NASO-RESPIRATORY FUNCTION AND
CRANIOFACIAL GROWTH
This volume includes the proceedings of a sponsored symposium
honoring
Professor Robert E. Moyers
Held February 23 and 24, 1979, in Ann Arbor, Michigan
Editor
JAMES A. McNAMARA, JR.
Associate Editor
KATHERINE A. RIBBENS
This volume is supported in part
by USPHS Grants DE 03610 and DE 04227
and a gift from the
Alpha Omega Foundation
Monograph Number 9
Craniofacial Growth Series
Center for Human Growth and Development
The University of Michigan
Ann Arbor, Michigan
1979
Copyright (@) 1979 by the Center for Human Growth and Development,
The University of Michigan
No part of this publication may be reproduced, stored in a retrieval
system, or transmitted, in any form by any other means, electronic,
mechanical, photocopying, recording or otherwise, without the prior
written permission from the Center for Human Growth and
Development.
SYMPOSIUM PARTICIPANTS
Speakers
CHARLES D. BLUESTONE, Director of Otolaryngology, Children's
Hospital of Pittsburgh; Professor of Otolaryngology, University of
Pittsburgh School of Medicine, Pittsburgh, Pennsylvania.
EGIL P. HARVOLD, Director, Center for Craniofacial Anomalies, Uni-
versity of California School of Dentistry, San Francisco, California.
STEN LINDER-ARONSON, Department of Orthodontics, Karolinska
Institute, Stockholm, Sweden.
ARTHUR J. MILLER, Associate Professor of Physiology, Center for
Craniofacial Anomalies, University of California School of Dentistry,
San Francisco, California.
WILLIAM R. SOLOMON, Professor of Internal Medicine (Allergy), The
University of Michigan School of Medicine, Ann Arbor, Michigan.
DONALD W. WARREN, Chairman, Department of Dental Ecology,
University of North Carolina School of Dentistry, Chapel Hill, North
Carolina.
Discussion Leaders and Panelists
ROBERT S. BUSHEY, Assistant Professor of Orthodontics, University
of Colorado, Denver, Colorado.
ROBERT J. ISAACSON, Chairman, Department of Growth and Devel-
opment, University of California School of Dentistry, San Francisco,
California.
CHARLES J. KRAUSE, Chairman, Department of Otolaryngology, The
University of Michigan School of Medicine, Ann Arbor, Michigan.
JAMES A. McLEAN, Professor of Internal Medicine (Allergy), The
University of Michigan School of Medicine, Ann Arbor, Michigan.
ROBERT M. RICKETTS, Professor of Orthodontics, Loma Linda Uni-
versity, Loma Linda, California.
BENI SOLOW, Associate Professor of Orthodontics, Royal Dental Col-
lege, Copenhagen, Denmark.
KENNETH. L. WATKIN, Assistant Professor of Speech and Hearing
Sciences, The University of Michigan, Ann Arbor, Michigan.
iii


SOLICITED CONTRIBUTORS
ELLEN GREVE, Clinical Orthodontist, 6 Bachsvej, Slagelse, Denmark.
BOB LANIER, Allergist, 5929 Lovell Avenue, Fort Worth, Texas.
NORMAN TREMBLAY, Allergist, 5929 Lovell Avenue, Fort Worth
Texas.
ROBERT M. RUBIN, Orthodontist, 300 E. Little Creek Road, Norfolk,
Virginia.
KAREN VARGERVIK, Associate Professor, Center for Craniofacial
Anomalies, University of California Medical Center, San Francisco,
California.
PETER VIG, Associate Professor of Orthodontics, School of Dentistry,
University of North Carolina, Chapel Hill, North Carolina.
DONALD G. WOODSIDE, Chairman, Department of Orthodontics,
University of Toronto, Toronto, Canada.
TABLE OF CONTENTS
Symposium Participants
Solicited Contributors
Preface
Neuromuscular Changes During Long-Term Adaptation of the
Rhesus Monkey to Oral Respiration
Arthur J. Miller and Karin Vargervik
The Growth in the Sagittal Depth of the Bony Nasopharynx in
Relation to Some Other Facial Variables
Sten Linder-Aronson and Donald G. Woodside
Aerodynamic Studies of Upper Airway: Implications for
Growth, Breathing and Speech
Donald W. Warren
Craniocervical Angulation and Nasal Respiratory Resistance
Beni Solow and Ellen Greve
Naso-Respiratory Function and Craniofacial Growth
Sten Linder-Aronson
Neuromuscular and Morphological Adaptations in
Experimentally Induced Oral Respiration
Egil P. Harvold
The Interdependence of the Nasal and Oral Capsules
Robert M. Ricketts
Adenoid Obstruction of the Nasopharynx
Robert S. Bushey
Respiratory Mode and Morphological Types: Some Thoughts
and Preliminary Conclusions
Peter S. Vig
The Role of Tonsils and Adenoids in the Obstruction of
Respiration
Charles D. Bluestone
Allergic Responses in the Upper Respiratory System
William R. Solomon
iii
ix
27
41
87
121
149
165
199
233
251
275
vii
An Approach to the Medical Management of Chronic
Mouthbreathing
Bob Lanier and Normand Tremblay 287
Diagnosis and Treatment Planning of Nasopharyngeal
Obstructions
Robert S. Bushey 301
The Orthodontist’s Responsibility in Preventing Facial
Deformity
Robert M. Rubin 323
viii
PREFACE
The topic of naso-respiratory function and craniofacial growth is of great
interest today, not only because it is an example of the basic biological
relationship of form and function, but also because it is of great practical
interest to pediatricians, otorhinolaryngologists, allergists, speech physi-
ologists, Orthodontists and other members of the medical and dental com-
munity. This relationship between the growth of the face and mouth-
breathing, tonsils, adenoids, allergies and other nasal obstructions was
examined during a multidisciplinary symposium held at The University of
Michigan on February 23 and 24, 1979.
The symposium was a “state of the art” look at our knowledge of the
effect of altered naso-respiratory function on the ultimate size and shape
of the craniofacial complex. Featured were presentations by six outstand-
ing investigators: Dr. Arthur J. Miller (neurophysiologist), Dr. Donald
W. Warren (speech physiologist), Dr. Charles D. Bluestone (otorhinolar-
yngologist), Dr. William R. Solomon (allergist), Dr. Egil P. Harvold
(orthodontist) and Dr. Sten Linder-Aronson (orthodontist).
As in past years, we have solicited a number of papers from individuals
throughout the world who are experts on this general topic in order to
make this volume as extensive a reference as is currently available. As
one can determine by reading the papers contained in this volume, there
is no universal agreement regarding the effect of altered nasal function on
the growth of the face. However, it is apparent that certain themes occur
repeatedly. -
The symposium honors Dr. Robert E. Moyers, Director of the Center
for Human Growth and Development and Professor of Dentistry. Dr.
Moyers has long been a renowned leader in the research of the relation-
ship of form and function in craniofacial growth.
The sponsors of the symposium, Dr. and Mrs. Verne Primack of Sagi-
naw, Michigan, once again have sought to provide a broad forum for new
concepts in the field of craniofacial biology. The goals of the sponsors
have apparently been met as evidenced by the continued attendance of
large numbers of individuals from varied backgrounds, including re-
searchers, students, practitioners and educators from a wide range of
medical, dental and other professional disciplines.
Mr. Kenneth E. Guire, Mr. Richard L. Miller and Mr. Robert L.
Wainright of the computer group of the Center for Human Growth and
Development are acknowledged for developing and implementing a new
ix
computer text editing procedure which greatly facilitates the editing, cor-
rection and final tape preparation of the manuscripts for publication. Ms.
Hattie Robertson was responsible for the typing using the text editing
process. Ms. Teryl Schessler was responsible for redrawing many of the
illustrations used in the text. We are most greatful for the assistance of
each of these individuals.
We also greatfully acknowledge the generous gift from the Alpha
Omega Foundation which, in part, made the publication of this volume
possible.
The person most responsible for the preparation of this volume is Ms.
Katherine A. Ribbens, Associate Editor. She was responsible for the
entire volume from the preparation of the manuscripts through editing
and rewriting to the painstaking examination of the galley and page
proofs. Without her it would have been difficult to produce this book at
the same level of quality in such a relatively short period of time.
J. A. McNamara
NEUROMUSCULAR CHANGES DURING
LONG-TERM ADAPTATION OF THE RHESUS
MONKEY TO ORAL RESPIRATION
Arthur J. Miller, Ph.D.
Karin Vargervik, D.D.S.
Center for Craniofacial Anomalies
University of California
Successful treatment of craniofacial anomalies and dental malocclusions is
inherently dependent on an understanding and proper use of the soft
tissue and muscle matrix which surrounds the craniofacial skeleton and
dental alveolar process. Stable treatment results depend upon establishing
a balanced neuromuscular function of the craniofacial muscles which sup-
port the structures in their position (Harvold, 75a, b, Vargervik, '78,
’79). Children who become mouth breathers due to partial or complete
blockage of the nasal airway demonstrate that changes in physiological
function of the upper respiratory tract result in skeletal adaptations
(Linder-Aronson, '75, '79; Bushey, '79).
Experimental Model
Studies at the Center for Craniofacial Anomalies, University of Califor-
nia, have been conducted on rhesus monkeys who adapt to oral respira-
tion. The studies have focused on correlating changes in cranioskeletal
morphology with adaptations of the neuromuscular system. Both nostrils
were blocked and the resulting neuromuscular and morphological modifi-
cations assessed. Data have been analyzed from two groups of experi-
mental animals. The first group consisted of animals who were 5 to 6
years of age and who had been mouth breathers for over three years prior
to neuromuscular assessment (Miller, '78a; Miller and Vargervik, '78).
The second group was comprised of younger monkeys, 2 to 4 years of
age, who were studied as they adapted to oral respiration within the first
six months after obstruction of the nasal airway (Miller and Vargervik, in
preparation).
The part of the neuromuscular study which is described in this paper
focuses on two issues: 1) which craniofacial muscles demonstrate changes
in neuromuscular patterns as the experimental animals adapt to oral res-
1
Neuromuscular Changes Following Altered Respiration

J ALVEOLAR SAC
S_-
BRONCHIOLES
C
ALVEOLAR DUCT
ALVEOLUS
Figure 1. The basic unit of the respiratory system, one of the over 300 million
alveoli used to exchange O2 and CO2 with the cardiovascular system.
piration; and 2) which type of neuromuscular patterns are exhibited by
the craniofacial muscles during this adaptation. It was postulated that
induced oral respiration establishes new neuromuscular patterns which, in
turn, are expected to correlate with morphological changes. The morpho-
logical adaptations of the skeleton include a significant increase in total
anterior face height and a more open gonial angle (Harvold et al., '73;
Harvold, '79; Harvold and Tomer, '79; Tomer and Harvold, '79). Soft
tissue adaptation can include the development of a notch in the upper lip
and various changes in the shape and size of the tongue.
RESPIRATORY PHYSIOLOGY
Function of the Pulmonary Alveoli and the Respiratory Tract
In order to understand the effects of oral respiration on the craniofacial
region, a concept of the underlying principles of neuromuscular function
of the primary and accessory respiratory muscles of the trunk and neck is
required. The major function of respiration is the exchange of oxygen and
carbon dioxide between the environment and the body’s cells. Oxygen is
used by the tissues in intracellular metabolism while carbon dioxide is the
end product of that metabolism. The respiratory system exchanges these
2
Miller
TOTAL AIRWAY RESISTANCE
(NASAL RESPIRATION)

| | |
NASAL LOWER AIRWAYS
PASSAGES vertºwa's (i.e. Bronchi, Bronchioles)
50% O % 30%
Table 1.
gases between millions of alveoli in the lungs and the capillaries of the
cardiovascular system (Fig. 1). The membranes of the alveoli are suffi-
ciently thin to allow oxygen and carbon dioxide to diffuse across them
and the adjacent membranes of the capillaries of the cardiovascular sys-
tem. Molecules of oxygen and carbon dioxide move between the gas
environment of air and the liquid environment of the blood vessels. The
rhythmic activity of respiration periodically alters the levels of these gases
within the alveoli and pulmonary capillaries, allowing these gases to re-
duce their pressure gradients.
The remainder of the respiratory system, consisting of the respiratory
tract, transfers the air between the alveoli and the environment. The
respiratory tract consists of the nasal and oral passages which connect
with the pharynx, larynx and trachea. The trachea divides into bronchi
which further divide into bronchioles with smaller diameters. This second
part of the respiratory system conducts the gases, protects the alveoli
from small particles, and humidifies and warms the incoming environ-
mental air before it reaches the alveoli (Fig. 2). -
The airflow through the respiratory tract is subject to resistance at
various levels (Table 1). Changes in the dimensions of the respiratory
tract, i.e., constriction or obstruction of the tract, will decrease airflow
(Solow and Greve, ’79; Warren, '79). Examples of changes in airflow due
to obstruction of the upper respiratory tract can be demonstrated in chil-
dren with large adenoids and tonsils. When changes in airway resistance
modifies airflow, respiratory muscles must increase their work to produce
changes in intrapulmonary pressure sufficient for air to be moved in and
out of the alveoli.
Modification of Respiration by Sensory Feedback
In the inital adaptation to the partial obstruction of the nasal airway,
the respiratory system increases its effort to compensate for the increased
nasal resistance. The augmented effort in motor output is initiated reflex-
3
Neuromuscular Changes Following Altered Respiration
CONCHAE
NASOPHARYNX
ORAL PHARYNX
LARYNX
TONGUE ARYTENOID
EPIGLOTTIS CRICOID
* -: , |
PLEURAL CAVITY tº TRACHEA
CHEST É "...
-D :
WALL =) :
AND $) & BRONCHUS
R|BS % CONDUCTING BRONCHUS
| i- PARIETAL PLEURA
— VISCERAL PLEURA
| – BRONCHIOLE
i-ALv. DUCT
§). * ALVEOL
DAPHRAGMs.
Figure 2. Schematic drawing of the respiratory system illustrating the two major
functional divisions: the respiratory tract which conducts air, and the alveoli
which allow exchange of gases between the environment and the blood.
ively by alterations in sensory feedback (Widdicombe, '74). Respiration is
modified by input from sensory receptors which are located within the
respiratory tract (Fig. 3). Receptors within the cardiovascular system in-
clude baroreceptors which respond to changes in blood pressure. The
baroreceptors are situated with the carotid and aortic vessels, the pul-
monary veins and the right auricle of the heart. Sensory receptors within
joints increase pulmonary ventilation during exercise. The respiratory





4
Miller
Emotions
Strong sensations
Pathologic afferents
Pain
JDoer air Dassages
OW 302 O(0ſ S
Sneeze
Ether, irritant gases
Reflexes
from chest wall
Extreme inflation Ether, irritant gases
or deflation
Chemoreceptors Baroreceptors
J. Pö. *co,
! pH, cyanide, etc. º
von Bezold p-A-"
~y_-
--- *..., Right auricle --
Nºy /* N-y
Veratrum alkaloids,
TP, etc.
... nºull' | 1 Pressure
(C) Chemoreceptors
Baroreceptors
Acid, alkali, K*, drugs Joint motion 1 Pressure
Figure 3. This diagram indicates sites of sensory receptors which modify respira-
tion altering its rate and depth (Lambertsen, '74; with permission).
system has receptors in the upper respiratory tract responding to irritant
gases, liquids and particles evoking a variety of reflexive effects that alter
respiration. The alveolar wall and chest wall have pulmonary stretch re-
ceptors that modify the respiratory phase and control respiratory freq-
uency (Clark and von Euler, '72). The first few inspirations following
nasal obstruction would be expected to be longer. This would be due to a
decreased tidal volume and a resulting lack of stretch of the lungs which
normally assist in terminating the inspiratory phase (Sant'Ambrogio and
Widdicombe, '65; Feldman and Gautier, '76).
However, the sensory receptors which are most affected by obstruction

















5
Neuromuscular Changes Following Altered Respiration
of the respiratory tract are chemoreceptors that monitor the levels of
oxygen and carbon dioxide in the body. These receptors are situated in
three regions: the carotid bodies at the junction of the external and
internal carotid arteries; the aortic bodies within the wall of the large
aortic vessel; and particular sites on the ventral surface of the medulla in
the brain stem of the central nervous system. The carotid bodies are the
most sensitive to changes in oxygen in the blood (Rosenstein et al., '74)
while the medullary site is particularly affected by levels of carbon diox-
ide (Mitchell et al., '63; Loeschcke, '73; Berger et al., 77).
The body protects its tissues by responding rapidly to changes in oxy-
gen and carbon dioxide within the blood. Obstruction of the upper respi-
ratory tract increases the resistance and decreases the airflow and oxygen
reaching the lungs. Simultaneously, airflow is impeded during expiration
so that carbon dioxide is not expelled at the normal rate. It is proposed
that bilateral obstruction of the nasal cavities leads to transient hypoxia
and hypercapnia and that these states stimulate neural receptors which
modulate the respiratory system (Fig. 4).
Response of the Respiratory Muscles to Changes in Sensory Feedback
The respiratory system increases its effort to compensate for decreased
airflow by using the muscles of the trunk and neck. This increased effort
is controlled by two nueromuscular mechanisms (Campbell, '58). One
mechanism increases the tension developed by the primary muscles
(Campbell et al., '64). The other mechanism recruits accessory respiratory
muscles which are normally not active in quiet respiration. Both mechan-
isms assist in decreasing resistance of the upper airway and increasing the
forces during inspiration and expiration (Gautier et al., '73).
The primary respiratory muscles are the diaphragm, the intercostal
muscles of the upper two intercostal spaces, the scaleni muscles and sev-
eral of the intrinsic and extrinsic laryngeal muscles (Andrews, '55; Green
and Neil, '55; Koepke et al., '55, 58; Murphy et al., '59; Petit et al., '60).
In normal, quiet breathing, most of these muscles contract during inspira-
tion. The laryngeal adductor muscles, the lateral cricoarytenoid and thy-
roarytenoid, are active in expiration (Green and Neil, '55; Faaborg-
Andersen, '57). The contraction of these primary respiratory muscles
enlarges the chest, lungs and respiratory tract during inspiration, as well
as maintaining the larynx in a stable position. At the completion of the
active inspiratory phase, the tension of the expanded chest and lungs is
sufficient to cause their recoil and expulsion of the air during quiet expi-
ration. These primary respiratory muscles will increase their electromy-
ographic activity (Fig. 5) and develop more tension during partial ob-
struction of the upper respiratory tract (Taylor, '60; Lourenco et al., '66).
Miller
Obstruction of Respiratory Tract
(i.e., Nasal plugs, large adenoids)
Increased Resistance of Respiratory Tract
W
Tronsient Decrease of Airflow
Transient Decrease of Oxygen (Hypoxia) and
Increase of Carbon Dioxide (Hypercapnia) in Blood
Alter Sensory Feedback from Carotid and
Aortic Bodies and Medullary Chemoreceptor Site
|
Central Respiratory Pathway Increases Work
(i.e., Pulmonary Ventilation)

W | W
Primary Respiratory Recruit Accessory
Muscles Increase Activity Respiratory Muscles
| _l

Increase Airflow by
using Orol Covity
F–––––––––––v––––––––––––
| Alteration of Neuromuscular Function of |
| Craniofacial Muscles |
| | |
| W W W
Alter Position of Alter Soft Tissue Alter Cronio-skeletol Form |
| Mandible ond Tongue (i.e., Upper lip, Tongue) |
— — — — — — — — — — — — — — — — — — — — — — — — — 4

Figure 4. Concepts of the physiological mechanism which contributes to changes
in the neuromuscular function of craniofacial muscles during obstruction of the
upper respiratory tract.
The accessory respiratory muscles are the abdominal muscles which
compress and force the diaphragm upward during expiration (Campbell,
‘52; Campbell and Green, '53a, b, Ogawa et al., '60; Hirschberg et al.,
'62). The serratus anterior, trapezius and sternomastoid muscles attach to
the chest wall at various points to assist in its movement during increased
pulmonary ventilation (Campbell, '55a; Raper et al., '66). The extrinsic
laryngeal muscles assist in the respiratory effort. Increased pulmonary
ventilation also recruits the intercostal muscles in descending interspaces
(Campbell, '55b; Fig. 6).
Neuromuscular Changes Following Altered Respiration
3OO
| FUWBAFTAF 23
O- - - - - - - - - - - - C COSTAL PART ~
e - – --e STERNAL PART 2:
2OO–
|
LOADS cm H2O
O I I I
º 4 8 |2 | 6 2O
—I l
Figure 5. The effect of increasing inspiratory loads on the electromyographic
discharge from three different regions of the diaphragm in the dog. Electromy-
ographic activity was recorded by implanted bipolar leads and integrated to obtain
relative levels. The animal was intubated with a tracheal tube. Inspiratory resis-
tance load was increased by lengthening the tracheal tube (Lourenco et al., '66;
with permission).
CRANIOFACIAL ADAPTATION TO NASAL OBSTRUCTION:
RHYTHMICITY
The principles underlying the adaptive responses of the muscles of the
trunk and limbs to obstruction of the respiratory tract have been pre-
sented. These concepts should apply also to the craniofacial muscles since
many of these muscles are involved in adaptation of the oral cavity as a
portion of the upper respiratory tract. The following series of experimen-
tal studies of adaptation to oral respiration in the rhesus monkey focuses
on these neuromuscular adaptations.
Rhythmicity in Craniofacial Muscles
The first goal of the experimental program was to determine which
craniofacial muscles were rhythmically active, discharging periodically
with primary respiratory muscles. Sixteen muscles were surveyed from
four regions in each experimental and control animal: the mandibular
elevators, mandibular depressors, tongue and facial muscles. Fine wires
(copper with nylon insulation, 50-75 micrometers in diameter) were
placed intramuscularly while the animals recovered from ketamine (3-10
mg/Kg). Electromyographic recordings were taken while the animal was
alert, unanesthetized, and sitting quietly in a chair.

8
Miller
7 5 .
7O -
75 -
6 O -
5 5-
5 O -
4 5 -
4 O -
3 5 -
3 O -
2 5 -
2 O -
O
| 5 -
| O - * }
| N S P J R A T O R Y V O L U M E AT PO | NT
OF ON SET OF M U S C L E ACT V | T Y
| N P E R C E N T OF PRE DI C T E O V | –
TAL CAPAC | T Y (PVC)
5 -
O -
W. W Wr W. W
| 2 3 4 5 6 7 8 9 || O || |
| N T E R COST AL MU S C L E S
Figure 6. The effects of increasing pulmonary ventilation on the recruitment of
intercostal muscles are shown. As inspiratory volume increases and becomes a
greater percentage of the vital capacity (i.e., maximum inspiratory effort), inter-
Costal muscles are successively recruited caudally. The graph depicts median value
of inspiratory volume at which the intercostal muscles begin to demonstrate an
electromyographic discharge (Campbell, '55b; with permission).



Neuromuscular Changes Following Altered Respiration
Rhythmicity After Long-Term Adaptation. The first study concentrated
on 16 adult rhesus monkeys, eight of which had exhibited long-term (3
years) adaptation to oral respiration and eight of which were controls
(Miller, '78a; Miller and Vargervik, '78). None of the control animals
demonstrated rhythmic activity in their jaw elevator muscles. In contrast,
three of the eight mouth-breathing monkeys rhythmically recruited their
temporalis, masseter and medial pterygoid muscles simultaneously.
None of the control monkeys exhibited rhythmic activity in the supra-
hyoid region, nor in the genioglossus or the dorsal fibers of the midline of
the tongue. Four of the experimental monkeys manifested rhythmicity in
all three regions when fully awake and unanesthetized.
The facial muscles demonstrated relatively little rhythmic discharge in
either the control or experimental monkeys. In the normal rhesus
monkey, muscles in the floor of the nares and in the lateral border of the
nasal cavity were rhythmically recruited. However, in four of the mouth-
breathing monkeys, muscles in a region just rostral to the horizontal
fibers of the orbicularis oris (designated as “lip elevator”) were also
recruited.
This study established that particular craniofacial muscles were rhyth-
mically recruited when the nasal cavity was obstructed. Yet some animals
demonstrated soft tissue changes in the shape of the tongue and upper lip
without measurable rhythmic recruitment. This suggests that neuromus-
cular changes might involve alterations in muscle discharge other than
rhythmicity (Miller, '78a, b, Miller and Vargervik, '79).
Rhythmicity During Early Adaptation. The next study included 26
young (juvenile-adolescent) rhesus monkeys, 13 of which were nose
breathers and were used as controls, and 13 of which had recently
adapted to mouthbreathing. In addition to assessing rhythmicity in this
study, the level of spontaneous discharge (i.e., tonic activity) was also
measured. Both rhythmic and tonic assessments were made with the ani-
mal sitting quietly and unanesthetized. Statistical analysis used both the
nonparametric Sign Test and Binomial Test (Siegel, '56).
Assessment of rhythmicity in the normal young nose-breathing
monkeys indicated that the dilator naris of the nares sometimes was
rhythmically active, as seen in the study using adult monkeys. In some of
the younger control monkeys rhythmicity was demonstrated in the genio-
glossus and dorsal fibers of the tongue, and the lip elevator and levator
labii of the upper lip region as well (Table 2).
In the experimental monkeys dramatic changes were demonstrated in
two ways during the first six months following obstruction of the nasal
cavity: 1) there was an increase in number of monkeys rhythmically re-
cruiting muscles from the upper lip and tongue (Table 2); and 2) rhythmic
10
Miller
CRANIOFACIAL MUSCLES
NORNWALLY RHYTHMICALLY ACTIVE
CONTROL EXPERIMENTAL
TONGUE REGION
GENIOGLOSSUS 5% 37% p=.00 l
(N=82) (N=63)
DORSAL FIBERS 3% 3.9% sº
(N=39) (N=23) p = .004
UPPER LIP REGION
LEVATOR LAB|| SUP. 10% 18%
(N=39) (N=28) NS
LIP ELEVATOR 13% 43% F.
(N=55) (N=55) p=.00 l
NARES (DILATOR NARIS) 6.8% 88% NS
(N=37) (N=26)
Non-parametric Sign Test; ot=.05
Table 2.
activity was induced in other craniofacial muscles, i.e., the geniohyoid
and digastric muscles of the suprahyoid region, the lateral lip and zygo-
maticus of the face, and the temporalis, medial and lateral pterygoid
muscles of the mandible (Table 3).
These results not only supported data gathered from adult mouth-
breathing monkeys but added new, pertinent data:
1. The rhythmic activity in the suprahyoid region of the adult mouth-
breathing monkey was now shown to recruit both the geniohyoid and
digastric muscles, but not the platysma. *
2. The horizontal fibers of the superior orbicularis oris were not re-
cruited, but the more rostral lip elevator region did demonstrate rhythmic
activity. The electromyographic pattern in the lip elevator could be distin-
guished from that of either the superior orbicularis oris or the dilator
Ila IIS.
3. While facial muscles other than the nares and upper lip were not
recruited in the eight adult experimental rhesus monkeys, there was evi-
dence in two of the young experimental animals that the zygomaticus and
lateral lip could be rhythmically recruited.
4. In some of the young rhesus monkeys who adapted to oral respira-
11
Neuromuscular Changes Following Altered Respiration
INDUCEMENT OF RHYTHMIC DISCHARGE IN
CRANIOFACIAL MUSCLES AFTER NASAL OBSTRUCTION
CONTROL EXPERIMENTAL
SUPRAH YOID REGION
GEN |OH YOID 0% 14% = .03 l
(N=78) (N=59) p = .
D|GASTRIC 0% 7 % -
(N=79) (N=59) p=.03 l
FACE & LIP REGION
LATERAL LIP (CANINUS) 0% 4% NS
(N=38) (N=28)
ZY GOMATICUS 0% 4% NS
* (N=37) (N=27)
MANDIBULAR REGION
ANT. TEMPORALIS l 9, 14% p=.03 l
(N=72) (N=59) e
NAED. PTERYGOID 0% 7% NS
(N=38) (N=27)
LAT. PTERYGOID 0% 10% p =.031
(N=68) (N=49) g
Non-parametric Sign Test; cº-.05
Table 3.
tion, individual jaw elevator muscles were rhythmically recruited. The
masseter did not demonstrate rhythmic activity in the first six months
following the onset of adaptation. Simultaneous recruitment of all jaw
elevator muscles, which was observed in the older animals, was not evi-
dent in the younger group.
The results, at both the onset of adaptation and after adaptation was
complete and patterns of oral respiration were well-established, indicated
that the central respiratory pathway controlling primary and accessory
respiratory muscles of the trunk, limbs and neck, could also synaptically
drive cranial motor neurons. These motor neurons were situated within
the hypoglossal nucleus innervating the tongue, in the trigeminal motor
neurons innervating the jaw opening or closing muscles and in those
select facial motor neurons specifically innervating the upper lip and
Ilaſ C.S.
12
Miller
LIP
ELEVATOR
DIAPHRAGM ºr =" 1000puV
Figure 7. Electromyographic recordings of the discharge patterns of the region of
the upper lip (craniofacial muscle) and the diaphragm (primary respiratory
muscle). The upper trace from each muscle is the electromyographic discharge
and the lower trace is the integration of that rectified signal with a mean voltage
integrator (time constant = 200 msec). The onset of diaphragmic discharge indi-
cates onset of inspiration. The lip elevator region refers to the area between the
floor of the nares and the horizontal fibers of the superior orbicularis oris. Note
that the maximum discharge of the lip elevator fibers occurs early in inspiration
and is distinctly different from that of the primary respiratory muscle.
Patterns of Rhythmicity
The rhythmic patterns of the craniofacial muscles were compared with
the discharge patterns of the primary respiratory muscles. Previous
studies have shown that the electromyographic discharge of the dia-
phragm muscle begins at the start of actual airflow during inspiration
(Koepke et al., '55; Lourenco et al., '66). The diaphragm and rostral
intercostal muscles reach their maximum discharge toward the end of
inspiration and complete their activity during the first phase of expiration.
There were two discharge patterns demonstrated by the craniofacial
muscles as compared to only one for the primary respiratory muscles such
as the diaphragm (Fig. 7). Muscles of the upper lip, nares and tongue
characteristically demonstrated maximum discharge at the onset of activ-
ity (Fig. 8). These electromyographic signals suggest that the actual ten-
Sion developed by the muscles is markedly different from that of the
diaphragm. The diaphragm slowly builds to its maximum tension while
the lip, nares and tongue muscles attain their maximum tensions immedi-
ately. These particular craniofacial muscles discharged during inspiration.
The second pattern was seen in muscles such as the mandibular eleva-
tors which gradually increased their electrical discharge to reach a maxi-
mum and were active predominantly during expiration. However, the

13
Neuromuscular Changes Following Altered Respiration
LEVATOR
LAB|| SUP.
NARES * ſº
(DILATOR NARIS)
Figure 8. Electromyographic discharge of two craniofacial muscles, the muscle
lateral to the nasal passage (levator labii Superioris proprius) and the muscle in
the floor of the nares (dilator naris). The upper trace from each muscle is the
discharge and the lower trace is the mean integration level. Both muscles demon-
strate maximum discharge early in inspiration.
discharge pattern of the lateral pterygoid muscle covered both inspiration
and expiration, as some experimental monkeys recruited the lateral ptery-
goid muscle at the onset of inspiration and others during expiration. If the
recording electrodes were placed in fibers of the lateral pterygoid muscle
which were active only during jaw opening, the rhythmic activity could be
present in either inspiration or expiration (Fig. 9). If they were placed in
fibers of the lateral pterygoid which were only active on closing of the jaw
(Miller and Vargervik, in preparation; Fig. 10), the rhythmic activity was
present only during expiration.
CRANIOFACIAL ADAPTATION TO NASAL OBSTRUCTION:
TONICITY
The adaptation of the craniofacial muscles during obstruction of the
nasal cavity led to a second, major neuromuscular change: an increase in
level of spontaneous background activity, i.e., tonic (Miller, '78a, b,
Miller and Vargervik, '78, '79; Fig. 11). Certain muscles of the head and
neck are normally active in the rhesus monkey who is sitting quietly
(Table 4). The normal young rhesus monkey can demonstrate a sustained
activity (i.e., greater than 10% of the observations) of the electromy-
ogram in either the geniohyoid or, less often, in the digastric muscle of
the suprahyoid region. The genioglossus muscle of the tongue demon-
strates sustained discharge. The region just lateral to the corner of the lip
is often tonically active without such tonic discharge for fibers of the
zygomatic, buccinator, superior or inferior orbicularis oris. The mentalis

14
Miller
LATERAL | 200LV
PTERYGOID
INTERCOSTAL 400, IV
l sec
Figure 9. The two distinct rhythmic patterns of the lateral pterygoid muscle are
compared to the respiratory cycle. The upper trace is the electromyographic
discharge and the lower trace is the mean voltage integration. Inspiration begins
with onset of electromyographic activity in the intercostal muscle. Left: Lateral
pterygoid activity during inspiration. The fibers of the lateral pterygoid muscle
discharged only during lowering of the mandible. Right: Lateral pterygoid activity
during expiration. The muscle fibers discharged only during closing of the jaw.
ſ t
ANI TEMPORALIS (R.I., --—— + t |200 av
LA I. PIERYGOID (RI.) —4-4-4–4–4– j400 Juv
| 400 pu"W
LA I. PIERYGOID (L.I.)
SUPRAH YOID |200 ºv
ZZZZ H Hº-
Clench TONGUE PRO TRUSION 4 SEC
—l———
Figure 10. Two types of discharge from the lateral pterygoid muscle recorded
during jaw opening and closing. The electrodes in the right lateral pterygoid
muscle are recording from fibers which are active during clenching and repeated
raising of the mandible; bursts of clenching coincided with those of a jaw elevator
muscle, the anterior temporalis. The electrodes in the left lateral pterygoid are
recording from fibers that contract only during jaw opening, which activity coin-
cided with that of the suprahyoid region. The jaw did not consistently deviate to
one side or protrude but repeatedly lowered as the tongue periodically protruded.
in both the rhesus monkey and human subjects monitored in our labora-
tory demonstrated a tonic discharge. The anterior temporalis maintained
a tonic discharge as one of the mandibular elevator muscles.
Adaptation to nasal obstruction does alter this tonicity. The number of
experimental animals that demonstrated tonicity of the above muscles
which were normally active in the control animals, did not significantly


15
Neuromuscular Changes Following Altered Respiration
A ronic-PHAsic B PHASIC
200 - TOTAL : 2248 400 H. TOT A L: 074
ME AN: 62 + 23 MSEC MEAN: 58 til 8 MSEC
o: 150 H MODE: 68 MSEC 300 H NAO DE: 25 M SEC
§ MEDIAN: 63 NASEC MEDIAN: 35 M SEC
; I OO H. BINW D: 5 M SEC 200 H. B|NW D: 10 MSEC
22
50 H IOO H 26 Days
7043
O —r-—I I I l O T- I -I I l
50 TOO 150 200 250 50 100 150 200 250
INTERVALS (msec)
EMG
INTEGRATION
\"\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\\!\!\!\!\!\ ||||||| | | -
\ \}, \"\"." º ~\-TV As
\\\\\\\\\\\\\|\ \"\"\\\\\\\ |\ \,\!\! |
\\ º - | | \\ \ w,
INTERVALS SHORT
W. v. ". ^..
.*.*. 8. - s *_ * *
pe º * - nº-" * "-- J-
~~~~ * 1. ºr * ". tº-
LONG - *ms *-
1–
l sec
Figure 11. Example of the two major types of muscle discharge (EMG) in experi-
mental monkeys adapting to oral respiration. EMG activity recorded from the lip
elevator in two animals is compared. (A) Display on left side in descending order
shows the distribution of intervals for the integration of a combined tonic-phasic
EMG; an example of the original EMG; the integration of the EMG; and the
density of the repeated integrations. (B) The right display indicates EMG activity
that is only phasic. In the example, the phasic activity is periodic and rhythmically
discharging in synchrony with respiration.
change. However, tonicity was induced in craniofacial muscles that do not
normally exhibit tonicity. In the young rhesus monkey, during the first six
months of adaptation to nasal obstruction, tonic discharge was initiated in
certain craniofacial muscles previously not engaged or only rarely active















16
Miller
CRANIOFACIAL MUSCLES
NORMALLY TONICALLY ACTIVE
CONTROL EXPERIMENTAL
SUPRAHYOID REGION
GENIOHYOID 45%
54%
NS p = .
(N=78) (N=59) p = .202
D|GASTRIC 19% 3 l 9% -
(N-79) (N=59) NS p- .212
TONGUE REGION p
GENIOGLOSSUS 57% 52% sº
O O N - .
(N=82) (N=63) S p=.500
FACE & LIP REGION
LIP ELEVATOR 26% 26% ~.
(N 69) (N 58) NS p-.6l3
LATERAL LIP (CANINUS) 37% 39% =
(N=38) (N=28) NS p-.254
MENTALIS 63% 71% =
(N=14) (N=16) NS p-.500
MANDIBULAR REGION
ANT. TEMPORALIS 53% 49% NS p- .2
(N=72) (N=59) S p=.29 l
Non-parametric Sign Test; oc=.05
Table 4.
(Table 5). The platysma, zygomaticus and buccinator were recruited toni-
cally in only a few observations of the thirteen experimental animals. The
dorsal fibers of the tongue were tonically active in a significant number of
experimental animals. Tonicity was initiated significantly in the constric-
tor muscle around the lips, the superior and inferior orbicularis oris. Both
the medial and lateral pterygoid muscles demonstrated significant in-
creases in the presence of tonic discharge.
CORRELATION OF NEUROMUSCULAR CHANGE WITH TIME
These results demonstrate that during the rhesus monkey’s adaptation
to oral respiration, either as a juvenile or adult, the neuromuscular sys-
tem of the craniofacial region undergoes modification in its mode of
17
Neuromuscular Changes Following Altered Respiration
INDUCEMENT OF TONIC DISCHARGE IN
CRANIOFACIAL MUSCLES AFTER NASAL OBSTRUCTION
CONTROL EXPERIMENTAL
SUPRAH YOID REGION
PLATYSNAA 0%
4%
(N=40) (N=27) NS
TONGUE REGION
DORSAL FIBERS 8% 35% =
(N=39) (N=23) p=.03 l
LIP REGION
SUP. ORBIC. ORIS 2% 25% = .05
(N=41) (N=24) p = .
|NF. ORBIC. ORIS 5% 32% tº-
(N=37) (N=28) p=.035
FACIAL REGION
ZY GOMATICUS 3% ll 9% NS
(N=37) (N=27)
BUCCINATOR O % 7%
(N=30) (N=29) NS
MANDIBULAR REGION
MED. PTERYGOID 3% 19% = .03 l
(N=38) (N=27) p=.
LAT. PTERYGOID 0% 14% º
(N=68) (N=49) p=.008
Non-parametric Sign Test; oc=.05
Table 5.
discharge pattern. These changes in discharge pattern do not affect all
craniofacial muscles. Furthermore, specific muscles are recruited differ-
ently in indvidual animals with nasal obstruction. However, a trend does
occur in the adaptation of a particular muscle over time, and we are in
the process of analyzing the significance of these findings. An example of
this approach is shown for three muscles: the anterior temporalis as a
mandibular elevator and postural muscle; the digastric as a jaw depressor;
and the genioglossus as a tongue protruding muscles (Fig. 12).
18
Miller
[...] NO CHANGE
(quiet, tonic, rhythmic)
TONIC p < .00 l
RHYTHMIC
+ l2 P-
- – ls? AMONTH
p < .02
+ 8 +
p < |
O
ºs
u +4 F , NS
> NS NS
: ź
†—OH –
>
2 ü
<!
# z – 4'- p < .001
3. + \ 4 T- | |
5 5th MONTH
§ ſ
ll- + l2.H.
O
Oz
Lll
É +8.
m)
2.
u + 4 HT
> NS
U
<ſ ſ { { -
i
ems
4
|-
ANTERIOR DIGASTRIC GENIO-
TEMPORALIS GLOSSUS
Non-parametric Binomial Test; oc=.05
Figure 12. Tonic and rhythmic neuromuscular patterns resulting from adaptation
to Oral breathing, varied with regard to time of onset for individual craniofacial
muscles. For each animal (N=13), data obtained before placement of the nose
plugs were compared with data obtained one month after nasal blockage (top)
and the one-month data were compared with the data recorded after five months
of oral respiration (bottom).



19
Neuromuscular Changes Following Altered Respiration
A few animals initiated rhythmic activity in the anterior temporalis
muscle during both the first and fifth months of adaptation, but not signifi-
cantly. In contrast, a significant number of animals established a tonicity of
the anterior temporal muscle after five months of oral respiration. In a few
experimental animals, rhythmicity in the digastric muscle was manifested
after both one and five months of oral respiration, but tonicity was a more
common finding. Tonicity of the digastric muscle was more significantly
evident in experimental animals after the first month than after five
months. By five months, several animals had lost this tonicity.
Blocking the nasal cavity induced rhythmicity in the genioglossus
muscle of many more experimental animals after one month than after
five months. In contrast, tonicity was recorded in a larger number of
animals after the fifth month than after the first month of oral respiration.
These temporal sequences in alterations in neuromuscular patterns for
individual craniofacial muscles suggest that morphological changes of the
soft tissue and cranioskeleton may be correlated ultimately with adapta-
tion to neuromuscular function.
MECHANISMS UNDERLYING NEUROMUSCULAR CHANGE
Neuromuscular adaptation of craniofacial muscles during oral respira-
tion is ultimately based on the neurophysiological reflex arcs and synaptic
contacts that modify the cranial motor neurons. The modification in syn-
aptic control of cranial motor neurons depends upon central and periph-
eral sensory feedback (Miller and Vargervik, '78). The organization of
the neural control for the head and neck exhibits certain properties that
differ from those for the limbs and the remainder of the body. The jaw,
facial and tongue muscles lack many control mechanisms evident at the
spinal cord level. The stretch reflex which uses the muscle spindle re-
sponding to length and is modulated by the gamma motor neuron system
is rare or absent in the jaw depressor muscles and facial muscles. The
physiological concept of reciprocal innervation between antagonistic
muscles around a joint is not demonstrated with the jaw depressor and
elevator muscles of the temporomandibular joint.
The concept of the spinal motor neuron serving as an error detector
between the centrally transmitted signal and the peripheral feedback re-
lies on the reciprocal interaction of sensory input from the muscle spindle
monitoring length and the tendon organ sensing tension. The jaw, facial
and tongue muscles demonstrate few such tension receptors indicating
that cranial motor neurons are modified synaptically by other types of
peripheral inputs. The absence of such proprioceptive interaction at the
cranial level is compensated for by sensory feedback from the facial skin,
oral-pharyngeal mucosa, periodontia and temporomandibular joint.
20
Miller

CEREBRAL CORTEX BASAL CEREBELLUM
(Position sense) GANGLIA (Rote, direction and
speed of movement)
EXCITATORY CENTRAL INPUTS INHIBITORY CENTRAL INPUT
Central Respiratory Drives 2^ Sleep states (i.e. REM)
*
Vestibular (Head position) S >> _2^
S \ * ^ + 2 *
EXCITATORY PERIPHERAL S \ SS- Pr’ INHIBITORY PERIPHERAL
INPUTS + N INPUTS
Stimulus: + MOTOR NEURONS Stimulus:
Temporomandibular — IN HYPOGLOSSAL tº a { Pressure or topping teeth
joint (Jaw depression) NUCLEUS (XII) Pinch tongue
Nerves: | Nerves:
Glossophoryngeal O + MOTOR UNITS Lingual
Superior Laryngeal Y— |N GENIOGLOSSAL —ſ Inferior Alveolar
\ MUSCLE O Infraorbitol
|
| Nerves:
º Mosseter
* : Digastric
Figure 13. Schematic diagram of the central and peripheral synaptic inputs that
modify the discharge of motor neurons in the hypoglossal nucleus innervating the
genioglossus muscle. Plus symbols indicate excitation of motor neurons and the
negative symbol demonstrates an inhibitory influence. The genioglossus is active
in tongue protrusion and exhibits both a rhythmic and tonic discharge which is
dependent on the synaptic control of its motor neurons.
The effects of these various inputs are illustrated in Figure 13 for one
group of cranial motor neurons, those hypoglossal neurons innervating
the genioglossus muscle. A similar concept could be applied to specific
motor neurons innervating jaw elevator or depressor muscles. The genio-
glossus motor neurons are excited by at least four central pathways: inter-
neurons governing central respiratory drive, and neurons within the swal-
lowing, masticatory and vocalization pathways. The same motorneurons
are affected by two major peripheral inputs: those from the temporoman-
dibular joint and those from sensory input with origins in the deep phar-
yngolaryngeal structures innervated by the glossopharyngeal and superior
laryngeal nerves.
In contrast, the inhibitory inputs on genioglossus motor neurons in-
clude stimulation of the facial and oral structures. These stimuli include
pressure applied to the teeth and touch applied to the dorsal surface of
the tongue. Sensory input from the mandibular muscles, both jaw eleva-
tors and depressors, has a sustained inhibitory effect on genioglossus
motor neurons through indirect inhibitory mechanisms modifying excita-
tory input. Sensory input predominantly over the trigeminal nerves is
21
Neuromuscular Changes Following Altered Respiration
inhibitory to the cranial motor neurons innervating this protruding
muscle. Loss of consciousness and particular stages of sleep modify the
tone of the tongue muscle. The sustained discharge of the tongue muscle
varies over a 24 hour period.
While neurophysiological studies have established that multiple inputs
modify cranial motor neurons to this tongue muscle, the final determina-
tion as to whether the genioglossus muscle will alter its level of discharge
depends on the balance of the total synaptic inputs. This balance depends
on the effect of excitatory inputs that decrease the threshold to discharge
the individual motor neuron, or on the inhibitory inputs which increase
the threshold. The shift in balance of the total synaptic input determines
whether or not a given motor neuron will discharge, a given motor unit
will contract, and a specific muscle will increase its discharge. Only by
analysis of natural or physiologically induced modifications in sensory
feedback or central control, can we begin to decipher which neurophysio-
logical mechanisms and pathways become critical factors in altering neu-
romuscular function.
SUMMARY
Bilateral obstruction of the nasal cavity in young rhesus monkeys alters
the electromyographic discharge of specific mandibular and facial
muscles. Rhythmic activity correlated with respiration is normally present
in five craniofacial muscles in the control animals using nasal respiration.
The experimental animals adapt to oral respiration increasing the prob-
ability of rhythmicity in those tongue and lip elevator muscles, and induce
rhythmicity in four additional muscles of the mouth-breathing monkey. A
second type of electromyographic discharge, sustained or tonic activity, is
evident in seven craniofacial muscles of the normal monkey. The experi-
mental animals induce sustained discharge in four additional muscles,
particularly, the constrictors of the lips and both pterygoid muscles.
CONCLUSIONS
Experimentally induced alterations of naso-respiratory function modi-
fies sensory feedback which reflexively induces changes in neuromuscular
function of craniofacial muscles. These neuromuscular changes involve
the alteration of the discharge of specific craniofacial muscles in one of
two modes: (1) inducing a periodicity in discharge correlated with rhyth-
mic respiration; and/or (2) initiating a sustained, tonic discharge. Long-
term changes in craniofacial function correlate with changes in soft tissue
and precede the morphological adaptations of the cranioskeleton.
22
Miller
ACKNOWLEDGEMENTS
This study was supported by a grant from the National Institute of Dental
Research, DE 02739.
REFERENCES
Andrews, B. L. The respiratory displacement of the larynx. A study of the inner-
vation of accessory respiratory muscles. J. Physiol. (London), 13:474-487,
1955.
Berger, A. J., R. A. Mitchell and J. W. Severinghaus. Regulation of respiration.
New Eng. J. Med. 297.92-97, 1977.
Bushey, R. S. Diagnosis and treatment planning of nasopharyngeal obstructions.
In: Naso-Respiratory Function and Craniofacial Growth. J. A. McNamara Jr.
(Ed.), Monograph 9, Craniofacial Growth Series, Center for Human Growth
and Development, The University of Michigan, Ann Arbor, 1979.
Bushey, R. S. Adenoid obstruction of the nasopharynx. In: Naso-Respiratory
Function and Craniofacial Growth. J. A. McNamara Jr. (Ed.), Monograph 9,
Craniofacial Growth Series, Center for Human Growth and Development,
The University of Michigan, Ann Arbor, 1979.
Campbell, E. J. M. An electromyographic study of the role of the abdominal
muscles in breathing. J. Physiol. 117:222-233, 1952.
Campbell, E. J. M. The role of the scalene and sternomastoid muscles in breath-
ing in normal subjects. An electromyographic study. J. Anat. 89:378-386,
1955a.
Campbell, E. J. M. An electromyographic examination of the role of intercostal
muscles in breathing in man. J. Physiol. (London), 129:72-76, 1955b.
Campbell, E. J. M. Respiratory Muscles and Mechanics of Breathing. Yearbook
Publishers, Chicago, 1958.
Campbell, E. J. M., C. J. Dickinson and J. B. L. Nowell. The immediate effects
of added loads on the inspiratory musculature of the rabbit. J. Physiol. (Lon-
don), 172:321-331, 1964.
Campbell, E. J. M. and J. H. Green. The variations in intra-abdominal pressure
and the activity of the abdominal muscles during breathing: A study in man. J.
Physiol. (London), 122:282-290, 1953a. *
Campbell, E. J. M. and J. H. Green. The expiratory function of the abdominal
muscles in man. An electromyographic study. J. Physiol. (London),
120:409–418, 1953b.
Clark, F. J. and C. von Euler. On the regulation of depth and rate in breathing.
J. Physiol. (London), 222:267-295, 1972.
Faaborg-Andersen, K. L. Electromyographic investigation of intrinsic laryngeal
muscles in humans. Acta Physiol. Scand. 41(Suppl. 140):1-148, 1957.
Feldman, J. L. and H. Gautier. Interaction of pulmonary afferents and pneumo-
taxic center in control of respiratory patterns in cats. J. Neurophysiol.
39:31-44, 1976.
23
Neuromuscular Changes Following Altered Respiration
Gautier, H., J. E. Remmers and D. Bartlett, Jr. Control of the duration of
expiration. Resp. Physiol. 18:205-221, 1973.
Green, J. G. and E. Neil. The respiratory function of the laryngeal muscles. J.
Physiol. 129:134-141, 1955.
Harvold, E. P. Experiments on mandibular morphogenesis. In: Determinants of
Mandibular Form and Growth. J. A. McNamara, Jr. (ed.), Monograph No. 4,
Craniofacial Growth Series, Center for Human Growth and Development,
The University of Michigan, Ann Arbor, pp. 155-177, 1975a.
Harvold, E. P. Centric relation. A study of pressure and tension systems in bone
modeling and remodeling. Dent. Clin. N. Am. 19:473–484, 1975b.
Harvold, E. P. Neuromuscular and morphological adaptations in experimentally
induced oral respiration. In: Naso-Respiratory Function and Craniofacial
Growth. J. A. McNamara, Jr. (ed.), Monograph No. 9, Craniofacial, Growth
Series, Center for Human Growth and Development, The University of Michi-
gan, Ann Arbor, 1979.
Harvold, E. P. and B. S. Tomer. Primate experiments on soft tissue adaptation to
oral respiration. J. Dent. Res. 58(Special Issue A):275, 1979.
Harvold, E. P., K. Vargervik and G. Chierici. Primate experiments on oral
Sensation and dental malocclusion. Am. J. Orthodont. 63:494-508, 1973.
Hirschberg, G. G., J. P. Adamson, L. Lewis and K. J. Robertson. Patterns of
breathing of patients with poliomyelitis and respiratory paralysis. Arch. Phys.
Med. 43:529-533, 1962.
Koepke, G. H., A. J. Murphy, J. W. Rae, Jr. and D. G. Dickinson. An electro-
myographic study of some of the muscles used in respiration. Arch. Phys.
Med. 36:217-222, 1955.
Koepke, G. H., E. M. Smith, A. J. Murphy and D. G. Dickinson. Sequence of
action of the diaphragm and intercostal muscles during respiration. I. Inspira-
tion. Arch. Phys. Med. 39:426-430, 1958. -
Lambertsen, C. J. Neurogenic factors in control of respiration. In: Medical Physi-
ology. V. B. Mountcastle (ed.), 13th Edition, C. V. Mosby, St. Louis, pp.
1423–1446, 1974.
Linder-Aronson, S. Effects of adenoidectomy on dentition and facial skeleton
over a period of five years. In: Transactions of the Third International Ortho-
dontic Conference. J. Cook (ed.), Crosby, Lockwood and Staples, Great Brit-
ain, pp. 85-100, 1975.
Linder-Aronson, S. Naso-respiratory function and craniofacial growth. In: Naso-
Respiratory Function and Craniofacial Growth. J. A. McNamara, Jr. (ed.),
Monograph No. 9, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, 1979.
Linder-Aronson, S. and D. G. Woodside. The growth in the sagittal depth of the
bony nasopharynx in relation to some other facial variables. In: Naso-
Respiratory Function and Craniofacial Growth. J. A. McNamara, Jr. (ed.),
Monograph No. 9, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, 1979.
Loeschcke, H. H. Respiratory chemosensitivity in the medulla oblongata. Acta
Neurobiol. Exp. (Warsaw), 33:97-112, 1973.
24
Miller
Lourenco, R. V., N. S. Chernicack, Jr., J. R. Malm and A. P. Fishman. Nervous
output from the respiratory center during obstructed breathing. J. Appl. Phys-
iol. 21:527–533, 1966.
Miller, A. J. Electromyography of craniofacial musculature during oral respira-
tion in the rhesus monkey (Macaca mulatta). Arch. Oral Biol. 23:145-152,
1978a.
Miller, A. J. Spectral analysis of the electromyogram of the temporal muscle in
the rhesus monkey (Macaca mulatta). Clin. Neurophys. Electroenceph.
44:317-327, 1978b.
Miller, A. J. and K. Vargervik. Neural control of oral respiration in the rhesus
monkey. In: Muscle Adaptation in the Craniofacial Region. D. S. Carlson and
J. A. McNamara, Jr. (eds.), Monograph No. 8, Craniofacial Growth Series,
Center for Human Growth and Development, The University of Michigan,
Ann Arbor, pp. 133-157, 1978.
Miller, A. J. and K. Vargervik. Recruitment of craniofacial muscles in oral respi-
ration. J. Dent. Res. 58(Special Issue A):334, 1979.
Mitchell, R. A., H. H. Loeschcke, W. H. Massion and J. W. Severinghaus.
Respiratory responses mediated through superficial chemosensitive areas on
the medulla. J. Appl. Physiol. 18:523-533, 1963.
Murphy, A. J., G. H. Koepke, E. M. Smith and D. G. Dickinson. Sequence of
action of the diaphragm and intercostal muscles during respiration. II. Expira-
tion. Arch. Phys. Med. 40:337-342, 1959.
Ogawa, T., N. C. Jefferson, J. E. Toman, T. Chiles, A. Zambetolglou and H.
Necheles. Action potentials of accessory respiratory muscles in dogs. Am. J.
Physiol. 199:569-572, 1960.
Petit, J. M., G. Milic-Emili and L. Delhez. Role of the diaphragm in breathing in
conscious normal men: an electromyographic study. J. Appl. Physiol.
15:1101-1106, 1960.
Raper, A. J., W. T. Thompson, Jr., W. Shapiro and J. L. Patterson, Jr. Scalene
and sternomastoid muscle function. J. Appl. Phsyiol. 21:497-502, 1966.
Rosenstein, R., L. E. McCarthy and L. L. Borison. Influence of hypoxia on tidal
volume response to CO2 in decerebrate cats. Resp. Physiol. 20:239-250, 1974.
Ruch, T. C. and H. D. Patton. Physiology and Biophysics. 19th Edition, W. B.
Saunders, Philadelphia, 1965.
Sant'Ambrogio, G. and J. G. Widdicombe. Respiratory reflexes acting on the
diaphragm and inspiratory intercostal muscles of the rabbit. J. Physiol. (Lon-
don), 180:766-779, 1965.
Siegel, S. Nonparametric Statistics for the Behavioral Sciences. McGraw-Hill, New
York, 1956.
Solow, B. and E. Greve. Craniocervical angulation and nasal respiratory resis-
tance. In: Naso-Respiratory Function and Craniofacial Growth. J. A. McNam-
ara, Jr. (ed.), Monograph No. 9, Craniofacial Growth Series, Center for Hu-
man Growth and Development, The University of Michigan, Ann Arbor,
1979.
Taylor, A. The contribution of the intercostal muscles to the effort of respiration
in man. J. Physiol. (London), 151:390-402, 1960.
25
Tomer, B. S. and E. P. Harvold. Experiments on mandibular rotation in growing
primates. J. Dent. Res. 58(Special Issue A):376, 1979.
Vargervik, K. New bone formation secured by oriented stress in maxillary clefts.
Am. Cleft Palate J. 15:132-140, 1978.
Vargervik, K. Temporalis and masseter activity in subjects with craniosynostosis.
J. Dent. Res. 58(Special Issue A):148, 1979.
Warren, D. A. Aerodynamic studies of upper airway: implications for growth,
breathing and speech. In: Naso-Respiratory Function and Craniofacial Growth.
J. A. McNamara, Jr. (ed.), Monograph No. 9, Craniofacial Growth Series,
Center for Human Growth and Development, The University of Michigan,
Ann Arbor, 1979.
Widdicombe, J. G. Reflex control of breathing. In: Respiratory Physiology. J. G.
Widdicombe (ed.), Ser. 1, Vol. 2, MTP International Review of Science,
Butterworth, London, pp. 273-302, 1974.
26
THE GROWTH IN THE SAGITTAL DEPTH OF
THE BONY NASOPHARYNX IN RELATION TO
SOME OTHER FACIAL VARIABLES
Sten Linder-Aronson, L. D.S., Ph.D.
Department of Orthodontics
Karolinska Institute
Donald G. Woodside, D.D.S.
Department of Orthodontics
University of Toronto
The size of the nasopharynx is of particular importance in determining
whether the mode of breathing is nasal or oral. The posterior wall of the
nasopharynx is covered by a layer of lymphoid tissue that often undergoes
hypertrophy during the period prior to puberty. This enlargement of
adenoids (adenoid vegetation) increases the chances of constricting the
nasopharyngeal airway. Consequently, the relationship between the size
of the bony nasopharynx and the size of the adenoids is crucial (Ricketts,
'54; Subtelny, '54; Linder-Aronson, '70).
The size and shape of the bony nasopharynx is determined by its
height, width and depth. Earlier studies agree that in growing children
both the height and width of the nasopharynx are largely dependent upon
age (Brodie, '41; King, '52; Bergland, '63; Handelman and Osborne,
’76). However, there appears to be some difference of opinion as to what
determines sagittal depth. Rosenberger (34) stated that the size of the
nasopharynx increases in conjunction with the growth of the cranial base
and forward development of the midface, while Brodie (’41) stated that
the depth of the nasopharynx is established during the first year or two of
life and thereafter remains constant.
King ('52) in a serial investigation of males and females examined
various nasopharyngeal dimensions from three months to 16 years. The
depth of the nasopharynx as measured from the atlas, the first cervical
vertebra, to pterygomaxillare increased during this period by an average
of 3.8 mm. King stated that the total depth of the nasopharynx is estab-
lished during the first or second year of life. He also thought that the
increase in depth of the nasopharynx due to growth at the spheno-
occipital synchondrosis is minimized by forward growth of the anterior
arch of atlas.
27
Growth in the Sagittal Depth of the Bony Nasopharynx
In contrast Subtelny ('57), in a serial cephalometric study of 30 sub-
jects, found that the depth of the nasopharynx increased from 3 months
to 17 years of age. During the first 11 years of life, approximately, there
were periods of apparent increase and decrease of the anteroposterior
depth of the nasopharynx. After 12 years of age, the anteroposterior
depth of the nasopharynx was found to increase steadily until 17 years of
age.
Handelman and Osborne ('76) measured the height, depth and area of
the nasopharynx of 12 subjects for 17 years, beginning at age 9 months.
In contrast with Subtelny's findings, they found that the nasopharyngeal
depth was constant from infancy to maturity in females but increased
moderately from three years and nine months to maturity in males.
Since opinions differ with regard to the sagittal development of the
bony nasopharynx, the present investigation was initiated to study longi-
tudinally the sagittal growth of the nasopharynx from 6 to 20 years of age
in a large sample.
MATERIALS
The sample consisted originally of 140 boys and 120 girls selected from
the serial Burlington Growth Center sample in Toronto, Canada. The
number of subjects examined in each group decreased through the years
as subjects dropped out of the study (Table 1). The Burlington popula-
tion is predominantly Caucasian and is considered to be representative of
the Province of Ontario (population 8,000,000), Canada (Burlington Or-
thodontic Research Center Progress Report, 1956). -
METHOD
The distances within the facial skeleton were measured from tracings of
lateral skull radiographs in the following manner (Fig. 1):
1. Posterior cranial base length was represented by a line drawn from
basion (ba) to sella turcica (s);
2. Anterior cranial base length was represented by a line drawn from
Sella turcica to nasion (n);
3. Sagittal depth of the nasopharynx was represented by a line drawn
from basion to pterygomaxillare (ptm);
4. Total cranial base length was represented by a line drawn from
nasion to basion;
5. Maxillary length was represented by a line drawn from pterygomaxil-
lare to subnasale (sn);
6. Lower facial height was represented by a line drawn from subnasale
to gnathion (gn); -
28
Linder-Aronson
Age 6 9 12 14 16 18 20
(years)
Male 140 139 132 121 114 101 60
Female 120 115 113 103 99 80 40
Table 1. The number of subjects in each age group.
7. Total facial height was represented by a line drawn from nasion to
gnathion; t
8. Upper facial height was represented by a line drawn from nasion to
Subnasale.
The measurements were made using the Burlington Research Center’s
Gradicon 100 digitizer which is accurate within +0.1 mm. In cases where
there was difficulty in locating certain intracranial reference points, the
corresponding radiograph taken in the rest position was used except for
the measurements of lower and total facial height. Values for mandibular
length and the gonial angle have been taken from an earlier investigation
of Woodside ('69) in which the same sample was used.
Measurement Error
The intra-observer error in determining the sagittal depth of the bony
nasopharynx was calculated using 20 randomly selected cases (Table 2)
and found to be no more than +0.37 mm. The variance of the intra-
observer error was 1.2% - 1.5% of the total variance for the sagittal
depth of the bony nasopharynx. This indicates a satisfactory degree of
accuracy in duplicating measurements. -
The inter-observer error was calculated from double determinations of
the sagittal depth of the bony nasopharynx in 55 males and 64 females.
No systematic difference could be seen in the measurements made by the
two observers. Correlation analyses were done, the results of which re-
vealed strongly significant correlations between the measurements made
by the two observers (r = 0.93 for males and r = 0.92 for females). The
rate of inter-observer error found in this study shows that there was
agreement between observers with regard to identification of the refer-
ence points. In some cases, however, differences of opinion were noted.
The size of the measurement error is particularly important in a study
of this nature where the average yearly growth increment is a mere 0.45
mm compared to an intra-observer measurement error of 0.37 mm. In
this study of 260 children, the possibility that measurement errors will
cancel each other were considered to be relatively good.
29
Growth in the Sagittal Depth of the Bony Nasopharynx
gn
Figure 1. Reference points used to measure total, anterior and posterior cranial
base length; Sagittal depth of the nasopharynx; maxillary length; and upper, lower
and total facial height.
Population standards for the sagittal depth of the bony nasopharynx
were established on both a mean and percentile basis, using the data
available from the total Burlington sample. Percentiles were plotted for
ages 6, 9, 12, 14, 16, 18 and 20 years, and velocity curves were prepared
also for the same ages. The mean and 50th percentile velocity curves for
male and females were then drawn.
A correlation analysis was done between the sagittal depth of the bony
nasopharynx and the different facial variables presented in Figure 1. In
addition, correlations between the bony nasopharynx and both the gonial
angle and mandibular length were calculated.

30
Linder-Aronson
Measurement error SD SD” in 96 of Sº SD in % of Sº
140 males 120 females
Intra-Observer
study based on
double determinations
by S. L-A.
XD°
SD = +0.37 1.2 1.5
N 2N p
Table 2. Measurement error.
RESULTS AND DISCUSSION
The population standards for the sagittal depth of the bony nasopha-
rynx in males and females are shown in Figures 2 and 3. There was a
steady increase in the sagittal depth of the nasopharynx of males (Fig. 2)
between 6 and 20 years of age. This increase was, on the average, smaller
during the period of 6 to 12 years of age (2.4mm) than during the period
of 12 to 18 years of age (4.7 mm). The increase in depth of the nasopha-
rynx of the females (Fig. 3) appeared to be negligible after 16 years of
age. During the first 6-year period, the average total growth increment
was 3.5 mm which was slightly more than double the corresponding incre-
ment (1.6 mm) for the second 6-year period. The mean and 50th percen-
tile velocity curves for both females and males differed very little.
There is a distinct difference between the sagittal growth of the bony
nasopharynx in males and females (Fig. 4). Growth velocity was found to
decline considerably earlier in females than in males. This reduction in
growth velocity in females occurred after 12 years of age, whereas the
corresponding growth reduction in males occurred after 14 years of age.
In females there was a negligible increase in sagittal depth of the na-
Sopharynx after 18 years of age. In males, however, a small average
increment in nasopharynx depth was found during the period of 18-20
years of age (Table 3).
The fact that the sagittal depth of the bony nasopharynx increases in
both sexes until at least 18 years of age indicates that it may contribute to
an increase in volume of the nasopharynx during the first 18 years of life,
as do the increases in height and width of the nasopharynx (Brodie, '41;
King, '52; Bergland, '63; Handelman and Osborne, '76). This increase in
31
Growth in the Sagittal Depth of the Bony Nasopharynx
nnnn
6OO +
__z. % percºue
550 + -T"

_T _-- 75 −"-
* = 2^
500 21.2T_T
sº me _-” Q • 10 tº —-
450 L-T _T _-T smºsºmº-
--T -* __T' 5 |
--~~
4CMO + LT —.-T
_-T
350 +
* —H —H } } } H {
6 9 12 14. 16 18 20 years of oge
Figure 2. Percentile distance curves for sagittal depth of the nasopharynx (ptm-
ba) for 140 to 60 males from ages 6 to 20 years.
volume is considered essential to maintaining a normal airflow in a grow-
ing person who has no nasal obstruction. This increase also may be de-
pendent partly upon the growth of the surrounding bones and partly on
the actual flow of air through the nasopharynx.
Figures 5 through 8 illustrate both the variability of the individual
velocity curves for sagittal depth of the nasopharynx in males and fe-
males, and the fact that none of the individuals illustrated exhibit the
same growth pattern as that representing the 50th percentile for the gen-
eral Burlington sample. Individual accelerations in growth in males (Figs.
5 and 6) did not peak at the same age as that of the 50th percentile of the
general population. Some rose to a higher or lower level and were more
sharply defined than that seen in the 50th percentile for the general
population. The averaging that occurs when individual values are com-
bined to produce population standards equalizes the differences of indi-
vidual behavior, which in this instance was highly variable. It is possible
that errors of measurement may assume more importance for individual
curves than for average curves owing to the smaller size of the measured
values. This may explain, to some extent, the irregular nature of the
individual curves. In addition, the intervals of two to three years between
measurements detracts from the preciseness of the age of peak velocity
32
Linder-Aronson
rnrn
6OO f
55.O +
__T • 90 º
--~~ -"

* • 50
_-T
450 = * ~. .--T _---- 25 – I —
_T. ~T_--— 1O — n—
_Ti_-T____ – --
4OO + 2–~
1
12 14 16 18 20 years of age
§
Figure 3. Percentile distance curves for sagittal depth of the nasopharynx (ptm-
ba) for 120 to 40 females from ages 6 to 20 years.
>I
>.
2
tº-º mole
# ———femole
O
§ 20 f O
§ *>===S_2^ \
º ~ O
z AO + Ne `s
Lll *
à Y ~ © sº- O
3. `----------.
: l | l l 1
T I I I I I -T
6 Q 12 {4 {6 {8 2O

years of age
Figure 4. Mean velocity curves for sagittal depth of the nasopharynx (ptm-ba) in
mm for males and females.
for individuals. Nonetheless, the presence of a small but distinct accelera-
tion in the male population standard indicates that a similar phenomenon
Occurs with individuals at possibly more variant ages.
In contrast, there was no distinct peak velocity in the 50th percentile
33
Growth in the Sagittal Depth of the Bony Nasopharynx
Growth Increments (mm/year)
6-9 9–12 12-14 14-16 16-18 18–20
years years years years years years
of age of age of age of age of age of age
Males 0.55 0.34 0.84 044 0.32 0.26
Females 0.48 0.52 0.33 0.19 0.12 0.07
Table 3. Average growth increments in the sagittal depth of the nasopharynx in
males and females as measured in mm/year for different age groups between 6-20
years.
5.of • — 50th percentile
* * * * * * * * * s = - e. COSe # 295
# •, — — I — 340
* = ./ \
: 40 2 \, — — — — — 652
I. / \ - - - - - – || — 763
H
E:
$2 30+
CO -
35
# 20+
#
à
- 1.0 +
20 years of oge
Figure 5. Individual velocity curves of increase in sagittal depth of the nasopha-
rynx of four males superimposed on the 50th percentile velocity curve for males.
population standard for females (Figs. 7 and 8) but, rather, a steady
decline in the velocity of growth after the period of 9 to 12 years until the
period of 12 to 14 years of age, after which it ceased. When the velocity
curve for the standard for females is compared to the individual velocity
curves of females, extreme variability is again evident, with individual
accelerations in growth only occasionally reaching or exceeding the great-
est velocity of growth seen in the population standard. Many of these
accelerations are within the limits for error of measurement and must be
regarded with care. Nonetheless, it would appear that in each individual
there is a consistent but very small acceleration in growth occurring at
variable ages between nine and sixteen years. Similar variability in ages

34
Linder-Aronson
5O + — 50th percentile
• * * * * * * * * * * * * * COSe # 135
# — — II — 144
# 40+ — — — — I – 320
F ––––– — I — 766
3.
É
30+
O
º
# 20 +
3.
:
1.O +
6 9 12 14 16 ſe 20 years of Oge
Figure 6. Individual velocity curves of increase in sagittal depth of the nasopha-
rynx of four males superimposed on the 50th percentile velocity curve for males.
and amounts of peak velocity was recorded by Woodside ('69) for males
and females.
Correlation Analyses
Correlation analyses were done between the sagittal depth of the na-
Sopharynx and various facial variables (Fig. 1) for both males and females
(Tables 4 and 5). Because males and females correspond very well with
regard to order and magnitude of correlation, the sexes will be discussed
together. -
The highest significant correlation coefficients were found between the
depth of the nasopharynx (ba-ptm) and the length of the total cranial
base (n-ba; r = 0.63-0.75). Within the different age groups, however, this
relationship only had Coefficients of Determination (R*) between 39%
and 56% in spite of the fact that basion was a common reference point.
Corresponding, but even lower, correlations were found between na-
sopharynx depth and the anterior cranial base (n-s; r = 0.45-0.60) and
posterior cranial base (s-ba; r = 0.22-0.43).
A very weak correlation exists between the depth of the nasopharynx
and the length of the maxilla (ptm-sn; r = 0.18-0.40) and the Coefficients
of Determination (R*) were only 3.2%-16%. It should be noted that
these two variables have one reference point in common, i.e. ptm. Thus,
a forward position of ptm should result in a large nasopharynx depth and
a short maxilla, if basion and subnasale are presumed to be unaffected.

35
Growth in the Sagittal Depth of the Bony Nasopharynx
5.O + --- 50th percentile
= | COSé # 356
>. — — — .454
T 4.0+ \ II.I.T. &
E \ 590
à
30+
O
2
;
§ 2.0+
§
1.O +
I
6
20 years of oge
Figure 7. Individual velocity curves of increase in sagittal depth of the nasopha-
rynx of four females superimposed on the 50th percentile velocity curve for
females. -
5.0 + ––– 50th percentile
# | “…” COSe # 118
: — — — |357
+ 4.0+ A. * * * * = • - it – 287
g - . . * * * * = – II – 455
O
Cº.
CD
5 50+
C/D
H.
2.
#
# 2.0+
C
2:
1.O-H-
20 years of age
Figure 8. Individual velocity curves of increase in sagittal depth of the nasopha-
rynx of four females superimposed on the 50th percentile velocity curve for
females.
The topographical relationship should, in this instance, lead to a negative
correlation. The correlation is positive, however, which should be inter-
preted as a true positive, but weak, association between the measured
distances.
No relationship could be established between the depth of the nasopha-


36
Linder-Aronson
ba-ptm (age in years)
Variable 6 9 12 14 16 18 20
Il-S 0.52 0.45 0.46 0.50 0.51 0.53 0.51
S-ba 0.36 0.29 0.43 0.42 0.33 0.29 0.30
n-ba 0.74 0.64 0.71 0.74 0.73 0.68 0.70
ptm-sn 0.29 0.27 0.34 0.29 0.31 0.36 0.32
Sn-gn 0.07 0.04 0.07 0.11 0.05 —0.03 –0.02
n-gn 0.17 0.07 0.08 0.14 0.03 –0.04 0.00
Il-SI) 0.22 0.11 0.08 0.12 –0.04 –0.01 0.04
mandibular length 0.28 0.21 0.27 0.31 0.19 0.25 -
gonial angle —0.11 –0.10 –0.07 –0.10 –0.05 –0.16 *
Table 4. Correlation analysis between sagittal depth of the bony nasopharynx
(ptm-ba) and various facial variables for males.
ba-ptm (age in years)
Variable 6 9 12 14 16 18 20
Il-S 0.46 0.60 0.53 0.49 0.48 0.18 0.47
S-ba 0.23 0.30 0.30 0.22 0.22 0.19 0.39
n-ba 0.63 0.72 0.71 0.68 0.70 0.73 0.75
ptm-sn 0.18 0.34 0.33 0.26 0.22 0.27 0.40
Sn-gn 0.07 0.02 –0.05 –0.04 –0.04 –0.06 0.10
n-gn 0.02 0.08 0.01 —0.03 –0.08 –0.04 0.01
Il-SI] –0.02 0.17 0.13 0.06 —0.07 0.09 –0.05
mandibular length 0.24 0.35 0.27 0.18 0.04 0.09 -
gonial angle –0.07 –0.08 –0.06 –0.06 –0.07 –0.23 -
Table 5. Correlation analysis between sagittal depth of the bony nasopharynx
(ptm-ba) and various facial variables for females.
rynx and the total face height (n-gn) or lower facial height (sn-gn), or the
length of the mandible.
The relationship between maxillary length (ptm-sn) and the total length
of the cranial base (n-ba) is shown in Table 6. These correlations (r =
0.37-0.59) were not as strong as those found between the depth of the
nasopharynx and total cranial base length (n-ba; r = 0.63-0.75). The
weak relationship between the length of the maxilla and the nasopharynx
on one hand, and total cranial base length and other variables on the
37
Growth in the Sagittal Depth of the Bony Nasopharynx
Age 6 9 12 14 16 18 20
Female 0.45 0.53 0.54 0.53 0.43 0.37 0.59
Male 0.48 0.48 0.53 0.52 0.50 0.49 0.55
Table 6. Correlation analysis between the length of the maxilla (ptm-sn) and the
cranial base (n-ba) for females and males.
other, could be due to the complexity of significant etiological factors
determining the size of the nasopharynx. The areas would appear to be
independent variables operating under independent factors. Environmen-
tal factors might influence one area more than the other.
In earlier investigations (Linder-Aronson, '72, '73), it was found that
the sagittal depth of the bony nasopharynx was influenced by the mode of
breathing. In children who were predominantly mouth breathers, the
nasopharynx was smaller than that found in nose breathers of the same
age. Following a change to nosebreathing, the depth of the bony na-
sopharynx was normalized. This may be explained, in part, by a change in
the muscle tone of the muscle ring consisting of the orbicularis oris, the
buccinator and the superior pharyngeal constrictor and, in part, by
altered muscle tone due to the accompanying change in posture of the
head and jaws (Ricketts, '58; Solow, '76). Also, pressure from the airflow
through the nasopharynx may influence growth of the nasopharynx (Moss
and Salentijn, '69; Fränkel, '76). -
No relationship could be found between the depth of the nasopharynx
and the anterior facial height. This finding agrees with those of earlier
investigations in which the subjects were nose breathers (Solow, '66;
Linder-Aronson, '70). However, investigations of Linder-Aronson ('70,
'73) and Harvold and co-workers ('73) have shown that total facial height
increases when there is posterior rotation of the mandible due to a reduc-
tion of the airflow through the nasopharynx. In this study, none of the
individuals examined showed any constriction of the nasopharyngeal air-
way. Therefore, the relationship between obstructed nosebreathing and
an increase in the facial height could not be studied.
SUMMARY AND CONCLUSIONS
1. The sagittal depth of the bony nasopharynx increases in small, steady
increments up to 16 years of age in females and 20 years of age in males.
2. In the population standards for males, the velocity of sagittal depth
increase peaked between ages 12-14.
38
Linder-Aronson
3. In the population standards for females, the velocity of sagittal depth
increase did not peak but, rather, decreased between ages 9-12.
4. There was great variation among individual velocity curves for males
in both the age at which velocity peaked and the magnitude of the growth
increments, which were frequently greater than the largest growth incre-
ment in the population standard for males.
5. Individual velocity curves for females showed that there were small
increments of growth occurring at highly variable ages. The magnitude of
these growth increments was small and usually less than the largest
growth increment in the population standard for females, although there
were a few very large growth increments (Fig. 8).
6. The sagittal depth of the bony nasopharynx is relatively independent
of other cephalometric dimensions of the facial complex. This suggests
that future research efforts should be directed toward determining what
the effects of environmental and physiological factors are on the size of
the airway.
ACKNOWLEDGEMENT
Original data presented in this study was made possible, in part, by the Medical
Research Council of Canada Grant MA-3600, United States Department of
Health, Education and Welfare Grant DE-01-2837-03 and by use of data from the
Burlington Growth Center, Toronto, Canada, which was funded, in part, by the
Evaluation of Interceptive Orthodontics Grant 605-7-299 of the National Health
and Welfare of Canada Grants Program.
The authors also wish to acknowledge the support of the Medical Research
Council of Canada which made it possible for Dr. S. Linder-Aronson to spend six
months at the University of Toronto as a Visiting Scientist.
The authors wish to thank Dr. Frank Popovich for his courtesy in making the
records of the Burlington Growth Center available and Dr. Gordon Thompson
for his assistance with statistics.
REFERENCES
Bergland, O. The Bony Nasopharynx. Acta Odont. Scand. Suppl. 35, 1963.
Brodie, A. G. On the growth pattern of the human head from the third month to
the eighth year of life. Am. J. Anat. 68:209, 1941.
Burlington Orthodontic Research Center Progress Report, Toronto, 1956.
Fränkel, R. Technik und Handhabung der Funktionsregler. Verlag Volk und Ge-
sundheit, Berlin, 1976.
Handelman, C. and G. Osborne. Growth of the nasopharynx and adenoid devel-
opment from one to eighteen years. Angle Orthodont. 44:243, 1976.
Harvold, E., K. Vargervik and G. Chierici. Primate experiments on oral sensa-
tion and dental malocclusions. Am. J. Orthodont. 63:494, 1973.
39
Growth in the Sagittal Depth of the Bony Nasopharynx
King, E. W. A roentgenographic study of pharyngeal growth. Angle Orthodont.
22:23, 1952.
Linder-Aronson, S. Adenoids - Their effect on mode of breathing and nasal
airflow and their relationship to characteristics of the facial skeleton and the
dentition. Acta Otolaryng. Suppl. 265, 1970.
Linder-Aronson, S. Effects of adenoidectomy on dentition and nasopharynx.
Trans. Europ. Orthodont. Soc. p. 177, 1972.
Linder-Aronson, S. Effects of adenoidectomy on the dentition and facial skeleton
over a period of five years. Trans. Third Int. Orthodont. Cong. p. 85, 1973.
Moss, M. and L. Salentijn. The primary role of functional matrices in facial
growth. Am. J. Orthodont. 55:566, 1969.
Ricketts, R. M. The cranial base and soft structures in cleft palate speech and
breathing. Plast. Recon. Surg. 14:47, 1954.
Ricketts, R. M. Forum on the tonsil and adenoid problem in orthodontics. Respi-
ratory obstruction syndrome. Am. J. Orthodont. 54:495, 1958.
Rosenberger, H. C. Growth and development of the nasorespiratory area in
childhood. Am. Otolaryng. 43:495, 1934.
Solow, B. The Pattern of Craniofacial Associations. Acta Odont. Scand. Suppl.
46, 1966.
Solow, B. and A. Tallgren. Head posture and craniofacial morphology. Am. J.
Phys. Anthrop. 44:417, 1976.
Subtelny, J. D. The significance of adenoid tissue in orthodontia. Angle Ortho-
dont. 24:59, 1954.
Subtelny, J. D. A cephalometric study of the growth of the soft palate. Plast.
Recon. Surg. 19:49-62, 1957.
Woodside, D. G. Distance, velocity and relative growth rate standards for man-
dibular growth for Canadian males and females aged three to twenty years.
American Board of Orthodontics Thesis, Library of American Association of
Orthodontists, 1969.
40
AERODYNAMIC STUDIES OF UPPER AIRWAY:
IMPLICATIONS FOR GROWTH, BREATHING
AND SPEECH
Donald W. Warren, D.D.S., Ph.D.
Department of Dental Ecology
The University of North Carolina
The nasal and oral cavities serve as pathways for respiratory airflow.
Ordinarily, the inspiratory and expiratory airstreams are channeled
through the nose because the mouth is usually closed. However, in some
individuals, because of nasal airway inadequacy or habit, the oral cavity
becomes the established and predominant route for the passage of respi-
ratory airflow.
There have been many attempts to establish a causal relationship be-
tween dentofacial deformities and nasal airway inadequacy. Unfortu-
nately, the documentation of airway inadequacy has usually been subjec-
tive and the conclusions drawn conflicting. Also, the judgement of mode
of breathing has differed among investigators, thus leading to additional
confusion. For example, an open anterior oral cavity does not necessarily
mean mouthbreathing. If the tongue occludes the oral cavity (Fig. 1A) or
linguo-palatal closure occurs (Fig. 1B), the oral airway is essentially
closed.
The most prevalent view has been that mouthbreathing resulting from
an inadequate nasal airway is often associated with such deformities as
retrognathic mandible, protruding maxillary anterior teeth, high palatal
vault, constricted maxillary arch, flaccid and short upper lip, flaccid pe-
rioral musculature and a somewhat dull appearance due to a constant,
open-mouthed posture.
Angle ('07), in a statement concerning Class II, division 1 malocclu-
sion, noted that “This form of malocclusion is always accompanied and,
at least in its early stages, aggravated, if indeed not caused by mouth-
breathing due to some form of nasal obstructions.” Allergists have ex-
pressed similar views in their concern for the allergic rhinitis patient and
for the patient with enlarged adenoids. Mouthbreathing is a common
characteristic in these cases, and there are reports of protruding maxillary
anterior teeth or constricted maxillary arches being present, as well as
other dental deformities.
41
Aerodynamic Studies of Upper Airway
Figure 1. Mode of breathing cannot be accurately judged by determining if the
mouth is open or closed. (A) Placement of the tongue against the alveolar ridge
can Seal the oral cavity even though the mouth appears to be open. (B) A
linguo-palatal seal can also completely occlude the oral airway.
Hunter ('71), however, did not find a relationship between allergic
rhinitis and malocclusion. His data did demonstrate that frequency of
mouthbreathing increases as nasal airway resistance increases.
Several investigators (Linder-Aronson and Aschan, '63; Tully, '66;
Linder-Aronson, '70) have described a special facial type as characteristic
of persons with enlarged adenoids and/or who are mouth breathers. Gen-
erally referred to as “adenoid facies”, this facial type reportedly is
marked by a long, narrow face, pinched nostrils, a short upper lip, promi-
nent maxillary incisors and lips-apart posture. - -
Moffatt ('63) related protrusion of the maxillary incisors to mouth-
breathing. When the mouth is open, the lower lip tends to fall between
the upper and lower incisors and in this retruded position it exerts an
anterior force on the upper incisors. Linder-Aronson and Bäckström
('60), however, found no relationship between mouthbreathing and either
inclination of the upper incisors or overjet.
Similarly, Harvold and co-workers ('73) have drawn attention to a
possible association between palatal anatomy and impaired nasal breath-
ing. These researchers simulated hypertrophied adenoids in primates with
acrylic blocks and found that within 9 to 15 months of placement of the
blocks, the palatal vault had increased in height creating an anterior open
bite. Harvold believes that an open, clear nasal airway is a prerequisite to
normal facial form and function.
On the other hand, Korkhaus ('60) suggested that maxillary arch form
is a primary factor in determining nasal cavity size and, hence, breathing
mode. His studies indicated that alterations of the maxilla due to inhibi-
42

Warren
tion of growth or deformation is not a local symptom, but rather a charac-
teristic of a complex anomaly which usually extends beyond the immedi-
ate region, and which includes the nose and sinuses.
Further complicating our understanding is the fact that dentofacial de-
formities can exist without airway inadequacy being present and vice
versa. For example, Derichsweiler ('56) argues against nasal obstruction
as a primary etiologic factor in dentofacial deformity based on three
subjects who had choanal atresia with normally developed jaws and denti-
tions. Similarly, Watson and colleagues ('68) measured nasal airway resis-
tance in orthodontic patients and noted that when resistance was high,
mouthbreathing invariably resulted but skeletal deformity did not always
occur. Interestingly, they noted that 23 percent of the mouthbreathers
apparently did so out of habit rather than from physiologic need.
Individuals with a high, narrow palate and posterior dental crossbite
often breath through their mouths (Hershey et al., '76). This type of
malocclusion is often associated with high nasal airway resistance. Treat-
ing such malocclusions with orthodontic appliances that expand the maxil-
lary arch not only corrects the malocclusion, but also, in many instances,
significantly reduces the nasal stenosis as well.
The only conclusion that can be drawn from these studies is that maloc-
clusion may or may not be associated with an inadequate nasal airway.
Whether upper airway obstructions produce dentofacial deformities or
whether the deformities produce airway impairment is still unclear in
cases in which both problems are present. Certain types of malocclusion,
such as that caused by a high palatal vault or a constricted maxilla, do
seem to be associated with nasal impairment, but which causes which
cannot be determined from the present data. The only positive statement
that can be made is that certain nasal or nasopharyngeal abnormalities
may produce a mouthbreathing pattern.
Since successful treatment of dentofacial deformities may depend on
recognizing the factors causing such defects, our research techniques
should be as objective as possible. The purpose of this paper is to present
the rationale for an approach which provides quantitative data that are
useful for assessing the nasal and oral airways. The instruments involved
are precise and simple to use, and when properly applied, yield accurate
and consistent information. However, the use of such aerodynamic tech-
niques does require that the investigator understand certain basic princi-
ples of fluid flow as well as the mechanics of respiration.
MECHANICS OF AIRFLOW
Air flows from one region to another (in this case from the outside to
the lungs and back) because of a difference in pressure between the two
43
Growth in the Sagittal Depth of the Bony Nasopharynx
this case the structure is the entire respiratory tract or a specific portion
of the tract such as the nasal airway), there is a pressure differential (or
pressure drop) across the structure in the direction of airflow. The rela-
tionship between this pressure drop and airflow depends upon a parame-
ter known in fluid dynamics as Reynolds number. Reynolds number (RA)
is defined
Rn = p-4
|L
where p is air density, - is air velocity, d is the diameter of the structure
and p is viscosity of the air.
In the respiratory tract whenever R, is less than about 2,000, the flow
is smooth or laminar. When Rn is more than 2,000, approximately,
airflow is considered to be turbulent (Comroe, '65). Each requires a
different amount of pressure to move a given amount of air through a
Structure. *
When airflow is laminar (Fig. 2), the relationship between pressure
drop and airflow is linear or
AP = kV
where P is pressure, k, is the proportionality constant which includes such
factors as air viscosity and the length and radius of the structure, and V is
airflow.
When branching and irregular shape of a structure cause eddying at
bifurcations, airflow is turbulent (Fig. 2). The relationship between air-
flow and pressure drop in this case is quadratic or
AP = k,Vº
where k, includes air density and the length and radius of the structure.
Constrictions which form along the vocal tract cause the air to flow
through an orifice producing a pressure drop, the results of which are
expressed as
•y TI 2
AP = --|Y
2k” | A
where k is the discharge coefficient which depends on the sharpness of
the edge of the orifice and on Reynold’s number, d is the diameter of the
structure and A is the area of the orifice. The coefficient has a value of
0.6-0.7 in the airflow domain corresponding to speaking or breathing at
rest (Warren and Dubois, '64).
44
Warren


7.) ſ zº N
( Z/
Mſ)//
C f- C sº ºf
\
OſłIFICE FLOW TURBULENT FLOW
LAMINAR FLOW
Figure 2. Types of airflow that occur in the respiratory tract.
MECHANICS OF RESPIRATION
Breathing, which is the movement of air into and out of the lungs,
results from contractions of the respiratory muscles which produce
changes in the volume of the chest cage. The lungs fill the thoracic cavity
and its outer surface (visceral pleura) is in intimate contact with the inner
surface of the thoracic cavity (parietal pleura). The two pleural layers are
in apposition, separated only by a thin film of fluid which enables the
lungs to slide freely within the cavity. Whenever the chest cage enlarges,
the lungs also enlarge.
At the end of expiration when the respiratory muscles are relaxed,
pressure within the lungs (pulmonary pressure) is atmospheric and there
is no airflow. This is the resting position. Both the lungs and the chest
wall contain considerable elastic tissue, and at resting position these pull
with equal force but in opposite directions, creating a balance of elastic
45
Aerodynamic Studies of Upper Airway
H
Figure 3. At resting level there is a balance of elastic forces as the lung and chest
wall pull in opposite directions (Warren, '76).
forces (Fig. 3). Although the lungs and chest operate as a unit, the two
would have different resting positions if separated. That is, the lungs
would collapse and the thoracic cavity would enlarge somewhat. Again, it
is the pleural linkage which prevents this from occurring and allows a
balance of elastic forces to exist at rest position. However, when contrac-
tion of the diaphragm and intercostal muscles occurs during inspiration,
the volume of the thoracic cage enlarges and the elastic forces of the two
units change. When the diaphragm contracts, its dome moves downward
into the abdomen, thus enlarging the thoracic cavity. Simultaneously, the
inspiratory intercostal muscles move the rib cage upward and outward,
also increasing the volume of the thoracic cavity. This enlarges the vol-
ume of air within the lungs, pressure falls below atmospheric and air is
drawn into the expanding lungs. While inspiration is an active process
involving muscle contraction, normal expiration is primarily a passive
event (Cherniack and Cherniack, '61). The elasticity of stretched tissues


46
Warren
and gravitational forces tend to return the thorax to its resting position
without any further expenditure of energy. Because the elements which
have been stretched during inspiration are elastic, they have a natural
tendency to return to their original position after relaxation of the inspira-
tory muscles. As the thorax and lungs spring back to their original sizes,
pulmonary air becomes temporarily compressed so that its pressure ex-
ceeds atmospheric and air flows from the lungs to the outside.
THE WORK OF BREATHING
During inspiration, active muscle contraction provides the energy re-
quired to expand the thorax and lungs. The primary forces which must be
overcome include stretching the elastic fibers in the tissues involved, air-
way resistance and surface tension. The elastic behavior of the respiratory
System is usually described in terms of its pressure-lung volume relation-
ship. The elastic forces of the lungs and chest wall vary with lung volume
(Agostini and Mead, '64). The relaxation pressure curve is obtained by
recording pulmonary pressure at different degrees of lung distension
while airflow is obstructed at the mouth and all muscles are relaxed
(Agostini and Mead, '64). The pressure obtained at any lung volume is a
result of the elastic forces of the lungs and chest wall. This is a measure of
effort previously exerted in order to overcome the elasticity of the tissues
involved. The curve illustrated in Figure 4 is the result of elastic recoil. At
60% of total lung capacity, the chest wall is at its natural size and since its
elastic fibers are not being stretched, they offer no recoil pressure. On the
other hand, the elastic fibers in the lung are being stretched so at that
volume, lung recoil pressure equals relaxation pressure. As inspiration
continues, both the lungs and chest wall recoil when the muscles relax
and the pressures are additive.
During expiration when the muscles are relaxed and the lungs are
deflated below resting level, a negative pressure develops. This negative
pressure indicates the effort previously exerted to overcome the elastic
resistance of the chest wall and lungs. Although the lungs would exert a
positive pressure until it completely collapsed, the lung pressure is more
than counter-balanced by that of the chest wall, as it exerts a greater
negative pressure when it is smaller than its natural size. -
Most of the work in fillings the lung involves overcoming the elastic
recoil, and the energy required to do this is stored during inspiration and
used during expiration. The compliance of the respiratory system, or the
degree of distensibility which occurs with the application of pressure, is
an important factor in determining the amount of energy required to
move air into and out of the lungs.
The second factor determining the degree of work required for breath-
47
Aerodynamic Studies of Upper Airway
RECOIL
RELAXATION PRESSURE CURVE Lung Chest Woll
|OO- / .” <- -º-
/ ."
* /
/
/
/
80 - /
/
/
To – W <!- O
OS /
*=s* /
>- /
E 60- /
C I
5. /
<[ == /
O /
CD / :
a 40 WT F -º- =>
—l / Resting Level
— /
# - /
C
2O—
;
O I I I l (-º- —- )
–|O O |O 2O 3O Compress Expond

PRESSURE (cm H2O)
— Reloxotion Pressure
g tº º º ºs tº 8 Lung
— — — Chest Woll
Figure 4. Illustration of the relaxation pressure curve. The pressure at any given
lung volume is a result of the elastic forces being exerted by the lungs and chest
wall. The curve is obtained by stopping airflow at various points of inspiration and
expiration. -
ing is the magnitude of airway resistance. When the airway is open,
airflow is mostly smooth (laminar) and resistance is low. However, in
disease states increased respiratory secretions or obstructions can increase
resistance greatly. Airflow becomes turbulent and greater effort is neces-
sary to move air in and out of the lungs.
The third factor relates to a very special surface film that lines the
alveoli of the lungs and produces surface tension. The fluid lining tends to
shorten the surface and resist further stretching. Thus, inspiration would
require additional energy to expand the alveolar sacs. Fortunately, a
surface-active substance, surfactant, is present which reduces surface ten-
sion. The recoil force of surface tension results in a pressure of about 20
cmH20 when the lung is fully inflated and about 2 cmH20 at lower vol-
umes (Comroe, '65).
48
Warren
Flowmeter
|
Differential
Pressure /
Transducer ſº Heated \-
Filament Filomen?
PNEUMOTACHOGRAPH WARM-WIRE ANEMOMETER
Figure 5. The pneumotachograph consists of a flowmeter and a differential pres-
sure transducer. As air flows across the mesh screen in the flowmeter, the pres-
sure drops and is recorded by the transducer. The pressure drop is proportional to
the rate of air flow. The warm-wire anemometer uses a heated wire as a sensing
unit. Air flows across the heated wire, cools it, and alters its resistance. The
change in voltage which results is proportional to the rate of airflow.
METHODOLOGY
Instruments capable of precisely measuring the respiratory parameters
of breathing have been used to assess upper airway structures. Aerody-
namic techniques are used routinely to estimate the area of constrictions,
resistances to airflow and volume displacements.
Airflow Measurement Devices
There are two types of flowmeters presently being used to measure
airflow rate. The most widely used instrument is the pneumotachograph,
the other less commonly used is the warm-wire anemometer (Fig. 5).
The pneumotachograph consists of a flowmeter and a differential pres-
Sure transducer and operates on the principle that as air flows across a
resistance the pressure drop which results is linearly related to the volume
rate of airflow (Lubker, '70). In most cases, the resistance is provided by
a wire mesh screen that is heated to prevent condensation. A pressure tap
is situated on each side of the screen, and both are connected to a very
sensitive differential pressure transducer. The pressure drop is converted
49




Aerodynamic Studies of Upper Airway
to an electrical voltage that is amplified and recorded either on magnetic
tape or on a chart recorder. Pneumotachographs are accurate, reliable,
linear devices for measuring ingressive and egressive airflow rates. In
addition, they are inexpensive and easily calibrated with a rotameter.
The warm-wire anemometer uses a heated wire as the sensing unit
(Subtelny et al., '66). The cooling effect of airflow on a heated wire,
through which an electric current flows, alters its resistance. The resultant
change in voltage is amplified and recorded. However, the anemometer
has poor linearity and does not sense direction of airflow. For this reason,
it is less popular than the pneumotachograph.
Air Pressure Measurement Devices
The pressure transducers presently in use are either variable resistance,
variable capacitance or variable inductance gauges. The resistance-wire
strain gauge manometers respond to changes in pressure with a change in
resistance when the strain-sensitive wire is exposed to stretch. A metal
bellows is compressed by pressure within the chamber of the strain gauge.
This action results in a resistance imbalance in a Wheatstone bridge that
is proportional to the applied pressure. The resulting output voltage from
the bridge is amplified and recorded.
The electrical capacitance manometer is a capacitor which is formed by
a pressure movable electrode separated from a stiff metal membrane by a
carefully adjusted air gap. Movements of the membrane in relation to the
electrode vary the capacitance, which can be measured by radio freq-
uency techniques. Membrane displacement is extremely small and sensor
response time is short, enabling measurements of instantaneous pressure.
However, this device is more temperature sensitive than the strain gauge
man Ometer.
Variable inductance pressure gauges can be made so small that they
can be placed directly on the site to be measured. The transducer utilizes
a soft iron slug placed within two coils of wire and fastened to the center
of an elastic membrane. Pressure moves the iron slug, and this movement
results in a change in magnetic flux. The change in inductance of the coils
is then recorded through an appropriate bridge circuit.
It is common practice to amplify the signal from transducers to provide
power to drive galvanometers. However, the mechanical inertia of some
direct writing galvanometers is so great that the frequency response is
limited, and amplification is required to produce any measurable re-
sponse at all. Usually a carrier wave amplifier is used in combination with
a strain gauge transducer. An oscillator supplies an alternating current,
and the amplitude is continuously affected by the varying resistance of the
Wheatstone bridge. The output of the transducer enters a capacitance-
50
Warren
coupled amplifier, which amplifies the modulated carrier wave. Then the
signals are rectified and the carrier wave is filtered out, leaving a DC
voltage which powers the recording instrument.
AERODYNAMIC TECHNIQUES
Resistance Measurements
Resistance to airflow is opposition to air motion caused by friction
(viscous drag). Friction dissipates mechanical energy in the form of heat
as air moves through the respiratory tract. This energy is supplied by the
respiratory muscles which require more forceful contractions as airway
resistance increases. As noted earlier, besides airway resistance there are
elastic and inertial forces which contribute to the work of breathing.
The measurement of airway resistance involves the simultaneous re-
cording of the rate of airflow and the pressure drop across a specific
Structure. The rate of airflow is measured by a pneumotachograph and
the pressure drop is measured by a differential pressure transducer.
The resistance to airflow is explained by an analogy to Ohm’s law for
electrical currents and for airflow is given by
AP
R = w (cmH2O/L/sec)
Since airflow through the respiratory tract is partly laminar and partly
turbulent, measurements must be made at a specific rate of flow if com-
parisons are to be meaningful. Usually flow rates of 250 or 500 cc/sec. are
used since these rates are comparable to normal breathing rates.
The procedure for measuring nasal airway resistance is illustrated in
Figure 6. The nasal pressure drop is measured with the differential pres-
sure transducer connected to two catheters. The first catheter is posi-
tioned in the subjects oropharynx as far posteriorly as can be tolerated
and the second catheter is placed within a nasal mask in front of the nose.
Both catheters are occluded at their tips but have side holes for measur-
ment of static pressures.
Nasal airflow is measured with a heated pneumotachograph connected
to a well-adapted nasal mask. Particular attention is given to positioning
the mask so that it does not contact the nostrils. After sitting in a
controlled environment of stable temperature and humidity for 30 min-
utes, each subject is asked to inhale as normally as possible through his
mouth, to close his lips, and then exhale through his nose. The resulting
pressure and airflow patterns are recorded by a direct writing recorder
(visicorder).
51
Aerodynamic Studies of Upper Airway
PRESSURE
AMPLIFIER
MONITOR
OSCILLOSCOPE
/ VISICORDER
Flow
AMPLIFIER
Figure 6. Airway resistance is measured by recording the pressure drop across the
structure and airflow through it.
NASAL AIRWAY RESISTANCE STUDIES
Watson and colleagues (68) compared nasal airway resistance to skele-
tal classification and mode of breathing in orthodontic patients. Skeletal
classification was assigned on the basis of the difference, in degrees, of
points A and B as each related to the Frankfort plane. An AB difference
equal to or greater than +4° was classified as skeletal Class II. An AB
difference equal to or greater than -4° was classified as skeletal Class III.
An AB difference of less than +4° or less than — 4° was classified as
skeletal Class I. This method of skeletal classification will not distinguish
those subjects with a retrognathic mandible from those with a prognathic
maxilla, and either or both conditions may result in a classification of
skeletal Class II. Similarly, a patient in whom both the maxilla and the
mandible are positioned mesially (or distally) may be classified as skeletal
Class I.
After analysis of the data, it appeared that a high incidence of what was
labeled “clinical mouthbreathing” occurred when nasal airway resistance
was greater than 4.5 cmH20/L/sec. (Fig. 7). Seventy-seven percent of the
Subjects whose nasal airway resistance was 4.5 cmH20/L/sec. or greater
were classified as mouth breathers. Again, it must be stressed that evalua-
tion of the breathing mode was subjective and does not rule out simulta-
neous oral and nasal breathing. Approximately 26% of this orthodontic
population were mouth breathers with a nasal airway resistance lower
than 4.5 cmH20/L/sec. Perhaps these individuals can be labeled habitual
mouth breathers.
Since clinically observable mouthbreathing occurred more frequently
when nasal airway resistance was above 4.5 cmH20/L/sec., the sample
52

Warren

74. 9/o
24 – M = mouth breathing
nasal breathing
H.
2
2
*
N
=
26 % 779,
4 - 23%
M N M N
R. 45CMH,0/L/SEC. R. 4.5 CMH,0/L/SEC.
Figure 7. Mouthbreathing was observed more frequently in those subjects whose
nasal resistance was about 4.5 cmH20/L/sec. than in those whose nasal resistance
was below this value. .
was divided into two groups: high resistance (above 4.5 cmH20/L/sec.)
and low resistance (below 4.5 cmH20/L/sec.). When the magnitude of
nasal resistance and the skeletal classification of individuals were com-
pared, they were found to be independent (Fig. 8). There was, however,
a tendency for Class II patients to have a higher nasal resistance than
Class I patients.
In our laboratory Hunter ('71) also compared mouthbreathing ten-
dency and nasal airway impairment to oral and facial characteristics. In
addition, he compared skeletal jaw relationships, dental anteroposterior
relationships, protrusion of maxillary incisors and palatal width and
height of perennial allergic rhinitis patients to a non-allergy sample.
Hunter reported that both allergy patients and mouth-breathing sub-
53
Aerodynamic Studies of Upper Airway
28
2 7
2 6–
25 —
24 –
Closs I AB difference < t 4 O 9
Closs II; AB difference > -- 4 O9
Closs III; AB difference > – 4 O*
Other Potient (s) discontinued
(ſ)
H
2
Lll
H
<[
O-
Li-
O
Or.
LL]
#
E 8
z 7–3.
g +%
A $.
3 -É ::::
: Tºš ... § 77 9, 7 7 %
::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: 3333333333. :::::::::::::::::::::::::::::::
CLASS I CLASS II CLASSIII OTHE SIT CLASSIII OTHER
LOW. R. 45 cmH2O/L/SEC. HIGH: R → 4.5 cm H.O/L/SEC
Figure 8. Number and percentage of subjects in each skeletal classification for the
high and low nasal resistance groups.
jects had high nasal airway resistance. However, he did not find an asso-
ciation between nasal airway impairment, mouthbreathing and skeletal
deformities. There was a suggestion of a higher incidence of retrognathic
mandibles in mouth breathers, but this did not correlate with nasal resis-
tance. An interesting finding was that the otorhinolaryngologist could
predict quite accurately through clinical evaluation that airway resistance
would be high whenever the nasal airway was severely obstructed. How-
ever, there were many instances of obstructions not producing nasal air-
way impairment, although the otorhinolaryngologist judged that it
should. Thus, clinical impressions of nasal airway impairment do not
always correlate with measurements of airway resistance.
Cleft Palate Studies
At flow rates of 0.5 L/sec., the airway resistance of normal subjects,
i.e., those with an adequate nasal airway, ranges between 1.0 and 3.5
cmH20/L/sec. (Warren et al., '69), with age of the subject affecting the
specific value. As Figure 9 indicates, this relates to the increase in cross-
sectional area of the nose with growth.






54
Warren
O
Lil
Oſ)
N.
—l
N.
Q
Tº 5.0 H
> *
5 4.0
LU 5 O – ºte) T
É (5)
<ſ 2. O – # (18)
5 &
op | O – +
Lil
Or
O
9 - || | 2 - |3 |5 8 OLDER
AGE
Figure 9. Nasal airway resistance decreases with age in normal subjects. Numbers
in () indicate number of subjects studied.
Nasal deformities and maxillary growth deficiencies result in increased
nasal airway resistance (Warren et al., '69). An example of this is the
cleft palate population in which resistance is about 20-30 percent higher
in each age group than that in a normal population (Fig. 10). Drettner
('60) has demonstrated that septal deformities, atresia of the nostrils and
turbinate hypertrophy diminish airway size. He noted that 45 percent of
the cleft plate subjects in his study presented narrower nasal airways
than was considered normal. Interestingly, in the studies performed in
our laboratory, otolaryngological examinations revealed that about 60
percent of the “normal” subjects demonstrated clinical evidence of sep-
tal defects, vomerine spurs, or turbinate hypertrophy in spite of the fact
that their nasal airway was judged to be normal. Approximately 70
percent of the cleft lip and palate subjects also presented similar nasal
defects although they were usually more severe. Those with cleft lip and
palate had a greater incidence of nasal deformities than those with cleft
palate alone.
Nasal abnormalities and a smaller cross-sectional area of the nose pro-
55
Aerodynamic Studies of Upper Airway
8 .O. r
O 7. O – Pºme
Lil
Oſ) -
~ 6 O H.
—l T
X 5.0 - » (9)
3. (
4 : O H.
3 (4) © ( ! 4 )
** **, (5)
* , e. 5
2 2 O - N C.P (18) L
<[
H. N CP
# | O H.
Lil N
Oº O
9 - || |2 - |3 |5 8 O LDER
AGE
Figure 10. Comparison of nasal airway resistance in a group of normal subjects
(N) to that in a cleft lip and/or palate population (C.P.). Nasal airway resistance is
increased in the cleft palate population but decreases with age as it does in the
normal group.
duce greater airway turbulence. The driving pressure which produces air
movement is expressed by the equation
AP = kV + k,Vº
where the first and second degree terms represent laminar and turbulent
flow, respectively. The constant k is proportional to the viscosity of the
air and k2 to its density. Nasal obstructions increase turbulence and hence
increase the pressure drop. Figure 11 illustrates an index of turbulence
comparing cleft subjects to normals. There is an approximate 50 percent
increase in the turbulence index in cleft palate individuals who have
Smaller airways. Again, growth diminishes airway turbulence but as Fi-
gure 11 illustrates, the difference between a normal size airway and a
Smaller one remains.
Restorative procedures for cleft palate patients which may alter the
nasopharyngeal airway can increase airway resistance in some cases (War-
ren et al., '74). Four groups of cleft palate patients were compared to a
normal sample. The cleft group included individuals with a prosthetic
speech appliance, those with repaired palates but no secondary proce-
dures, those with repaired palate and posterior pharyngeal flaps and,
56
Warren
2.2–

2.0-
1.8-
1.6-
1.4-
1.2-
1.0-
0.8-
0.6-
0.4-
O. 2-
normal A
cleft O
O.O
9–11 Yrs. 12–14 Yrs. 15 Yrs.--
Figure 11. Index of turbulence in cleft palate and normal individuals. Turbulence
is increased in the nasal airway of cleft palate individuals. Although turbulence
diminishes with age in both groups, the difference between the normal population
and the cleft palate population remains about the same.
finally, a group with cleft palate who had undergone no corrective sur-
gery. Figure 12 illustrates the relative effects of restorative procedures on
the nasal airway of adults. These data indicate that such procedures,
although they substantially fill the nasopharynx, do not usually have a
significant effect on airway resistance. This is of interest since a prosthetic
Speech appliance may have a pharyngeal section as large as 200 mm. In
57
Aerodynamic Studies of Upper Airway
A GE |5 AND OLDER T-
6 O –
T
T
3 5 O-
Q1)
Cſ)
N
—l
N. T ©
O 4.O –
CN
I
5 * *
LL T
3. O –
O
2 ©
<ſ
H
90
§ -l
# 2 O- t -
—l —l- he
<ſ
º -1-
2 | O- -
O
Normo | Unoperated Cleft Palate Cleft Palate Cleft Polate
Cleft Palate Surgical Clo- with Flap with Appliqnce
sure with no
Secondory
Procedure
Figure 12. Comparison of the effect of different cleft palate restorative procedures
on nasal airway resistance.
fact, of sixteen patients studied with and without their appliances, only
four demonstrated a clinically significant increase in airway resistance
when the appliance was in position. What these data indicate is that most
of the resistance to airflow occurs in the nasal chamber and not in the
nasopharynx, at least in adults.
Data for children are somewhat different (Fig. 13). In this case, poste-
rior pharyngeal flaps were used to decrease nasopharyngeal size and as a
result airway resistance was substantially increased. Apparently, as the
nasopharynx increases in size with growth, the flap becomes smaller in
comparison and airway resistance is reduced. In a way, these data are
similar to those presented by Linder-Aronson ('70). He found that ade-
58
Warren
G T
Lil
Q e - Clef f Polote
sº |O – with Posterior
O Pharyngeal Flaps
+" X - Cleff Poldfe
> A – Normal
C 8 —
LL
# O
f
Or X
2. 4 — | T
3: X
Or. * • X
amºe A
§ 2 — -- l A
<ſ
2 1.
o-
7 - || |2 – 14 |5 and older
A GE
Figure 13. Cleft palate restorative procedures, such as posterior pharyngeal flaps,
can increase nasal airway resistance significantly in children and produce mouth-
breathing.
noid tissue mass relative to overall nasopharyngeal size is the important
consideration rather than the presence itself of the adenoid tissue mass.
Thus, one might infer that growth has an important effect on airway
resistance within the nasopharynx.
Maxillary Expansion and Nasal Airway Resistance
Resistance in the nasal airway can be reduced by certain orthodontic
procedures. Hershey and co-workers ('76) reported a 45 percent reduction
in nasal airway resistance after rapid maxillary expansion. Turbyfill ('76),
studying the long-term effects of rapid maxillary expansion on nasal airway
resistance, noted that an average 53 percent decrease occurred in the 17
subjects studied (Fig. 14). This decrease was stable for at least one year
59
Aerodynamic Studies of Upper Airway
ol NASAL RESISTANCE AT 500 cc/sec
D Expansion Group
9 – Control Group
8 –
O 7.7
(l)
Š
S 7–
º s
; P- -
= 6- F-
O
Q)
E 5– l
e
.* 4.4
(M) 4.2
& 4–
tº 3.6
º
O
Z 3– - +”
2- |<-3 wis->| | |<–3 mo->| #elyr-
-l—
1 —
Initial M dximum Appliance 1 Year Post
Expansion Removal Removal
Figure 14. Orthodontic procedures such as maxillary expansion can decrease nasal
airway resistance, on the average, about 50%, bringing it within normal levels.

60
Warren
after removal of the expansion device. The mean change in resistance at
500 cc/sec. was 4.1 cmH20/L/sec. for the expansion group as compared to
a mean change of 0.1 cmH20/L/sec. for the control group. Rapid maxil-
lary expansion is apparently the primary cause of this decrease in nasal
resistance, since no significant decrease occurred in the control group.
Before maxillary expansion the mean binasal cavity width in the expan-
sion group was significantly less than that in the control group. After com-
pletion of expansion no difference remained. Although the increase in upper
binasal cavity width was small (an average of 0.5 cm), it should be remem-
bered that airflow varies inversely as the fourth power of the radius of the
tube through which it passes. The much larger increase in lower binasal
cavity width (3.5 mm) had an even greater effect on nasal airway resistance.
Maxillary Osteotomy and Airway Resistance
Recently there has been new interest in facial reconstructive surgical
procedures involving the maxilla, prompted by improvement in surgical
techniques, confidence obtained from revascularization research (Bell,
'69, '73), and from the decision of many clinicians to treat deformities at
the site of origin (Bell, 71; Schendel et al., '76).
Although clinical documentation has shown that maxillary surgery is
successful, one sequela which has not been adequately studied is the
effect of such surgery on the nasal airway. Turvey and Hall (77), in our
laboratory, have been following the effects of maxillary osteotomies on a
longitudinal basis by measuring nasal airway resistance prior to surgery,
and at three and 12 months post-surgery. The direction and amount of
movement of maxillary segments, as well as the type of surgery, are being
considered in relation to changes in nasal airway resistance.
The study is ongoing but the results to-date are of interest. The mean
nasal airway resistance before surgery is 6.67 cmH20/L/sec. and 3 months
after surgery is 4.18 cmH20/L/sec. This is a significant mean decrease of
almost 40 percent. Only one of 17 individuals showed an increase in nasal
airway resistance and only one showed little or no change.
Nasal obstructions which were noticed in presurgical clinical examina-
tions of the nostrils of seven of the subjects could have caused some of
the nasal airway resistance. These obstructions were removed during sur-
gery since all were located in the inferior third of the nasal cavity and may
have accounted for some of the decrease in nasal airway resistance in the
patients. Superior repositioning of the maxilla does impinge on the nasal
cavity and presumably would lead to a decrease in the size of the airway.
However, grooving the nasal crest to the maxilla for placement of the
nasal septum and some resection of the inferior portion of the septum
apparently prevents this and results in decreased nasal airway resistance
61
Aerodynamic Studies of Upper Airway
COMPA RISON OF NASAL RESISTANCE IN DIFFERENT GROUPS

n-
T T
10 -
9 -
t T
* 8–
sº
Cº. mnſ
# 7– - r
Wº 6 —
2:
5
2 * * * * * * = * * * * * = * = t-º gº tº º tº dº tº gº sº. tº sº tºº ſº tº Eº º tº
‘C . l |-
Cº. 4 — -
5.
# 3 – l
l
CONTROL NASAL PALATAL MOUTH- ALLERGY PRE-OP POSI.OP
GROUP BREATHERS EXPANSION BREATHERS SUBJECTS MAXILLARY SURGERY
STEWART HUNTER STEWART HUNTER HUNTER
1974 197] 1974 197] 197]
Figure 15. Comparisons of nasal resistance of groups studied in our laboratory.
Areas above the broken line indicate high nasal resistance. Nasal airway resis-
tance in the pre-op maxillary osteotomy group compares closely to that in the
allergy group and the mouthbreathing group.
posteriorly. Figure 15 illustrates how this group compares to the others
we have studied.
MODEL STUDIES
When the mouth is closed, it is obvious that all air must flow through
the nose. Similarly, when the nose is completely blocked all air must flow
through the mouth. However, there are many individuals who use a
combination of oral and nasal breathing. Since the magnitude of oral and
nasal airway resistance depends upon many factors, model studies are
useful in providing an understanding of the effects of resistance changes
62
Warren
| 3| 5 : 65 Diom
: 18 ||
: W ) : 34
: # {–
: N-2soon
* 68.5
All Meosurements in MM
19.5 K–19.5 ->
Dig m. Diom
Figure 16. An analog model of the upper respiratory tract. The mouth and ve-
lopharyngeal port can be opened in 0.05 cm increments and nasal airway resis-
tance can be varied.
on airflow patterns. In this investigation a simple mechanical model of the
upper airway was used to evaluate such effects. Briefly, it was assumed
that if a model could be designed to adequately simulate the physiological
parameters of breathing, then the data observed from it could be viewed
with a fair degree of confidence and possibly could produce a better
understanding of the breathing process.
The plastic model employed in this study is illustrated in Figure 16.
Dimensions, such as oral cavity and nasal pathway length, were approxi-
mated from cephalometric measurements of normal subjects. Structures
which could not be approximated from X-ray measurements, such as the
cross-sectional area of the nose and mouth, were constructed so as to
offer resistance to airflow comparable to known values in normal indi-
viduals. The velopharyngeal and oral ports could be varied from 0 to 1
cm”. Respiratory airflow was simulated by a pump which produced air-
flow in the form of sinusoidal waves. Nasal airway resistance could be
increased by changing the size of the velopharyngeal orifice and/or by
inserting corks of known resistances into the nasal airway.
A slight opening of the oral port causes a major decrease in nasal
airflow (Fig. 17). This is the result of normally greater resistance to
airflow in the nasal passages. Opening the mouth 0.10 cm reduces nasal
airflow to approximately 50 percent while opening the mouth 0.30 cm."

63
Aerodynamic Studies of Upper Airway
RESPIRATORY AIR FLOW .250 L/SEC.
wo- e oral port closed
§
80-
> |>
9|C 60– i.e.
I lº e or al port size . 10 cm?
Oz l oz
< |3:
, || 40- e
< | < e oral port size .20 cm2
º 6 20- e oral port size .30 cm2
Z I H
O

VELOPHARYNGEAL ORIFICE OPEN
Figure 17. Nasal airflow as a percentage of total respiratory airflow. Note that
slight opening of the oral port shunts most of the air through the mouth.
reduces nasal airflow to 20 percent. What this suggests is that an individ-
ual does not have to open his mouth very much to mouth breathe if his
nasal cavity is obstructed. Figure 18 illustrates the fall in nasal airflow
when the oral port is opened. What the model studies demonstrate quite
clearly is that the amount of airflow moving through the nose or mouth or
both depends upon the magnitude of resistance within each portal.
While the nasal airway resistance is usually constant at any given time,
it can be modified considerably by elevation of the soft palate which
occurs in some individuals during breathing (Fig. 19). If adenoids were
present, airway resistance in the nasal port would be quite high. How-
ever, in most instances the oral port would control the movement of air
since it can act as a variable resistance.
These data do raise some interesting questions. For example, if open-
ing the mouth only 0.30 cmº reduces oral airway resistance below that of
the unobstructed nasal airway, why then should facial or oral morphology
be affected by a need to mouth breathe? One possible explanation is that
in certain instances enlarged tonsils, a large tongue or long, draping pos-
terior pillars may obstruct the posterior oral cavity. In this case, tongue
position would have to be altered to open the mouth 0.30 cm and this
could produce a greater anterior oral opening than would normally be
necessary. However, this is only speculation.
64
Warren
RESPIRATORY AIR FLOW .250 L/SEC.
O I I I I I
..] O . 20 .30 . 40 .50
ORAL PORT SIZE (cm2)
Figure 18. Nasal airflow decreases rapidly as the mouth is opened. This is due to
the fact that nasal airway resistance is higher than oral airway resistance.
Congenital Palatal Incompetency and Adenoids
As interest in the nasopharyngeal airway and especially the adenoids
increases, the importance of the adenoids in speech must not be over-
looked (Subtelny and Baker, '56). Removal of the adenoids in patients
with cleft palate, congenital palatal incompetency or neuromuscular defic-
its can result in hypernasality and articulatory deficits. Most clinicians are
aware of the importance of the adenoid tissue in augmenting palatopha-
ryngeal closure in cleft palate. However, in congenital palatal incompe-
tency where there is a tissue deficiency, speech may be normal until the
adenoids are removed. Often it is only after such surgery that the clini-
cian becomes aware of a defect masked by the adenoids such as submu-
cous cleft palate, short soft palate, deep pharynx or neuromuscular defic-
its (Figs. 20-21). In these cases, the importance of the adenoids dictates
their retention as long as possible. The slow process of adenoid involution
sometimes allows the palate to compensate for such defects. If the ade-
noids are considered a hazard to an individual’s health, then the safest
course to follow is a peritubular adenoidectomy.

65
Aerodynamic Studies of Upper Airway
º zºº, º ſº.
º º
Figure 19. If the Soft palate is elevated during breathing, nasal airway resistance
would increase.
PLETHYSMOGRAPHIC TECHNIQUES FOR TOTAL AIRWAY
STUDIES
Body plethysmographs are used to study the relationship between pres-
Sures, airflow rates and lung volume during breathing (DuBois et al., 56).
The total airway resistance can be evaluated using either the oral or nasal
airways (Fig. 22). There are two basic types of plethysmographs: the
closed box type and the open box type. In the closed box type, the
Subject sits and breathes inside the plethysmograph, which is basically an
airtight chamber about the size of a telephone booth (Fig. 23). Its use is
based upon the application of Boyle's law relating gas volumes and pres-
Sures. When the subject breathes, lung volume changes and this change
66

Warren
NEUROMUSCULAR DEF|CITS SHORT FUNCTIONAL PALATE
Figure 20. Congenital palatal incompetency due to (A) a short soft palate, (B) a
deep pharynx, (C) neuromuscular deficits, and (D) a short functional palate. In
this case the levator muscle inserts too far anteriorly and most of the palate hangs
vertically.
ADENOID PAD CLOSURE NO CLOSURE AFTER ADENOIDECTOMY
Figure 21. (A) Congenital palatal incompetency is often masked by the adenoids
and (B) can often only be seen after surgical removal of the adenoids.


67
Aerodynamic Studies of Upper Airway
- ..”**** -
Figure 22. Measuring the pressure drop between the lungs and outside the mouth
or nose simultaneously with airflow provides an estimate of total airway resis-
tance. Pi is pressure in the lungs and P2 pressure outside the mouth.
alters box pressure. A very sensitive pressure transducer is attached to the
box and it measures the pressure changes within the box with reference to
atmospheric pressure. Since the total amount of gas in the plethysmo-
graph-lung system is constant, any increase in gas pressure inside the lungs
of the subject must cause a decrease in pressure in the gas in the plethys-
mograph. Therefore, at any instant, the resulting pressure change in the
gas in the box must be opposite in sign to the pressure change in the lungs.
There are several factors which, if not carefully controlled, influence
box pressure and cause measurement artifacts. There is a uniform and
continuous effect on pressure which results from heat production by the
subject in the box. This heat produces a baseline drift if it is not compen-
sated for by creating a small leak in the chamber, introducing a compen-
sating electronic signal or airconditioning the box.
Another problem that must be dealt with is the nonuniform and discon-
tinuous effect of warming and humidifying the inspired air and water

68
Warren
In cose of
Emergency
Hed fed Break Glass :
Pneumotochograph
E= —O—
Ma-Aaaa-
:^-
—[−H-T
O O O O
Pressure
Tronsducer
Recorder
Figure 23. The closed box body plethysmograph. V, volume rate of airflow; PM,
mouth pressure; PP, plethysmograph pressure.
vapor condensation of the cooled expired air. This problem can be over-
come by electronic compensation, rebreathing in a bag, or keeping the
chamber at 100 percent humidity with a cool air vaporizer. Although
there are several other possible sources of error, they are negligible com-
pared to the effects of uncontrolled temperature and humidity. -
The open box plethysmograph employs a technique involving displace-
ment of some air during chest movement (Fig. 24). The displacement is
recorded by a pneumotachograph, which provides an indication of the
volume change occurring as the subject breathes. Changes in the lung
volume are measured by recording volumes displaced by the body sur-
face. As described by Hixon ('72), the subject is seated in a wooden body
chamber and is totally encased except for his head and neck. A collar
seals the chamber and suction is used to make it airtight. As the subject
breathes, chamber pressure decreases with chest volume. This change in
chamber volume and subsequent lowering of pressure results in air flow-
ing into the chamber through a pneumotachograph screen. The flow mea-
sured by the pneumotachograph is then integrated to provide an estimate
of volume displacement. The same pressure transducer also provides a

69
Aerodynamic Studies of Upper Airway
SUCTION
WS
NECK SEAL
SCREEN
|- Pchamber
AIR
CONDITIONER
Figure 24. The open box body plethysmograph with which changes in lung volume
can be measured (from Hixon, '72).
measure of the displacement related to gas compression; since the total
volume is the sum related to compression and displacement of gas, true
lung volume can be determined by summing the two electronically.
With slight modification, the open box plethysmographic technique can
be used for measuring subglottal pressures (Fig. 25). In this case, a lucite
dome is used so that the entire body is encased in the plethysmograph.
Subglottal pressure changes are determined from the measurements of
compressional volume changes, and the pressure-volume relationships are
70








Warren
Poirway
opening
#screen
T PChamber
ſº º
- º
CONDITIONER
Figure 25. Chamber configuration for making plethysmographic measurements of
alveolar pressure (from Hixon, '72).
71





Aerodynamic Studies of Upper Airway
quantified by using Boyle's law. As in the closed box method, the experi-
menter must be extremely careful to minimize measurement artifacts.
Seen in this light, the body plethysmograph offers several real advantages
over other techniques for measuring subglottal pressure, airway resistance
and volume displacements.
AERODYNAMICS OF SPEECH
A constant subglottal pressure must be maintained to power the speech
mechanism. In spite of the complex interplay between muscular and non-
muscular forces, the actual generation of pressure in the lower airway and
the air movement which results appears to be well controlled. Since
speech occurs during the expiratory phase of breathing, normal expira-
tory pressure must be modified to some extent. The subglottal pressure
during normal expiratory breathing fluctuates between 20 cmH20 and
atmospheric, depending upon the phase of expiration. However, the sub-
glottal pressure head for speech is maintained at approximately 6-10
cmH20. Thus, expiratory forces must be modified so that an appropriate
and consistent magnitude of subglottal pressure is generated during the
speech process (Fig. 26). That is, in order to maintain a constant subglot-
tal pressure, relaxation pressure resulting from the recoil of elastic fibers
in the lung and chest wall must be checked initially by active contraction
of the inspiratory muscles (Hixon, '73; Fig. 27). Similarly, as lung volume
decreases, relaxation pressure falls and activation of the expiratory
muscles is necessary at Some stage to maintain subglottal pressure. Lade-
foged and colleagues ('58) observed electromyographically that the exter-
nal intercostals remain in action at the beginning of the utterance to
check the descent of the rib cage and to counteract relaxation pressure As
lung volume decreases, external intercostal activity diminishes; it ceases
completely when lung volume is slightly less than what it is after a normal
inspiration. At that point, relaxation pressure seems to be sufficient to
provide the necessary pressure for the utterance. Expiratory muscle activ-
ity is then required to maintain pressure, with the internal intercostals
gradually increasing activity. Supplemental activity may occur in the later
stage, with the external oblique, rectus abdominus and latissimus dorsi
contracting when lung volume is below that of resting level (Campbell,
'68). Maintenance of subglottal pressure requires more than checking or
enhancing elastic recoil forces. Compensation for the sudden changes in
respiratory load that occur when the upper airway closes or opens must
be almost instantaneous if pressure is to be maintained at a near constant
level. Otherwise, sound intensity and fundamental frequency would be
unstable. This poses a considerable error control problem that is not
encountered in breathing. For example, phonation of the word /papa/
72
Warren

Ps /~1
Po /\!\ ^_^– I

My T |EN|1|||s|MER"clean
Vº y^_^^ ~~~~ I
O _/U/~2^^-v-Vºr
Vo


S —º-ºº-º-º-º-º-º-esº-
P CAL = 50 mm H2O
W CAL= |OOcc/sec
Figure 26. Comparison of subglottal pressure (Ps), intraoral pressure (Po), nasal
airflow (Va), oral airflow (Vo) and sound (S) during phonation of the sentence,
“My tent is very clean.” A nearly constant subglottal pressure is modulated into
discrete patterns of pressure and airflow.
involves abrupt closure of the lips and impounding of air. Subglottal
pressure is maintained by labial closure. The lips open for the vowel and
Vocal folds adduct to maintain pressure in the lungs. The flow of air from
the lungs does not appreciably affect pulmonary pressure because the
respiratory muscles adjust recoil forces. The lips close again for /p/ and
the glottis opens. Once again pressure is sustained by closure of the oral
port.
Undoubtedly a complicated feedback system regulating pressure and
airflow must be involved. Although there is some general information
73
Aerodynamic Studies of Upper Airway
IOO-
–
8
O
*
-
6
O
•=
–
4
O
Resting Level
O I-T I I I I I I I I I I I
–4O –2O O 2O 4O 6O 7O
SUBGLOTTAL PRESSURE (cm H2O)
* * * * * * * * *
§ Expiratory muscle pressure
§ needed to mointain subglottal
Inspiratory muscle pressure
needed to prevent excessive
pressure during phonation subglottal pressure during
phonotion
Figure 27. Lung volume and pressure relationships during speech. At high lung
volumes, inspiratory muscle activity is required to check recoil pressure of elastic
fibers in the lung and chest wall and prevent excessive subglottal pressure. At low
lung volumes, expiratory muscle activity is required to maintain subglottal pres-
sure for speech (modified from Hixon, '73).
available, current models are still highly speculative. One possible system
is illustrated in Figure 28. It consists of a controller unit or computer
coordinating center, sensors or receptors to transmit information, and
effectors to power the system and produce articulatory movements (War-
ren, '76). The controller most certainly is in the brain, and presumably
not only the medulla but higher centers as well are involved. Sensors may
be located in the lung and along the vocal tract. The effectors are the
respiratory muscles which power the pump and the articulatory structures
are the variable resistances which modulate the airstream. This hypotheti-
cal model is presented only for the purpose of demonstrating our limited
knowledge. Receptors for sensing such parameters as pressure and air-
flow have not been identified, yet monitoring is necessary if errors are to
be corrected. For example, in breathing, overinflation of the lungs is


74
Warren
º º
[
/S-2 \ RESPRATORY
PUMP
Ç) Resistance Control
[...I. Possible Sensing Mechanisms
------ Motor
— Sensory
Figure 28. Theoretical representation of a possible feedback mechanism con-
trolling subglottal pressure (from Warren, '76).
75













Aerodynamic Studies of Upper Airway
prevented by receptors which transmit information on volume to the
respiratory centers. Breathing is a slow process in comparison to speech,
however, and regulation of volume can be accomplished, to a great ex-
tent, by the alpha motoneuron system, although the gamma efferent sys-
tem is available for rapid readjustments when required. More rapid and
frequent adjustments of pressure and airflow would be necessary for
speech. Gross muscle activity such as checking elastic recoil may be con-
trolled by the alpha system, but changes in respiratory load in response to
events in the upper ariway require a faster response. The gamma efferent
system may provide the rapid, sensitive adjustments necessary to main-
tain constant pressure. In addition, simultaneous preprogramming for the
respiratory muscles, as well as for the articulators, is also a possibility.
There is evidence that the brain prepares the articulators for the pro-
duction of speech sounds well in advance (Kozhevnikov and Chistovich,
'65; Ohman, '66, '67; Daniloff and Moll, '68; Moll and Daniloff, '71).
There is an interval of preparation for a specific sound, and this interval
presumably involves advanced neural input to the articulators. This same
advanced programming may provide simultaneous input to the respira-
tory muscles to prepare for possible events such as transient back pres-
sures. Indeed, coarticulation seems to be a reflection of advanced pro-
gramming. The gamma loop and the small motor fiber system associated
with it would still operate as a servo to drive the main muscle fibers, but
their operating range would be smaller with preprogramming of the alpha
system.
Upper Airway Dynamics
Structures in the upper airway play an essential role in the speech
process by modulating the airstream into precise patterns. The direction
and velocity of air movement are controlled primarily by changes in air-
way size. These changes occur well in advance of the sounds to be pro-
duced and, therefore, influence the preceding segments of speech as well
(Warren, '64a).
Most speech activity is directed through the oral airway and the airway
resistance to airflow varies from less than 1.0 cmH20/L/sec. for low vowels
to an infinite resistance or complete obstruction in the case of plosives.
Air actually flows more readily through the oral cavity than it does
through the nasal cavity because airway resistance of the oral airway is
approximately half that of the nasal airway, providing the tongue is not
elevated to any great extent. That is, for low vowels, airflow would pass
through the oral cavity even if the palatopharyngeal orifice were open.
Whether air exits from the mouth or nose under these circumstances
depends upon the relative amounts of resistance in each cavity. In normal
situations nasal airway resistance is between 1.0 and 3.0 cmH20/L/sec.
76
Warren
30-
25 -
2O –
G
QD
Oſ)
N.
sº-> — V P ORIFICE .IO cm?
2|** Q, |5 - — — V P ORIFICE 20 cm
I | N - - - - - , V P ORIFICE .4Ocm?
E
C)
|O –
O,
5 | N
N
TO-
*-
Te—
©----........ T-e——
***O--------------- ©--------...... -O -O
O U I I I U
O O5 ..[O |5 2O
ORAL PORT SIZE (cm”)
Figure 29. The relationship between velopharyngeal orifice resistance and oral
port size at varying degrees of velopharyngeal closure (respiratory airflow, 0.250
L/sec.).
(Warren et al., '69). Lip, tongue and soft palate movement can modify
resistance to airflow considerably and shunt airflow through the nose as is
the case when nasal sounds are produced.
Figure 29 illustrates the effect of the size of the oral airway opening on
velopharyngeal orifice resistance at different degrees of velopharyngeal
closings. It should be evident that, in spite of an open velopharyngeal
orifice, the nasal chamber with its smaller cross-sectional area and higher
resistance receives substantial amounts of airflow only when the oral
airway is constricted. This relationship between oral airway resistance and
nasal airway resistance becomes very important in individuals with a cleft
palate (Warren and Ryon, '67).


77
Aerodynamic Studies of Upper Airway
A Rºyal H| 0 |Me P|A |P|A|
S —ºº-º-º-º-
V - || | ~~~. Ll- I
O.5 Se C.
8 O T- | |
Pressure Col. = 50 mm. H.O
- 6 O H |
*: | Flow Col = |OOCC./SeC.
E |
* Fº |
<ſ 4O |
Lil |
º: |
2 O H.
w | | | A
º | | | g
N ſ
– | | |
O | | | | | | | | | | |
A IRIY IOI H | O | ME | P |A | P | A
E U
Figure 30. A typical intraoral pressure (Po), sound (S), nasal airflow (Va) and
velopharyngeal orifice area record of the sentence, “Are you home, papa?” Op-
ening of the orifice occurs well in advance of the nasal consonant. This nasalizes
the vowel and results in nasal emission of air prior to the actual voicing of the
nasal Sound.
The Effects of the Velopharyngeal Orifice. During the production of
non-nasal sounds, the soft palate and pharyngeal walls form a valve that
prevents airflow from entering the nasal cavity. Ordinarily, closure is
tight and complete in most individuals. However, there are some normal
speakers who demonstrate very small openings (0.02-0.03 cm’) at times
(Warren, '64a). Also, there is variability among speakers in terms of the
period of time the orifice is open for nasal sounds. Figure 30 illustrates an
opening sequence and demonstrates that nasalization may occur two pho-
netic segments ahead of the point at which the nasal consonant is voiced.
Similarly, the closing phase nasalizes a portion of the plosive consonant.



78
Warren
7O H.
6 O H e
5
O
}-
3
4
O
}*
H
O O
O
O
3 O H
| - -
.."
2O H- * ee
O
O
©
| O H. O O O O
• * © O O O
ºs- O O © e * ,
O l I l l I I 1 l l 1–1–1 l 1 l l —l I l s l 1 1.
O IO 2O 3O 4 O 5 O 6 O 7O 8O 9 O |OO |||O
AREA ( mm2 )
Figure 31. The relationship between orifice size and intraoral pressure during
consonant production. The consonants /b/, /t/ and /m/ were studied. A nonlinear
pattern is evident, which indicates that adequate intraoral pressure for non-nasal
consonants cannot be attained when the orifice is larger than 10-20mmº.
Nasal emission of air occurs during this entire interval. In the specific
example shown, the velopharyngeal orifice opened well in advance and,
in this instance, began as far back as at the voiceless /h/ in preparation for
the nasal /m/. For example, the duration of theſm/ segment is 120 msec.,
compared to an opening interval of 284 m.sec. prior to the initiation of its
sound. The orifice, therefore, was open 404 m.sec., or nearly 3.5 times
longer than the actual voicing of the /m/ segment. When the velopharyn-
geal orifice is closed, pressure in the nasal cavity is atmospheric during
speech because of open communication with the outside. When it is open,
as in the speech sample just cited or in the case of cleft palate, its effect
on speech aerodynamics can be substantial.
As indicated earlier, an intraoral pressure of 3-7 cmH20 is normal for
pressure consonants (Brown and McGlone, '69). If the velopharyngeal
mechanism is open more than 0.20 cmº for non-nasal sounds, intraoral
pressure cannot be maintained at this level (Fig. 31) unless the nasal
cavity is obstructed (Warren and DuBois, '64). Actually most speakers
would demonstrate audible nasal emission and some hypernasality with
openings between 0.1 and 0.2 cmº. However, other structures besides the
velum influence nasal airflow. The amount of oral airway opening, airway
resistance of the nasal cavity and oral cavity volume all influence pressure
79
Aerodynamic Studies of Upper Airway
and airflow in an interactive way (Warren and Devereaux, '66; Warren
and Ryon, '67). If the velopharyngeal mechanism is open during a pres-
Sure-consonant sound, the relationship between intraoral pressure and
size of the opening can be described by the equation
V 2 • yº)
For plosive sounds, A relates to size of the velopharyngeal orifice while in
the case of fricatives, A relates to opening at the oral port as well. The
portion of the equation
indicates an orifice type airflow through the oral and/or nasal ports and
1/2(k,V* + k,V)
indicates that flow through both chambers has laminar and turbulent
components. If respiratory effort is increased, the laminar components
are diminished and the equation changes to
W T2 tº
P F k3 [...] + k,Vº
A
Nasal resonance is also modified if the palatal orifice is not open
enough for nasal sounds (Warren, '64b). Denasal voice quality results
when the opening is small (possibly below 0.20 cm3) or the nasal airway is
blocked. This may occur with upper respiratory infections, enlarged ade-
noids or after treatment for cleft palate. Figure 32 indicates that the
velopharyngeal orifice must not only be opened an adequate amount for
nasalization but should begin to open at least with the vowel preceding
the nasal consonant, otherwise, denasal voice quality results.
APPLICATION OF AERODYNAMIC TECHNIQUES
Pressure and airflow devices have been used in a variety of ways to
measure the aerodynamics of speech production. Intraoral pressure can
be recorded by placing a small catheter in the mouth and attaching it to a
pressure transducer, amplifier and recorder (Fig. 33). Similarly, subglot-
tal pressure can be measured by inserting a needle attached to a catheter
into the trachea below the glottis. Pressures can be measured anywhere
along the vocal tract as long as access can be provided.
Airflow along the vocal tract can be recorded with a pneumotacho-
graph appropriately attached by tubing or a mask to the mouth or
80
Warren
| ſi\
B |E|SS|| E S | | |A YED A L L | S |U|M|ER
S
V. --→– I
O.5 Sec.
3O H Pressure Cal-50mm. Ho
2O p Flow Col. = 2 OO co./sec.
.
|O
o! —”
| | | | | | | | | | | |
B|E|S| || S |T|AYE|D| ALL | S |U|M|ER
S E M
Figure 32. Denasal speech results when the velopharyngeal orifice does not open
sufficiently nor in advance of the nasal consonant. Nasal emission of air is dimin-
ished and the preceding vowel is not nasalized.
PRESSURE
TRANSDUCER
O O O O
PRESSURE Poocoozzº
AMPL | FIER O O
M| CROPHONE
OOOO
L
RECORDER
Figure 33. Intraoral pressure is measured by using an oral catheter which is
attached to a pressure transducer from which the signal is amplified and recorded.
nose or both (Fig. 34). Integrating airflow values over time provides a
measure of air volumes used in speech.
Aerodynamic techniques have been used to obtain important informa-
tion about normal and abnormal speech production. The techniques usu-
ally involve the application of hydraulic principles (Warren, '75). Upper
airway structures such as the tongue, teeth, lips and palate form numer-
ous constrictions which affect airflow and pressure. Hydraulic equations
are used to estimate the size of these constrictions. The basis for such
measurements can be explained in terms of airflow through simple pipes.
The size of a constriction in a pipe can be calculated by measuring the





81
Aerodynamic Studies of Upper Airway
2 ~
` Ali Wiº
\
*
FLOW
HEATED dP
FLOWMETER y avºuries
VISI CORDER
MICROPHONE __
Figure 34. Airflow is measured using a face mask, pneumotachograph, amplifier
and recorder.
A
To Different id | Pressure
Trons ducer
To Flow meter
AP
6– Posterior
- Ph ed
Co the fer in Gryng
* WO ||
NOS tril SOff
To Differentid <- P :
Pressure Tronsducer <- O || Of e
CO the fer
in Mouth
Figure 35. Catheters are placed above and below the orifice to measure the
differential pressure. The catheter placed in the left nostril is secured by a cork,
which plugs the nostril and creates a stagnant air column above the orifice (A).
The second catheter is placed in the mouth (B). Both catheters are connected to a
differential pressure transducer. The pneumotachograph is connected to the right
nostril and collects orifice airflow through the nose (from Warren, '76).






82
Warren

Cotheters
<1 Different id
Pressure
Transducer Pressure
/2 U-sº-2 Amplifier
* Monitor
(2%
&lº Heated – Oscilloscope
WN T) Flow meter -\ 0 &
& y VisiCorder
NS
F|O Flow
W o gº •
A
Transducer mplifier
Figure 36. Catheters are placed on both sides of the oral constriction to measure
oral port opening for fricative sounds. Airflow is collected in a face mask and goes
to the pneumotachograph.
airflow through the pipe (V) and the pressure drop across the pipe (P -
P2). Area of the constriction is then calculated from the equation
V
2AP
k d
A =
The size of articulatory constrictions can also be estimated in this man-
ner (Warren, '76; Fig. 35). Thus, if one wanted to measure the size of the
velopharyngeal orifice, it would be necessary to record the pressure dif-
ference between the nose and the mouth and the volume rate of airflow
through the nose during speech. This measurement is especially impor-
tant in cleft palate cases. Similarly, the size of the oral opening during
fricative productions can be estimated by placing catheters and a face
mask in positions illustrated in Figure 36 (Claypoole et al., '74; Smith et
al., '78). This technique has been used to measure oral port opening in
individuals with open-bite malocclusion (Klechak et al., '76).
SUMMARY
Aerodynamic techniques provide a useful tool for objectively assessing
the resistance to air flow in the oral and nasal airways during breathing
83
Aerodynamic Studies of Upper Airway
and speech. The instruments involved provide accurate information and
the procedures are fairly simple. The limited number of aerodynamic
studies presently available do not support the assumption of some that
nasal airway inadequacy produces dentofacial deformities. The data do
demonstrate, however, that abnormalities of oral and nasal structures can
seriously compromise speech performance.
REFERENCES
Agostini, E. and J. Mead. Statics of the respiratory system. In: Handbook of
Physiology, Respiration, I., W. Fenn and H. Rahn (eds.), American Physio-
logical Society, Washington, D.C., 1964.
Angle, E. H. Treatment of Malocclusion of the Teeth, S. S. White, Philadelphia,
7th edition, 1907.
Bell, W. H. Revascularization and bone healing after anterior maxillary osteot-
omy: a study using adult rhesus monkeys. J. Oral Surg. 27:249-255, 1969.
Bell, W. H. Correction of skeletal type anterior open bite. J. Oral Surg.
29:706-714, 1971.
Bell, W. H. Biological basis for maxillary osteotomies. Am. J. Phys. Anthrop.
38:279-290, 1973.
Brown, W. W. and R. E. McGlone. Constancy of intraoral air pressure. Folia
Phoniat. 21:332-339, 1969.
Campbell, E. and J. M. The respiratory muscles. In: Annals of the New York
Academy of Science, A. Bouhuys (ed.), Sound Production in Man,
155:135-139, 1968.
Cherniack, R. M. and L. Cherniack. Respiration in Health and Disease. W. B.
Saunders, Philadelphia, 1961.
Claypoole, W. H., D. W. Warren and D. P. Bradley. The effect of cleft palate on
oral port constriction during fricative productions. Cleft Palate J. 11:95-104,
1974.
Comroe, J. H. Physiology of Respiration. Year Book Medical Publishers, Chi-
cago, 1965.
Daniloff, R. G. and K. L. Moll. Coarticulation of lip rounding. J. Speech and
Hear. Res. 11:707-721, 1968.
Derichsweiler, H. Gaumennahrterweiterung. Karl Hanser, Munchen, 1956.
Drettner, B. The nasal airway and hearing in patients with cleft palate. Acta
Otolaryng. 52:131-142, 1960.
DuBois, A. G., S. Y. Bothelho and J. H. Comroe. A new method for measuring
airway resistance in man using a body plethysmograph. Values in normal sub-
jects and in patients with respiratory disease. J. Clin. Invest. 35:327-335, 1956.
Harvold, E. P., K. Vargervik and G. Chierici. Primate experiments on oral
sensation and dental malocclusions. Am. J. Orthodont. 63:494-508, 1973.
Hershey, H. G., B. L. Stewart and D. W. Warren. changes in nasal airway
resistance associated with rapid maxillary expansion. Am. J. Orthodont.
69:274-284, 1976.
Hixon, T. J. Respiratory function in speech. In: Normal Aspects of Speech, Hear-
84
Warren
ing and Language, F. Minifie, T. Hixon and F. Williams (eds.), Prentice-Hall,
Englewood Cliffs, New Jersey, 1973.
Hixon, T. J. Some new techniques for measuring the biomechanical events of
speech production: One laboratory's experiences. ASHA Rep. 7:68-103, 1972.
Hunter, B. M. Nasal airway resistance, breathing patterns and dentofacial charac-
teristics. M. S. Thesis, University of North Carolina, Chapel Hill, 1971.
Klechak, T. L., D. P. Bradley and D. W. Warren. Anterior open bite and oral
port constriction. Angle Orthodont. 46:232-242, 1976.
Korkhaus, G. Present orthodontic thought in Germany: Jaw widening with active
appliances in cases of mouth breathing. Am. J. Orthodont. 46:187-206, 1960.
Kozhevnikov, V. A. and L. A. Chistovich. Speech: articulation and perception.
U.S. Department of Commerce, Joint Publications Research Service, Wa-
shington, D.C., 1965.
Ladefoged, P., M. H. Draper and D. Whitteridge. Syllables and stress. Misc.
Phon. 3:1-15, 1958.
Linder-Aronson, S. Adenoids: Their effect on mode of breathing and nasal air-
flow and their relationship to characteristics of the facial skeleton and the
dentition. Acta Oto-Lar. Supple. 265:1-132, 1970.
Linder-Aronson, S. and G. Aschan. Nasal resistance to breathing and palatal
height before and after expansion of the median palatine suture. Odont. Revy.
14:254-270, 1963.
Linder-Aronson, S. and A. Bäckström. A comparison between mouth and nose
breathers with respect to occlusion and facial dimensions. Odont. Revy.
11:343-376, 1960.
Lubker, J. F. Aerodynamic and ultrasonic assessment techniques in speech-
dentofacial research. In speech and the dentofacial complex: The state of the
art. ASHA Rep. 5:207-223, 1970.
Mead, J. and E. Agostini. Dynamics of breathing. In: Handbook of Physiology,
I., W. Fenn and H. Hahn (eds.), American Physiological Society, Washington,
D.C., 1964.
Mead, J., A. Bouhuys and D. F. Procter. Mechanisms generating subglottic pres-
sure. In: Annals of the New York Academy of Science, A. Bouhuys (ed.),
Sound Production in Man. 155:177-181, 1968.
Moffatt, J. B. Habits and their relation to malocclusion. Aust. Dent. J. 8:142-149,
1963.
Moll, K. L. and R. G. Daniloff. Investigation of the timing of velar movements
during speech. J. Acoust. Soc. Am. 50:678-684, 1971.
Ohman, S. E. G. Coarticulation in VCV utterances: Spectrographic measure-
ments. J. Acoust. Soc. Am. 39:151-168, 1966. 47
Ohman, S. E. G. Numerical model of coarticulation. J. Acoust. Soc. Am.
41:310-320, 1967.
Schendel, S. A., J. Eisenfeld, W. H. Bell, B. N. Epker and D. J. Mishelwich.
The long face syndrome: vertical maxillary excess. Am. J. Orthodont.
70:398-408, 1976.
Smith, H. Z., G. D. Allen, D. W. Warren and D. J. Hall. The consistency of the
pressure-flow technique for assessing oral port size. J. Acoust. Soc. Am.
64:1203–1206, 1978.
85
Aerodynamic Studies of Upper Airway
Subtelny, J. D. and H. K. Baker. The significance of adenoid tissue in velopha-
ryngeal function. Plast. Reconstr. Surg. 17:235-250, 1956.
Subtelny, J. D., J. H. Worth and M. Sakuda. Intraoral pressure and rate of flow
during speech. J. Speech and Hear. Res. 9:498–518, 1966.
Tully, W. J. Abnormal functions of the mouth in relation to the occlusion of the
teeth. In: Current Orthodontics, John Wright & Sons Ltd., Bristol, 1966.
Turbyfill, W. J. The long-term effect of rapid maxillary expansion. Master's The-
sis, University of North Carolina, Chapel Hill, 1976.
Turvey, T. A. and D. J. Hall. Alterations in nasal airflow, resistance and ve-
lopharyngeal competency following maxillary surgery for correction of dento-
facial deformities: A preliminary report. Third Intern. Cong. Cleft Palate,
#115, 1977.
Warren, D. W. Velopharyngeal orifice size and upper pharyngeal pressure-flow
patterns in normal speech. Plast. Reconstr. Surg. 33:148-162, 1964a.
Warren, D. W. Velopharyngeal orifice size and upper pharyngeal pressure-flow
patterns in cleft palate speech: A preliminary study. Plast. Reconstr. Surg.
34:15-26, 1964b. -
Warren, D. W. The determination of velopharyngeal incompetence by aerody-
namic and acoustical techniques. Clin. Plast. Surg. 2:299-304, 1975.
Warren, D. W. Aerodynamics of sound production. In: Contemporary Issues in
Experimental Phonetics, Norman Lass (ed.), C C Thomas Co., Springfield,
Ill., 1976.
Warren, D. W. and A. B. DuBois. A pressure-flow technique for measuring
velopharyngeal orifice area during continuous speech. Cleft Pal. J. 1:52-71,
1964.
Warren, D. W. and J. D. Davis. Effects of oral structures on airway conductance
during normal speech. J. Dent. Res. 56:232, 1977.
Warren, D. W. and J. L. Devereux. An analog study of cleft palate speech. Cleft.
Pal. J. 3:103-114, 1966. -
Warren, D. W., L. F. Duany and N. D. Fischer. Nasal pathway resistance in
normal and cleft lip and palate subjects. Cleft Pal. J. 6:134-140, 1969.
Warren, D. W. and D. J. Hall. Intraoral pressures in whispered speech: differ-
ences among voiced and voiceless consonants. Presented at the American
Speech and Hearing Association annual Meeting, 1969.
Warren, D. W. and W. E. Ryon. Oral port constriction, nasal resistance and
respiratory aspects of cleft palate speech: An analog study. Cleft Pal. J.
4:38-46, 1967.
Warren, D. W., W. C. Trier and A. G. Bevin. Effect of restorative procedures on
the nasopharyngeal airway in cleft palate. Cleft Pal. J. 4:367-373, 1974.
Watson, R. M., D. W. Warren and N. D. Fischer. Nasal resistance, skeletal
classification and mouthbreathing in orthodontic patients. Am. J. Orthodont.
54:367-379, 1968.
86
CRANIOCERVICAL ANGULATION AND NASAL
RESPIRATORY RESISTANCE
Beni Solow, dr. odont.
Ellen Greve, dr. odont.
Institute of Orthodontics
The Royal Dental College
In the study of the biological mechanisms that control postnatal craniofa-
cial morphogenesis, information about the relationship between naso-
respiratory function and craniofacial growth may be of considerable
value.
It is generally recognized that certain characteristics in craniofacial
morphology, such as a narrow, upper dental arch, posterior crossbite and
high V-shaped palate, sometimes are seen in connection with pathological
conditions which cause long-term obstruction of the nasopharyngeal air-
way. Mouthbreathing, which often accompanies obstruction of the na-
Sopharyngeal airway, has been considered to be the cause of these mor-
phological characteristics. However, studies of the relationship between
mouthbreathing, malocclusion and craniofacial morphology have yielded
conflicting results. (See the following for a review of the literature on this
subject: Emslie et al., 52; Linder-Aronson and Bäckström, '60; and
Linder-Aronson, '70).
In a comprehensive study of children with nasal respiratory obstruction
due to adenoids, Linder-Aronson ('70) demonstrated that there were
significant differences in the craniofacial morphology of these children as
compared with normal controls (Fig. 1). Follow-up studies of children
who underwent adenoidectomies (Linder-Aronson, '74, '75) showed that
the differences between patients and controls decreased significantly. Evi-
dence for altered craniofacial morphology in patients with nasal obstruc-
tion due to adenoids, particularly as regards mandibular form, has also
been found by Dunn and co-workers ('73) and Koski and Lähdemäki
(75). Wankewicz (31) and Harvold (75) reported that changes did occur
in the craniofacial morphology of animals after experimental inducement
of nasopharyngeal airway obstruction.
Linder-Aronson ('70, '74, '75) considered the preoperative differences
between children with nasal obstruction due to adenoids and controls to
be caused by mouthbreathing which lowered the tongue position relative
87
Craniocervical Angulation
— CONTROL-CHILDREN (GROUP 1)
- - - - ADENOIDEC TOMY - CHILDREN (GROUP 5)
Figure 1. Tracings of lateral cephalometric radiographs showing differences be-
tween 60 children who underwent adenoidectomy for obstructed nose breathing
(Group 5) and 81 control children (Group 1). Note the significant differences in
such variables as the adenoids, the dentition, the skeleton, lips and position of the
tongue (from Linder-Aronson, '70, with permission).
to the facial skeletal structures. He considered the postoperative changes
to be due to a raised tongue position caused by the transition to nasal
respiration which was made possible by the adenoidectomy. The very com-
prehensiveness of the craniofacial differences documented in Figure 1 sug-
gests, however, that perhaps the changed tongue position is not the only
factor responsible for the characteristic craniofacial morphology of these
patients. In particular, recent studies of head posture and craniofacial
morphology (Solow and Tallgren, '76; Opdebeek et al., 78; Thompson
Posnick, '78) suggest that a changed head posture might also be involved.
The observation, that in children with nasal obstruction due to adenoids,
the head is bent backwards in relation to the neck, was reported as early as
1926 by Schwarz. Increased craniocervical angulation in subjects with ade-

88
Solow
noid induced nasal obstruction has also been described by Ricketts ('68),
Koski and Lähdemäki (75) and Quinn and Pickrell (78).
HEAD POSTURE
Anthropological Studies
The natural head position in man has been the subject of considerable
interest in the literature. In the field of physical anthropology this interest
was first motivated by the requirement for comparison of craniofacial
morphology in different population groups (von Baer and Wagner, 1861;
Broca, 1862; von Ihering, 1872; Schmidt, 1876; Lüthy, '12). Later, par-
ticular attention was devoted to the phylogenetic implications of the si-
multaneous development of the brain, the cranial base flexion and the
erect posture in man (Bolk, '15; Cameron, 27; Kraus, 27; Dabelow, '29,
'31; Weidenreich, 24, 41; Schultz, '42; de Beer, '47; DuBrul, '50; Björk,
'57; Delattre and Fenart, '59, '60; Riesenfeld, '67). Experimentally, the
presence of a relationship between morphology and posture was sup-
ported by the demonstration of craniofacial morphological changes in
animals following artificially induced changes in body posture (Lisowski et
al., '61; Moss, '61; Riesenfeld, '66, '69).
Orthopedic Studies
The motility in the craniocervical articulation and the cervical spine is
important in the diagnosis of pathological conditions related to the cervi-
cal vertebrae and has been extensively studied from an orthopedic point
of view. The main interest has been focussed on the maximal ranges of
movement of the individual joints as assessed from cadavers and skeletal
material (Weber, 1827; Henke, 1859; Hultkrantz, 12; Virchow, '28) or
from radiographic studies of living subjects (Bakke, 31; Albers, '54;
Exner, '54; Aho et al., '55; Brocher, '55; Werne, '57; Baldini and Guares-
chi, '58; Kottke and Mundale, '59; Bugyi, '60; Penning, '60; Zeitler and
Markuske, '62; Lewit and Krausová, '62, '63). The anteroposterior mobil-
ity in the middle part of the cervical column was found to be lower than
in the craniocervical joints and in the lower part of the cervical column.
Orthodontic Studies
In the Orthodontic area, the need for assessment of facial esthetics lead
to a search for a craniofacial reference plane, which in the natural head
position would exhibit a relatively constant relationship to the true hori-
zontal or vertical plane (Downs, '56; Bjerin, '57; Moorrees and Kean,
'58; Schonherr, '67; Mills, '68). The natural head position has also been
89
Craniocervical Angulation
used for orientation of the head in studies of the mandibular rest position
(Tallgren, '57, '66), of the oropharyngeal structures (Carlsöö and Leijon,
'60; Bench, '63; Cleall, '65; Cleall et al., '66; Fromm and Lundberg, '70;
Cleall, '72), and of the relationship between head posture and craniofa-
cial morphology (Solow and Tallgren, 71a, b, '76, ’77; Opdebeek et al.,
’78; Thompson Posnick, '78).
The methods used to determine the natural head position have varied.
They included use of a mirror (Bjerin, '57; Moorrees and Kean, '58;
Opdebeek et al., '78), a light source placed in front of the patient (Cleall,
'65; Cleall et al., '66) and no external reference (Carlsöö and Leijon, '60;
Fromm and Lundberg, '70). Solow and Tallgren ('71a, b) recorded a
position determined by the use of a mirror and one determined without
external reference. In most studies the subjects were placed in a sitting
position. However, Bjerin (57) compared the head position of sitting and
standing subjects, and Solow and Tallgren ('71a) recorded the head posi-
tion while their subjects were standing.
In the analysis of head posture, most authors related the position of the
head to the true vertical or horizontal. It was pointed out by Solow and
Tallgren ('71b), however, that in order to analyze changes in head pos-
ture, it is useful to divide the total change in the position of the head
relative to the true vertical into its two components; i.e., the position of
the head relative to the cervical column and the position of the cervical
column relative to the true horizontal. Their analysis of the 3 degree
difference between head position determined without external reference
and that determined with a mirror suggested that change in cervical incli-
nation accounted for the major part of the positional change of the head,
whereas changes in craniocervical angulation accounted for the detailed
positional adjustments.
HEAD POSTURE AND CRANIOFACIAL MORPHOLOGY
The relationship between head posture and craniofacial morphology
was emphasized by Schwarz (.26, ’31), who found that extension of the
head in relation to the body, particularly during sleep, led to distal dis-
placement of the mandible and the development of Class II malocclusion.
Björk ('55, '60, '61) noticed that individuals with a flattened cranial base
and a retrognathic facial type carried their head in an extended position,
while those with a marked bend of the cranial base and a prognathic
facial type carried their head in a lower position. Bench ('63) in a radio-
graphic study of the growth of the cervical vertebrae noted a tendency for
the neck to be curved in subjects with square faces, and straight with a
long cervical column in subjects with long faces.
90
Solow
A systematic analysis of the correlations between craniofacial morphol-
ogy and the positional relationship of the head to the true vertical and to
the cervical column was carried out by Solow and Tallgren ('76). They
found that of the postural variables, the craniocervical angulation showed
the most comprehensive correlation with craniofacial morphology, i.e.,
the position of the head in relation to the cervical column seemed to be
more closely related to craniofacial form than the position of the head to
the true vertical. The correlations indicated that, on the average, exten-
Sion of the head relative to the cervical column was seen in connection
with large anterior and small posterior facial heights, small anteroposte-
rior craniofacial dimensions, large inclination of the mandible relative to
the anterior cranial base and to the palatal plane, facial retrognathism, a
large cranial base angle, and a small nasopharyngeal space. Subjects cha-
racterized by extreme flexion of the head in relation to the cervical col-
umn would be characterized, on the average, by small anterior and large
posterior facial heights, large anteroposterior craniofacial dimensions,
small inclination of the mandibular plane relative to the anterior cranial
base and to the palatal plane, facial prognathism, a small cranial base
angle and a large nasopharyngeal space (Fig. 2). The findings regarding
the relationship between craniocervical angulation and craniofacial mor-
phology were confirmed by Thompson Posnick ('78).
Solow and Tallgren ('76) further observed that differences in craniofa-
cial morphology between subjects with large and small craniocervical an-
gulations were remarkably similar to those between subjects with large
and small mandibular plane inclinations. A direct comparison showed
that the average craniofacial morphology of a group of subjects who had
a large craniocervical angulation resembled that of a group of subjects
who had a large mandibular plane inclination (Fig. 3A). Similarly, the
craniofacial morphology of a group of subjects characterized by a small
craniocervical angulation was very like that seen in a group of subjects
characterized by a small mandibular plane inclination (Fig. 3B). This
suggests that the factors responsible for the postural differences may also
be responsible for differences in mandibular plane inclination and facial
type. A similar relationship between facial type and craniocervical angu-
lation was reported by Opdebeek and co-workers (78).
Hypothesis of Soft-Tissue Stretching
In order to explain the relationship between head posture, craniocervi-
cal angulation and craniofacial morphology, a hypothesis was suggested
by Solow and Kreiborg ('77) according to which posturally induced
stretching of the facial soft-tissue layer might influence craniofacial mor-
phological development. Hypothetically, an extension of the head in rela-
91
Craniocervical Angulation
Max. NSL/OPT
sº tº ſº ºn mº tº Min. NSL/OPT
NSL - Orientation
Figure 2. Superimposed mean facial diagrams illustrating differences in craniofa-
cial morphology between ten subjects who had a large craniocervical angulation,
i.e., a large angle between the nasion-sella line (NSL) and the posterior tangent
to the odontoid process of the second cervical vertebra (OPT, Max. NSL/OPT),
and ten subjects who had a small craniocervical angulation (Min. NSL/OPT). The
diagrams are superimposed on the nasion-sella line using the sella point for align-
ment. The nasion-sella line is placed horizontally (from Solow and Tallgren, '76).
tion to the cervical column would entail a passive stretching of the facial
Soft-tissue layer draping the face and neck, which consists of skin, fasciae
and some superficial musculature (Schwarz, 26). The effect of this would
be slight backward and downward forces exerted by the soft-tissue layer
on the facial skeleton which might influence facial development, e.g., by
restraining the forward component and increasing the downward compo-

92
Solow
\!; N. N.S.), /()|''|' \) in NS|, /()|''|'
- - - - - - \l;t x . NS1, / \||. –––––– Mlin. NS]./\ll,
Figure 3. Mean facial diagrams illustrating similarity in the craniofacial morphol-
ogy of (A) ten subjects with a large craniocervical angulation (Max. NSL/OPT)
and ten subjects with a large mandibular plane (ML) inclination (Max. NSL/
ML), and (B) ten subjects with a small craniocervical angulation (Min. NSL/OPT)
and ten subjects with a small mandibular plane inclination (Min. NSL/ML). The
diagrams were superimposed in the same way as those in Figure 2 (from Solow
and Tallgren, '76).
Soft-tissue —) Differential forces
stretching on skeleton
y \
Postural change Morphologic change
^ /
Neuromuscular . Obstruction
feedback of airways
Figure 4. Suggested chain of factors relating craniocervical angulation and cranio-
facial morphology to each other. In principle each factor may be the site of a
primary affliction triggering the cycle (from Solow and Kreiborg, '77).
nent of maxillary and mandibular growth relative to the cranial base.
Since one of the vital functions of head posture is to maintain an ade-
quate airway, a control mechanism linking airway adequacy, neuromus-
cular feedback, head posture, soft-tissue stretching and facial develop-
ment could be hypothesized (Figs. 4 and 5). The hypothesis predicts the
developmental consequences if any of these factors in the chain are

93
Craniocervical Angulation
Figure 5. Facial morphology and craniocervical posture in a subject with man-
dibular bicondylar hypoplasia. Notice the extremely large craniocervical angle. a,
suggested restraining influence of soft-tissue layer on facial development; b, Sug-
gested traction from cervical investing fascia responsible for gonial apposition and
antegonial notching (from Solow and Kreiborg, '77).
changed. In the case of adenoid obstruction of the nasopharyngeal air-
way, the hypothesis predicts increased craniocervical angulation and
changes in craniofacial morphology corresponding to this changed head
posture. Removal of adenoid airway obstruction should result in a re-
duction of craniocervical angulation and corresponding changes in cra-
niofacial morphology.
A systematic demonstration of the predicted increase in craniocervical
angulation due to obstructed nasopharyngeal passage has not been made,
although Woodside and Linder-Aronson (79) have demonstrated that the
94

Solow
position of the head is raised relative to the true vertical plane in subjects
with nasopharyngeal obstruction due to adenoids.
The purpose of the present study, therefore, is to examine the relation-
ship between nasopharyngeal respiratory obstruction and craniocervical
angulation in a group of children referred for adenoidectomy.
MATERIAL
The sample consisted of children referred by physicians for nasal respi-
ratory obstruction, otitis media or recurrent upper airway infections, and
hospitalized at the ENT department of the Copenhagen Municipal Hospi-
tal. The children were examined on the day before adenoidectomy was
performed and again two to three months after surgery. A total of 32
children were examined. However, eight children were later excluded
from the sample due to the diagnosis of sinuitis maxillaris, pneumonia,
etc., or because the adenoidectomy was accompanied by tonsillectomy.
The sex and age distribution of the remaining sample of 24 children are
given in Figure 6. The mean age was 8.7 years, with a range from 4.7 to
12.5 years.
METHODS
The registrations comprised determination of the nasal respiratory re-
sistance and the recording of a lateral cephalometric head film in the
natural head position and of a posteroanterior head film.
Rhinomanometric Recordings
In analogy with the definition of electrical resistance (R) as the voltage
drop (V) divided by the current (A) or R = V/A, the fluid dynamic
concept of nasal respiratory resistance (NRR) is usually defined as the
pressure drop (A p) across the nose divided by the air flow through the
nose (V), NRR = A pſW. However, due to turbulent air flow, the nasal
respiratory resistance is not constant but increases at higher flow rates.
The methodology developed for recording nasal respiratory resistance
has been reported in detail by Solow and Greve ('79). Therefore, only the
the main points of the recording procedure will be described here.
The recording of pressure drop and flow was made with a modified
version of the Mercury Electronics Nasal Resistance Meter, NR1, which
is based on two membrane-type pressure transducers (Fig. 7). Nasal air-
flow was routed via a nose mask to a pneumotachygraph (a flow head) in
which a calibrated mesh produced a small pressure drop proportional to
the flow. This was recorded by one of the transducers in the NR1. The
95
Craniocervical Angulation
N
|- [] M
8 H 3 F
6 H
4 |
TOTETSTV.I.
Age
Figure 7. Nasal Resistance Meter, NR1 (Mercury Electronics, Glasgow, Scot-
land). a, flowhead; b, extra digital display.
pressure drop across the nose is defined as the difference between the
retropharyngeal pressure and the pressure outside the nose.
In the posterior rhinomanometric procedure, the retropharyngeal pres-
sure is recorded by an oral tube. This recording can easily be obstructed
by contact between the tongue and the soft palate. To prevent this, the
oral tubing was fitted with a small collar made from a disposable tip for a
fibre otoscope (Fig. 8A). To prevent air slippage due to poor fit of the
nose mask, the rim of the mask was lined individually at every recording
96







Solow
Figure 8. Posterior rhinomanometric recording. (A) Preparation of oral tubing.
(B) Recording procedure with individually lined mask.
Session with impression material (Fig. 8B). The recordings were moni-
tored on a storage screen oscilloscope. This proved particularly valuable
for conditioning the children to elevate the soft palate in order to avoid
blockage of the retropharyngeal pressure recording.
The NR1 equipment has a built-in threshold feature which produces a
digital display of the pressure drop corresponding to a preselected flow
threshold. A light bulb and a tone indicates that the threshold has been
reached. In the present study, all the posterior recordings were made at a
flow threshold of 0.2 L/sec. (12 L/min.). This was the highest flow rate that
could be reached without excessive effort on the part of all of the children.
The output from the recording procedure can be recorded in three
ways: (1) as a strip chart record of pressure drop and flow versus time
(Fig. 9); (2) as an oscilloscope display of pressure drop versus flow (Fig.
10); and, (3) as the digital readout of the pressure drop corresponding to
a preselected flow threshold. In the present study, the oscilloscope dis-
play was used only for monitoring the recording, the actual numerical
data being obtained from the digital display.
Each measurement of nasal respiratory resistance was based on four
Series of recordings, each of which comprised readouts from four respira-
tions; i.e., each measurement was calculated as the mean of 16 record-
ings. Before each recording session the children were administered a few
drops of 0.5% Neosynephrine® after which they blew their noses to
thoroughly clear them.
The method error, s(i), within a session, i.e., the standard deviation of
the individual measurement, was found to be 0.2 cm H20/L/sec. Compari-
Son of recordings from two sessions two weeks apart, a comparison which
included the physiologic variability in nasal resistance, showed a method
error of 0.5 cm H20/L/sec.
97

Craniocervical Angulation
- - -
L^ º - ".
- -
- ".
- ". - *_ _
- - -
- -
/ N
| / N
4. -
/ \
Z Pºssure, AP
ºf - -
| FLOW ſol/MIN | SEC
PRESSURE IOMM H2O
Figure 9. Strip chart recording of transnasal flow and pressure drop.
Cephalometric Recordings
The radiographic equipment consisted of the motorized, vertically ad-
justable Dana Cephalix with an attached Lumex Special headholder and
a Philips Rotapractix rotating anode x-ray source with a focus of 0.8 by
0.8 mm. The vertical adjustability permits the recording of standing
subjects. The focus-median plane distance was 180 cm. The film-median
plane distance was 10 cm for the lateral cephalometric films and 15 cm
for the posteroanterior (p-a) films, with enlargements of 5.6% and
8.3%, respectively.
The lateral cephalometric radiographs of the natural head position
were recorded as previously described by Solow and Tallgren ('71a). The
procedure used for obtaining the natural head position consisted of two
phases. First, a reproducible body posture, “orthoposition”, was obtained
by letting the subject “walk on the spot” in order to eliminate excessive
curvature of the spinal column. Secondly, the head position was defined
by asking the subject to look into his own eyes in a mirror placed on the
wall in front of him (mirror position). The position was rehearsed before
the subject was placed in the cephalometer. The subject was then posi-
tioned under the raised head holder, and the positioning procedure was
repeated. If the ear rods of the head holder, when lowered, did not match
98


Solow
Figure 10. Oscilloscope display of flow (V) and pressure drop (Ap) during a
respiratory cycle.
the ears, the subject was instructed to move his feet slightly forward or
backward. During this phase of the positioning, it is essential that the
Operator does not move the head of the subject forward or backward with
his hands, as this will affect the craniocervical angulation. When a correct
position of the subject’s ears had been obtained, the ear rods were in-
Serted. Finally the head position was corrected for possible lateral rotation
or tilting, while at the same time care was taken to ensure that the sagittal
position of the head was not affected.
In a sample of adults, the method error for this procedure was found to
be 1.4° for the position of the head relative to the true vertical and to the
cervical column, and 1.9° for cervical inclination (Solow and Tallgren,
’71a).
99

Craniocervical Angulation
N X S Skewness
Vbſ
NSL/VER" 24 97.22 3.91 0.47
NSL/OPT9 24 98.00 6.73 0.01
OPT/HOR* 24 89.22 6.40 0.28
pm-ad1 mm 24 11.53 5.20 –0.26
pm-adz mm 24 8.45 3.53 —0.52
NRR 23 2.99 1.58 1.43**
(cm H2O/L/sec)
**p < 0.01
Table 1. Statistical description of postural and respiratory variables before adenoi-
dectomy was performed.
The reference points and lines used in the present study are shown in
Figure 11. The digitizing and data processing procedures have been previ-
ously described by Solow and Tallgren ('76). The statistical analyses were
performed using the SAS computer program (Barr et al., '76) and the
IBM 370/165 computer at the Northern Europe University Computing
Centre (NEUCC) in Copenhagen.
FINDINGS
The results of the cephalometric and rhinomanometric examinations
done before the adenoidectomy was performed are presented in Table 1.
The mean position of the head in relation to the true vertical (NSL/
VER) was 97.2°. This agrees with the findings of Woodside and Linder-
Aronson ('79) who found a mean of 96.9° in 16 children with nasopharyn-
geal obstruction due to adenoids. The mean craniocervical angle (NSL/
OPT) of the children considered in the present study was 98.0°, and the
mean cervical inclination (OPT/HOR) was 89.2°.
The mean sagittal extent of the free nasopharyngeal airway (pm-ad1
and pm-ad?) was 11.5 mm and 8.5 mm, respectively, which agrees with
the means of 11.0 mm and 8.9 mm reported by Linder-Aronson and
Henrikson ('73) for 8 to 9-year-olds who were mouth breathers.
For nasal respiratory resistance (NRR) the mean was 3 cm H20/L/sec.
at a flow rate of 0.2 L/sec., and the distribution form showed a significant
positive skewness of 1.4 (Fig. 12). A logarithmic transformation, LNRR
= log(NRR - 1.0), normalized the distribution form and was included in
the subsequent correlation analysis.
100
Solow

FML
NSL-W- tº
FH ) ad2
2–=.”
NL —w. º
º
y
VER
HOR
OPT CVT
Figure 11. Reference points and lines used in the present study. NSL, nasion-sella
line; FH, Frankfort horizontal line; NL, nasal line; FML, foramen magnum line;
OPT, odontoid process tangent; CVT, cervical vertebra tangent; VER, true verti-
cal; HOR, true horizontal; pm, pterygomaxillare; ad1, intersection of adenoid
contour with a line from pm to basion (the most posteroinferior point of the
clivus); ad2, intersection of adenoid contour with a line from pm to the midpoint
of the sella-basion line (Linder-Aronson and Henrikson, '73).
101
Craniocervical Angulation
Respiratory variables
before adenoidectomy
POStural NRR LNRR pm-adl pm-adz
variables N=23 N = 23 N = 24 N = 24
before
adenoidectomy
NSL/VER .15 .05 — .24 — .23
FHſVER .13 .05 — .24 — .24
NL/VER .31 .16 — .43 — .47°
FML/VER .38 .30 — .32 — .26
NSL/OPT .47% .41* — .56** — .55**
FH/OPT .50* .45* — .60% + — .60**
NL/OPT .57++ .47% — 67*** — 70***
FML/OPT • .63** .57++ – .59% + .55**
OPT/HOR — .42* — .43 .44* .44*
CVT/HOR — .35 — .37 .26 .23
OPT/CVT — .07 — .06 .32 .40
NRR — .47% — .48*
LNRR — .44* — .43*
*p < 0.05
**p < 0.01
***p < 0.001
Table 2. Correlations between postural and respiratory variables before adenoi-
dectomy was performed. NRR, nasal respiratory resistance; LNRR, log (NRR-
1.0); pm-ad] and pm-ad?, sagittal depth of free nasopharyngeal airway. Postural
variables are defined in figure 11.
The postural and respiratory variables were correlated before the aden-
oidectomy was performed, and the results are given in Table 2. The
correlations between craniocervical angles (NSL/OPT, FH/OPT, NL/
OPT, FML/OPT) and nasal respiratory resistance (NRR, LNRR) ranged
from 0.41 to 0.63 and were significant at the 5% and 1% levels. A
scattergram illustrating this relationship is seen in Figure 13. There was
no significant correlation between the position of the head relative to the
true vertical (NSL/VER, FH/VER, NL/VER, FML/VER) and nasal res-
piratory resistance (NRR, LNRR).
The sagittal depth of the free nasopharyngeal airway (pm-ad1 and pm-
ad2) showed markedly negative correlations (-0.55 to -0.70) with the
craniocervical angles, significant at the 1% and 0.1% levels (Fig. 14). The
102
Solow
1O-
8-
2-
T
I I
1 2 3 4 5 § 7 8
I
I
NRR before adenoidectomy (cm H2O/I/sec)
Figure 12. Distribution of nasal respiratory resistance (NRR) before adenoidec-
tomy.
correlations between the position of the head relative to the true vertical
and pm-ad1 and pm-ad? were considerably lower and only reached the
5% level for NL/VER.
Thus, on the average, extension of the head relative to the cervical
column was seen in connection with a large nasal respiratory resistance
and a narrow passage between the adenoid tissue and the choanae.
The changes that occurred after the adenoidectomy was performed are
given in Table 3. The surgical removal of adenoid tissue resulted in a
marked increase in the sagittal depth of the free nasopharyngeal airway
(pm-adl and pm-ad2) of about 10.0 and 6.6 mm, respectively. The post-
surgical values of these dimensions (not in table) were 21.5 mm and 15.1
mm, which agrees well with the means of 20.1 mm and 15.1 mm reported
by Linder-Aronson and Henrikson ('73) for 8 to 9-year-olds who were
nose breathers.
The position of the head relative to the true vertical was lowered sig-
nificantly by 2.6°, resulting in a mean of 94.6°, which agrees with the
postsurgical value of 93.3° found by Woodside and Linder-Aronson ('79).
103
Craniocervical Angulation
NSL/OPT O
11O°H
O
O
H O
O
O O O O
1OO°H
O
O O
• • * *
* O O O
O
O
90°F
O
O
8O” l 1 l l ſl 1– l —1–
1 2 3 4 5 6 7 8
NRR (cm H2O/I/sec)
Figure 13. Scattergram illustrating the correlation between nasal respiratory resis-
tance (NRR) and craniocervical angulation (NSL/OPT) before adenoidectomy (r
= 0.47; p < 0.05).
The craniocervical angulation was reduced by 2.4°, which was signifi-
cant at the 5% level, whereas cervical inclination showed no significant
change.
Nasal respiratory resistance decreased significantly by a mean of 1 cm
H.0/L/sec (Fig. 15). The significantly skewed distribution was normalized
by the transformation LNRR = -log(abs(NRR - 1.1)].
The pattern of change in nasal respiratory resistance was further exa-
mined by correlating the change in nasal respiratory resistance with the
presurgical values of the postural and respiratory variables (Table 4).
Significant correlations were found only with the presurgical values of
nasal respiratory resistance. The scattergram (Fig. 16) shows, moreover,
104
Solow
X S skewness
Vbſ
NSL/VER" 24 –2.63” 3.58 –0.11
NSL/OPT° 24 —2.36* 4.18 0.18
OPT/HOR* 24 –0.27 3.67 0.14
pm-ad 1 (mm) 24 9.95% ++ 4.15 0.11
pm-adz (mm) 24 6.64*** 2.95 0.76
NRR 23 – 1.05% + 1.45 — 1.08° “
(cm H2O/L/sec)
*p < 0.05
**p < 0.01
***p < 0.001
Table 3. Changes after adenoidectomy: Statistical description of changes in pos-
tural and respiratory variables from presurgical to postsurgical stages.
NSL/OPT O
110 -
O
O
O
O
O e e^
1OO° -
O
O O
O O O O
}= O O O
O
o O
90° H O
O
O
80° _l A —1—
O 2 4 6 8 10 12 14 16
pm - ad2 (mm)
Figure 14. Scattergram illustrating association between the sagittal depth of the
free nasopharyngeal airway (pm-ad2) and craniocervical angulation (NSL/OPT)
before adenoidectomy was performed (r = -0.55; p < 0.01).
105
Craniocervical Angulation

N -
1O –
Change in NRR (cm H2O/I/sec)
Figure 15. Distribution of changes in nasal respiratory resistance (NRR) after
adenoidectomy was performed.
that the reduction in resistance occurred only in those subjects who pre-
Surgically had displayed an increased resistance.
The correlations between the changes in the postural and respiratory
variables are given in Table 5. The correlation between the change in
nasal respiratory resistance and the change in craniocervical angulation
ranged from 0.30 to 0.39. This association did not reach the 5% level of
significance. However, the scattergram illustrating this relationship (Fig.
17) shows that while the craniocervical angulation of the subjects with an
almost unchanged nasal resistance could either increase or decrease, the
craniocervical angulation of subjects with a marked reduction in nasal
resistance only decreased. To statistically represent this, the subjects were
divided into two subgroups according to change in NRR. The mean
change in NSL/OPT for 7 subjects with a reduction of NRR larger than 1
cm H20/L/sec was -4.6° E 1.1, significant at the 1% level. The mean
change for the remaining group was -1.3° E 1.1, and did not differ signifi-
106
Solow
Variables before Change in nasal
adenoidectomy respiratory resistance
after adenoidectomy
NRR LNRR
NSL/VER –0.10 0.02
NSL/OPT –0.35 –0.20
OPT/HOR y 0.32 0.24
pm-adl 0.31 0.19
pm-ad2 0.31 0.18
NRR –0.90% + + —0.75+++
LNRR –0.85*** –0.76***
***p < 0.001
Table 4. Correlations between postural and respiratory variables before adenoi-
dectomy and change in nasal respiratory resistance after adenoidectomy. N=23.
cantly from zero. The difference between the mean changes in craniocer-
vical angulation in the two groups was significant at the 0.1% level. After
adenoidectomy, the craniocervical angle thus, on the average, was re-
duced by almost 5° in the subjects in whom nasal respiratory resistance
had been reduced.
DISCUSSION
The more than 30 methods developed for measurement of nasal respi-
ratory resistance reflect the practical and theoretical problems involved in
the assessment of this physiological parameter (Stoksted, '51; Stoksted
and Nielsen, '57; Aschan et al., '58; Masing, '65; Solomon et al., '65;
Ingelstedt et al., '69; Fischer, '70; Kern, '73; Bachmann, '73; Masing and
Frimberger, '74; Solow and Greve, ’79). A survey of the different metho-
dologies and terminologies currently in use is given by Kern ('77).
In the method used in the present study (Solow and Greve, ’79), par-
ticular emphasis was placed on eliminating the variability in the record-
ings due to air slippage around the mask and on reducing the failure rate
for the posterior method of recording.
Due to the turbulence created at high airflow rates, the relationship
between pressure drop and airflow is not constant during the respiratory
cycle, and the pressure-flow diagram has a typical reverse sigmoid shape.
The ratio between pressure drop and airflow at any single point of the
107
Craniocervical Angulation
:
N RR before (cm H2O/I/sec)
Figure 16. Association between nasal respiratory resistance before adenoidectomy
(NRR before) and the change in resistance after adenoidectomy (NRR change).
A large change was seen only in those subjects who had great nasal respiratory
resistance before surgery (r = -0.90; p < 0.001).
curve, therefore, cannot be used to characterize all aspects of nasal respi-
ratory resistance in a given physiologic situation. A number of authors
have argued that for various values of x, the ratio Ap/V* would remain
constant during the entire respiratory cycle (Aschan et al., '58; Spoor,
'63; Masing, '65; Drettner, '69; Fischer, '70; Kern, '73). It has been
shown, however, that these ratios actually were not constant for all flow
rates (Solomon and Stohrer, '65; Bachmann, '73).
In the present study the pressure drop was measured only at a single,
relatively low airflow rate under standardized conditions. The recorded
values, therefore, can be used only for intra- and inter-individual com-
parisons of subjects measured under the same standardized experimental
conditions.
Analysis of nasal respiratory resistance before surgery showed a
skewed distribution of the recordings. The data suggests that the children
108
Change in respiratory variables
Change in
postural NRR LNRR pm-ad! pm-ad?
variables N = 23 N = 23 N = 24 N = 24
NSL/VER .33 .30 .10 — .40
FHAVER .35 .32 .10 — .41*
NL/VER .35 .31 .08 — .44*
FML/VER .30 .26 .10 — .40
NSL/OPT .33 .38 .15 .00
FHAOPT .35 .39 .15 .00
NL/OPT .35 .39 .14 — .04
FML/OPT .30 .34 .16 .01
OPT/HOR — .07 — .16 — .08 — .39
CVT/HOR — .04 — .11 — .06 — .39
OPT/CVT — .11 — .15 — .05 .00
NRR — .46° — .48*
LNRR — .40 — .47%
*p < 0.05
Table 5. Correlations between changes in postural and respiratory variables after
adenoidectomy. NRR, change in nasal respiratory resistance; LNRR, -log [abs
(NRR-1.1)]; pm-ad1 and pm-ad?, change in sagittal depth of free nasopharyngeal
airways. Postural variables defined in Figure 11.
might be classified into two groups: children with obstructed nasal respi-
ration after use of nose drops, and children with no such obstruction after
use of nose drops. This agrees with clinical observations that adenoidec-
tomy is performed sometimes due to otitis media, and sometimes due to
nasal obstruction as evidenced by snoring, mouthbreathing and rhinolalia.
On the other hand, a retrospective examination of the presurgical hospi-
tal records did not permit any such clear distinction, as most of the
children showed symptoms of both otitis media and nasal obstruction due
to adenoids.
The correlation analysis of the relationship between head posture and
nasal respiratory resistance (Table 2) confirmed the prediction that sub-
jects with obstruction of the nasopharyngeal airway would display in-
creased craniocervical angulation. From the scattergram illustrating this
association (Fig. 13), it may be seen, furthermore, that while the subjects
with a low nasal respiratory resistance had a full range of craniocervical
109
Craniocervical Angulation
NSL/OPT
6. O
NRR change (cm H2O/I/sec)
Figure 17. Scattergram illustrating association between the change in nasal respi-
ratory resistance (NRR) and the change in craniocervical angulation (NSL/OPT)
after adenoidectomy. Thin lines indicate zero change (r = 0.33; p > 0.05).
angulations, the subjects with a high respiratory resistance generally had
a large craniocervical angle. No association was found with the position of
the head relative to the true vertical.
The relationship between obstruction of nasopharyngeal airway and
craniocervical angulation was further supported by the marked negative
correlation between the sagittal depth of the free nasopharyngeal airway
(pm-ad1 and pm-ad?) and craniocervical angulation. The smaller the dis-
tance between the adenoids and the choanae on the lateral head film, the
larger the craniocervical angle. Also, the correlations of the position of
the head relative to the true vertical were considerably lower.
The finding that the craniocervical angulation (NSL/OPT) was more
strongly correlated to nasal respiratory resistance than to the position of
the head relative to the true vertical (NSL/VER) agrees with the findings
of Solow and Tallgren ('76) that NSL/OPT showed a more systematic
correlation with craniofacial morphology than NSL/VER. This supports
the contention that the craniocervical angulation is the postural variable
which is most strongly correlated to craniofacial development.
110
Solow
Figure 18. Facial appearance of patient before (A) and 2 months after (B) adenoi-
dectomy.
As seen in Figure 18, removal of the adenoids sometimes results in a
dramatic improvement of facial appearance. As would be expected, the
Surgical procedure resulted in a considerable increase in the distances
pm-ad] and pm-ad2.
Nasal respiratory resistance, on the average, was reduced by 1 cm
H20/L/sec. However, analysis of the distribution of the changes in NRR
(Fig. 15) showed that about 60% of the sample displayed only small
fluctuations around zero, while the remaining 40% showed changes from
-1 to -5 cm H20/L/sec. Thus, the small average change for the whole
group was due to a rather large reduction of nasal respiratory resistance
in the subjects with nasal obstruction.
Craniocervical angulation decreased on the average by about 2° after
Surgery, a change significant at the 5% level. A detailed analysis showed,
moreover, that in the sub-group with a marked reduction of nasal respira-
tory resistance, the craniocervical angle was reduced by almost 5°, signifi-
cant at the 1% level. These findings confirm the prediction that removal
of adenoid airway obstruction should result in a reduction of the cranio-
cervical angulation.
The morphological changes observed in subjects with adenoid obstruc-
111

Craniocervical Angulation
tion of the airway have generally been attributed to the lowered tongue
and mandibular position caused by mouthbreathing, which itself is an
adaptive response to the respiratory obstruction. On the other hand, the
changes in craniofacial morphology seen in subjects with adenoid obstruc-
tion (Fig. 1) are remarkably similar to those found in subjects with a large
craniocervical angulation (Fig. 2).
The two postural factors thus related to craniofacial morphology, i.e., a
lowered position of the tongue and the mandible and a raised position of
the head relative to the cervical column, might seem to be different. It
should be noted, however, that statements regarding a lowered position
of the tongue and the mandible usually imply that it is lowered in relation
to the cranial base/maxillary complex. Perhaps the same findings could
also have been described as a raised cranial base/maxillary position rela-
tive to the tongue and the mandible.
The distinction between the two descriptions of the postural relation-
ship is not unimportant. First, the neuromuscular patterns of activity are
not the same when the head is tilted upward relative to a stable linguo-
mandibulo-cervical complex as when the tongue and the mandible are
lowered relative to a stable craniocervical complex (Thurow, '70, 75;
Davies, '79). Second, different patterns of distortion of the soft-tissue
envelope of the face would result from the two types of postural change,
with possible different effects on craniofacial morphology. In view of
these considerations, considerable caution should be exerted in the inter-
pretation of previous studies of the position of the tongue and the mandi-
ble before and after adenoidectomy, when the changes relative to the
cervical column and the true vertical have not been analyzed.
The finding in the present study that removal of adenoid airway ob-
struction resulted in a reduction of the craniocervical angulation is in
agreement with the prediction of the soft-tissue stretching hypothesis.
According to the hypothesis, this change might contribute to the explana-
tion of the reversibility of the morphological changes in children who
have undergone adenoidectomy documented by the follow-up studies of
Linder-Aronson ('74, '75).
The general question of whether form determines function or function
determines form has been much debated in the Orthodontic literature in
the last decades. In particular, the concept of the functional matrix has
received much attention (Moss and Young, '60; Moss, '68; Moss and
Rankow, '68; Moss and Salentijn, '69; Johnston, '76). While providing an
elaborate conceptual framework for how function can affect form, the
functional matrix hypothesis has not provided predictions of the effect on
craniofacial morphology of adenoid obstruction of the airways, or of the
effect of changes in craniocervical angulation. Thus, the hypothesis of
soft-tissue stretching (Solow and Kreiborg, '77) and the findings of the
112
Solow
present study neither support nor contradict the tenets of the functional
matrix hypothesis.
The fact that the findings of the present study confirm the predictions
of the soft-tissue stretching hypothesis, on the other hand, does not
“prove” that this hypothesis is correct. Rather, the results indicate that
the hypothesis has resisted an attempt at refutation (Popper, '69). The
hypothesis predicts increased craniocervical angulation and specific mor-
phological changes for a number of conditions which cause obstruction of
the nasopharyngeal airways. Observation of such relationships have been
made by several authors (Bosma, '57; Cleall, '72; Pruzansky, '73; Quinn
and Pickrell, '78). This encourages continued efforts to examine the pre-
dicted relationships in order to improve our understanding of the mech-
anisms that control normal and abnormal craniofacial development.
SUMMARY
In order to examine a predicted relationship between craniocervical
angulation and obstruction of the nasopharyngeal airway, 24 children,
aged 4 to 12 years, were examined before and after adenoidectomy.
Cephalometric recordings of the natural head position and rhinomano-
metric recordings of nasal respiratory resistance were obtained for each
subject. Before adenoidectomy, a large craniocervical angulation was
seen in connection with a large nasal respiratory resistance and a narrow
passage between the adenoid tissue and the choanae. After adenoidec-
tomy, reduction of the craniocervical angulation occurred in the children
in whom nasal respiratory resistance was reduced.
These findings confirmed the predictions of the soft-tissue stretching
hypothesis and provide an explanation for the reversible craniofacial mor-
phological changes previously observed in subjects in whom adenoid na-
sal obstruction had been removed. Examination of other factors causing
obstruction of nasopharyngeal airways should shed further light upon the
mechanisms controlling craniofacial morphogenesis.
ACKNOWLEDGEMENTS
The study was funded by grant 512-8080 from the Danish Medical Research
Council. The authors wish to express their indebtedness to Professor, Dr. Med.
Henning Sorensen, E.N.T. Department, Hvidovre Hospital, Denmark, for pro-
viding the sample, and to laboratory assistant, Mrs. Jytte Norgaard, for efficient
assistance.
REFERENCES
Aho, A., O. Vartiainen and O. Salo. Segmentary antero-posterior mobility of the
cervical spine. Ann. Med. Intern. Fenn. 44:287–299, 1955.
113
Craniocervical Angulation
Albers, D. Eine Studie über die Funktion der Halswirbelsäule bei dorsaler und
ventraler Flexion. Fortschr. Roentgenstr. 81:606-615, 1954.
Aschan, G., B. Drettner and H. E. Ronge. A new technique for measuring nasal
resistance to breathing, illustrated by the effects of histamine and physical
effort. Ann. Acad. Regiae Sci. Upps. 2:111-126, 1958.
Bachmann, W. Probleme der Rhinomanometrie - Ihre Lösung durch X - Y
Schreibung. Z. Laryngol. Rhinol. Otol. 52:872-878, 1973.
von Baer, K. E. and R. Wagner. Bericht liber die Zusammenkunft einiger Anthro-
pologen im September 1861 in Göttingen zum Zwecke gemeinsamer Bespre-
chungen. Leopold Voss, Leipzig, 1861.
Bakke, S. N. Röntgenologische Beobachtungen über die Bewegungen der
Wirbelsäule. Acta Radiol. (Stockholm), Suppl. 13, p. 1-75, 1931.
Baldini, G. and B. Guareschi. Rilievi sull'esame radiologico funzionale del ra-
chide cervicale. Minerva Med. 49:117-122, 1958.
Barr, A. J., J. H. Goodnight, J. P. Sall and J. T. Helwig. A user's guide to
SAS-76. SAS Institute Inc., Raleight, N.C., 1976.
deBeer, G. R. How animals hold their heads. Proc. Linnean Soc. (London),
158:125-139, 1947.
Bench, R. W. Growth of the cervical vertebrae as related to tongue, face and
denture behavior. Am. J. Orthodont. 49:183-214, 1963.
Bjerin, R. A comparison between the Frankfort horizontal and the sella turcica-
nasion as reference planes in cephalometric analysis. Acta Odont. Scand.
15:1-12, 1957.
Björk, A. Some biological aspects of prognathism and occlusion of the teeth.
Angle Orthodont. 21:3-27, 1951.
Björk, A. Cranial base development. Am. J. Orthodont. 41:198-225, 1955.
Björk, A. The relationship of the jaws to the cranium. In: Introduction to Ortho-
dontics. A. Lündstrom (ed.), McGraw-Hill, London, pp. 104-140, 1960.
Björk, A. Roentgencephalometric growth analysis. In: Congenital Anomalies of
the Face and Associated Structures. S. Pruzansky (ed.), CC Thomas, Spring-
field, Illinois, pp. 237-250, 1961.
Bolk, L. Über Lagerung, Verschiebung and Neigung des Foramen magnum am
Schädel der Primaten. Z. Morphol. Anthrop. 17:611-692, 1915.
Bosma, J. F. Significance of the pharynx in rehabilitation of poliomyelitis disabili-
ties in the cervical area. Arch. Phys. Med. 38:363-368, 1957.
Broca, M. Sur les projections de la tête, et sur un nouveau procede de
céphalométrie. Bull. Soc. Anthrop. (Paris), 3:514-544, 1862.
Brocher, J. E. W. Die Occipito-Cervical-Gegend. Eine diagnostischpathogene-
tische Studie. G. Thieme, Stuttgart, 1955.
Bugyi, B. Untersuchungen zum Vergleich der röntgenologischen funktionellen
Halswirbelsäulen-Methoden. In: Die Wirbelsäule in Forschung und Praxis. H.
Junghanns (ed.), Hippokrates-Verlag, Stuttgart, 15:137-140, 1960.
Cameron, J. Craniometric studies, No. 5-8. Am. J. Phys. Anthrop. 10:275-295,
1927.
Carlsöö, S. and G. Leijon. A radiographic study of the position of the hyo-
114
Solow
laryngeal complex in relation to the skull and the cervical column in man.
Trans. R. Sch. Dent. (Stockholm and Umea), 5:13-34, 1960.
Cleall, J. F. Deglutition: A study of form and function. Am. J. Orthodont.
51:566-594, 1965.
Cleall, J. F. Circumstances limiting the development and verification of a compre-
hensive theory of craniofacial morphogenesis. In: Mechanisms and Regulation
of Craniofacial Morphogenesis. B. C. Moffett (ed.), Swetz and Zeitlinger,
Amsterdam, pp. 115-126, 1972.
Cleall, J. F., W. J. Alexander and H. M. McIntyre. Head posture and its relation-
ship to deglutition. Angle Orthodont. 36:335-350, 1966.
Dabelow, A. Uber Korrelationen in der phylogenetischen Entwicklung der
Schädelform. I. Die Beziehungen zwischen Rumpf und Schädelform. Morphol.
Jahrb. 63:1-49, 1929.
Dabelow, A. Uber Korrelationen in der phylogenetischen Entwicklung der Scha-
delform. II. Beziehungen zwischen Gehirn und Schadelbasisform bei den
Mammaliern. Morphol. Jahrb. 67:84-133, 1931.
Davies, P. L. Electromyographic study of superficial neck muscles in mandibular
function. J. Dent. Res. 58:537-538, 1979.
Delattre, A. and R. Fenart. La méthode vestibulaire. Appliquée à l'étude du
crane. Son champ d'applications. Z. Morphol. Anthrop. 49:90-114, 1959.
Delattre, A. and R. Fenart. L'Hominisation du Crane. Editions du Centre Na-
tional de la Recherche Scientifique, Paris, 1960.
Downs, W. B. Analysis of the dentofacial profile. Angle Orthodont. 26:191-212,
1956.
Drettner, B. Nasal and oral maximal voluntary ventilation in persons with normal
and reduced pulmonary function. Int. Rhinol. 7:15-22, 1969.
DuBrul, E. L. Posture, locomotion and the skull in lagomorpha. Am. J. Anat.
87:277-313, 1950.
Dunn, G. F., L. J. Green and J. J. Cunat. Relationships between variation of
mandibular morphology and variation of nasopharyngeal airway size in mono-
zygotic twins. Angle Orthodont. 43:129-135, 1973.
Emslie, R. D., M. Massler and J. D. Zwemer. Mouthbreathing: I. Etiology and
effects (a review). J. Am. Dent. Assoc. 44:506-521, 1952.
Exner, G. Die Halswirbelsäule, Pathologie und Klinik. G. Thieme, Stuttgart,
1954.
Fischer, R. Die Messung und graphische Auswertung des Stromungswieder-
standes der Nase. Arch Klin. Exp. Ohren Nasen Kehlkopfheilkd. 197:72-84,
1970.
Fromm, B. and M. Lundberg. Postural behavior of the hyoid bone in normal
occlusion and before and after surgical correction of mandibular protrusion.
Sven. Tandlaek. Tidskr. 63:425-433, 1970.
Harvold, E. P. Experiments on mandibular morphogenesis. In: Determinants of
Mandibular Form and Growth. J. A. McNamara, Jr. (ed.), Monograph 4,
Craniofacial Growth Series, Center for Human Growth and Development,
The University of Michigan, Ann Arbor, pp. 155-178, 1975.
115
Craniocervical Angulation
Henke, W. Die Bewegung des Kopfes in den Gelenken der Halswirbelsäule. Z.
Rat. Med. (3. Reihe) 7:49-62, 1859.
Hultkrantz, J. V. Zur Mechanik der Kopfbewegungen bein Menschen. Kungl.
Sven. Vetenskap.-Akad. Handl. 49 (8):1-38, 1912.
von Ihering, H. Ueber das Wesen der Prognathie und ihr Verhaltniss zur Schadel-
basis. Arch. Anthrop. 5:359-407, 1872.
Ingelstedt, S., B. Jonson and H. Rundcrantz. A clinical method for determination
of nasal airway resistance. Acta Otolaryngol. (Stockholm), 68:189-200, 1969.
Johnston, L. E., Jr. The functional matrix hypothesis: Reflections in a jaundiced
eye. In: Factors Affecting Growth of the Midface. J. A. McNamara, Jr. (ed.),
Monograph 6, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, pp. 131-168, 1976.
Kern, E. B. Rhinomanometry. Otolaryngol. Clin. North Am. 6:863-874, 1973.
Kern, E. B. Standardization of rhinomanometry. Rhinology, 15:115-119, 1977.
Koski, K. and P. Lähdemäki. Adaptations of the mandible in children with ade-
noids. Am. J. Orthodont. 68:660-665, 1975.
Kottke, F. J. and M. O. Mundale. Range of mobility of the cervical spine. Arch.
Phys. Med. 40:379-382, 1959.
Kraus, W. M. Erectness in man. Arch Neurol. Psychiat. 17:1-11, 1927.
Lewit, K. and L. Krausová. Beitrag zur Flexion der Halswirbelsäule. Fortschr.
Roentgenstr. 97:38-44, 1962.
Lewit, K. and L. Krausová. Messungen von Vor- und rúckbeuge in den Kopfge-
lenken. Fortschr. Roentgenstr. 99:538-543, 1963.
Linder-Aronson, S. Adenoids. Their effect on mode of breathing and nasal air-
flow and their relationship to characteristics of the facial skeleton and the
dentition. Acta Otolaryngol. Suppl. 265, pp. 1-132, 1970. -
Linder-Aronson, S. Effects of adenoidectomy on dentition and nasopharynx. Am.
J. Orthodont. 65:1-15, 1974.
Linder-Aronson, S. Effects of adenoidectomy on the dentition and facial skeleton
over a period of five years. In: Transactions of the Third International Ortho-
dontic Congress. J. T. Cook (ed.), Crossby Lockwood Staples, London, pp.
85-100, 1975.
Linder-Aronson, S. and A. Bäckström. A comparison between mouth and nose
breathers with respect to occlusion and facial dimensions. Odont. Revy.
11:343-376, 1960.
Linder-Aronson, S. and C. O. Henrikson. Radiocephalometric analysis of antero-
posterior nasopharyngeal dimensions in 6- to 12-year-old mouth breathers
compared to nose breathers. ORL, 35:19-29, 1973.
Lisowski, F. P., A. van der Stelt and J. H. Vis. Upright posture: An experimental
investigation. Acta F. R. N. Univ. Comen. 5:127-136, 1961.
Lüthy, A. Die vertikale Gesichtsprolifilierung und das Problem der Schadelhori-
zontalen. Arch. Anthrop. N. F. 11:1-87, 1912.
Masing, H. Die klinische Bedeutung der Nasenwiederstandmessung. Arch. Ohren
Nasen Kehlkopfheilkd. 185:763-767, 1965.
Masing, H. and R. Frimberger. Ein neues Rhinomanometer fur die Praxis. La-
ryngol. Rhinol. Otol. (Stuttgart), 53:717-722, 1974.
116
Solow
Mills, P. B. A grid and visual head positioning as adjuncts to cephalometric
analysis. Am. J. Orthodont. 54:521-531, 1968.
Moorrees, C. F. A. and M. R. Kean. Natural head position, a basic consideration
in the interpretation of cephalometric radiographs. Am. J. Phys. Anthrop.
16:213–234, 1958.
Moss, M. L. Rotation of the otic capsule in bipedal rats. Am. J. Phys. Anthrop.
19:301-307, 1961.
Moss, M. L. A theoretical analysis of the functional matrix. Acta Biotheor.
18:195-202, 1968.
Moss, M. L. and R. M. Rankow. The role of the functional matrix in mandibular
growth. Angle Orthodont. 38:95-103, 1968.
Moss, M. L. and L. Salentijn. The primary role of functional matrices in facial
growth. Am. J. Orthodont. 55:566-577, 1969.
Moss, M. L. and R. W. Young. A functional approach to craniology. Am. J.
Phys. Anthrop. 18:281–292, 1960.
Opdebeek, H., W. H. Bell, J. Eisenfeld and D. Mishelevich. Comparative study
between the SFS and LFS rotation as a possible morphogenetic mechanism.
Am. J. Orthodont. 74:509-521, 1978.
Penning, L. Functioneel Röntgenonderzoek Bij Degeneratieve en Traumatische
Aandoreningen der Laag-Cervicale Bwegings-segmenten. van Denderen, Gro-
ningen, 1960.
Popper, K. R. Conjectures and Refutations. 3rd ed., Routledge and Kegan Paul,
London, 1969.
Pruzansky, S. Concluding comment. II. Fourth Symposium on Oral Sensation and
Perception. J. F. Bosma (ed.), DHEW Publ. No. NIH 73-546, Bethesda, Md.,
pp. 390-408, 1973.
Quinn, G. W. and K. L. Pickrell. Mandibular hypoplasia and airway interference.
N. Carolina Dent. J. 61:19-24, 1978.
Ricketts, R. M. Respiratory obstruction syndrome. Am. J. Orthodont.
54:495-507, 1968. -
Riesenfeld, A. The effects of experimental bipedalism and upright posture in the
rat and their significance for the study of human evolution. Acta Anat. (Ba-
sel), 65.449-521, 1966.
Riesenfeld, A. Biodynamics of head form and craniofacial relationships. Homo,
18:233-251, 1967.
Riesenfeld, A. Head balance and brachycephalization. Homo, 20:81–90, 1969.
Schmidt, E. Die Horizontalebene des menschlichen Schädels. Arch. Anthrop.
9:25-60, 1876.
Schultz, A. H. Conditions for balancing the head in primates. Am. J. Phys.
Anthrop. 29:483-497, 1942.
Schwarz, A. M. Kopfhaltung und Kiefer. Z. Stomatol. 24:669-744, 1926.
Schwarz, A. M. Prophylaxe und Frühbehandlung der Bissanomalien. Fortschr.
Orthodont. 1:635-660, 1931.
Schönherr, E. Natürliche Kopfhaltung, individuelle Kauebene und ihr Wert für
die kieferorthopädische Profil- und Modell-analyse. Fortschr. Kieferorthop.
28:297-312, 1967.
117
Craniocervical Angulation
Solomon, W. R., J. A. McLean, C. Cookingham, G. Ahronheim and G. De-
Muth. Measurement of nasal airway resistance. J. Allergy, 36:62-69, 1965.
Solomon, W. R. and A. W. Stohrer. Consideration in the measurement of nasal
patency. Ann. Otol. Rhinol. Laryngol. 74:978-990, 1965.
Solow, B. and E. Greve. Rhinomanometric recording in children. Rhinology, in
press, 1979.
Solow, B. and S. Kreiborg. Soft-tissue stretching: A possible control factor in
craniofacial morphogenesis. Scand. J. Dent. Res. 85:505-507, 1977.
Solow, B. and A. Tallgren. Natural head position in standing subjects. Acta
Odont. Scand. 29:591-607, 1971a.
Solow, B. and A. Tallgren. Postural changes in craniocervical relationships.
Tandlaegebladet, 75:1247-1257, 1971b.
Solow, B. and A. Tallgren. Head posture and craniofacial morphology. Am. J.
Phys. Anthrop. 44:417-436, 1976.
Solow, B. and A. Tallgren. Dentoalveolar morphology in relation to craniocervi-
cal posture. Angle Orthodont, 47:157-164, 1977.
Spoor, A. Aerodynamics. Int. Rhinol. 1:19-22, 1963.
Stoksted, P. Rhinometric examinations of schoolchildren with adenoid vegeta-
tions. Acta Otolaryngol. (Stockholm), 39:44-55, 1951.
Stoksted, P. and J. Z. Nielsen. Rhinomanometric measurements of the nasal
passage. Ann. Otol. Rhinol. Laryngol. 66:187-198, 1957.
Tallgren, A. Changes in adult face height due to ageing, wear and loss of teeth
and prosthetic treatment. Acta Odont. Scand. 15(Suppl. 24):1-122, 1957.
Tallgren, A. The reduction in face height of edentulous and partially edentulous
subjects during long-term denture wear. Acta Odont. Scand. 24:195-239, 1966.
Thompson Posnick, B. Craniocervical angulation and morphologic variables in
children: A cephalometric study. M.S.D. Thesis, University of North Carolina,
Chapel Hill, 1978.
Thurow, R. C. Atlas of Orthodontic Principles. Mosby, St. Louis, 1970.
Thurow, R. C. The survival factor in orthodontics. In: Transactions of the Third
International Orthodontic Congress. J. T. Cook (ed.), Crossby Lockwood
Staples, London, pp. 17-25, 1975.
Virchow, H. Die sagittal-flexorische Bewegung der menschlichen
Halswirbelsäule. Arch. Orthop. Unfall- Chir. 26:1-42, 1928.
Wankewicz, M. M. Zur Aetiologie der sogenannten Bissanomalien. II. Teil. Ver-
suche der künstlichen Erzeugung von Kiefer-Gesichts-Skelettsdeformationen
bei Tieren. Z. Zahnaerztl. Orthop. 23:41-59, 1931.
Weber, E. H. Anatomisch physologische Untersuchung über einige Einrichtun-
gen im Mechanismus der menschlichen Wirbelsäule. In: Archiv für Anatomie
und Physiologie. J. F. Meckel (ed.), Leopold Voss, Leipzig, pp. 240-274, 1827.
Weidenreich, F. Die Sonderform des Menschenschädels als Anpassung an den
aufrechten Gang. Z. Morphol. Anthrop. 24:157-189, 1924.
Weidenreich, F. The brain and its role in the phylogenetic transformation of the
human skull. Trans. Am. Phil. Soc. N. S. 31:321-442, 1941.
Werne, S. Studies in spontaneous atlas dislocation. Acta Orthop. Scand. Suppl.
23, pp. 1-150, 1957.
118
Solow
Woodside, D. G. and S. Linder-Aronson. The channelization of upper and lower
anterior face heights compared to population standard in boys between ages 6
to 20 years. Europ. J. Orthodont. 1:25-40, 1979.
Zeitler, E. and H. Markuske. Röntgenologische Bewegungsanalysen der
Halswirbelsäule bei gesundenen Kindern und Jugendlichen. Fortschr. Roent-
genstr. 96:87–93, 1962.
119
NASO-RESPIRATORY FUNCTION AND
CRANIOFACIAL GROWTH
Sten Linder-Aronson, L. D. S., Ph. D.
Department of Orthodontics
Karolinska Institute
In order to be in a position to discuss respiratory function and its effects
on craniofacial growth, one first must be able to clearly distinguish be-
tween nose and mouth breathers. However, this distinction is not easily
made, since most mouth breathers usually have some nasal respiratory
capacity as well.
Therefore, only those individuals with total blockage of the nasal air-
way (e.g., bilateral chonanalatresi or alea nasii insufficiency) should be
described as being pure mouth breathers. In all other cases a combination
of nasal and oral respiration is found. The term mouth breather, there-
fore, refers to those individuals who have a certain degree of nose-breath-
ing capacity but, for one reason or another, breathe mainly through the
mouth.
One group of patients who usually exhibit reduced nasal respiratory
function are those with enlarged adenoidal masses. The growth changes
occurring following adenoidectomy can be studied in order to determine
the effects of a change in the mode of breathing on subsequent craniofa-
cial growth. Consequently, much of this paper is based on results ob-
tained from studying the effects of adenoidectomy on patients with en-
larged adenoids and comparing them to data taken from a control group
with normal respiratory function.
What are the effects of reduced nasal respiratory function on the devel-
opment of the facial skeleton and occlusion? This is a question which has
aroused the interest of many researchers during the last 100 years. As
early as 1868, a Danish physician, Wilhelm Meyer, postulated that pa-
tients with reduced nasal respiration often suffered from poor hearing and
poor general health. Some years later, Tomes (1872) reported that chil-
dren who were mouthbreathers often had narrow dental arches which
were sometimes V-shaped.
By disturbing the balance between the tongue and cheek musculature,
it was thought that the alveolar process in the premolar and molar regions
became compressed medially, driving the upper anterior segment for-
ward. This theory of compression was developed by the otolaryngologist
121
Naso-Respiratory Function and Craniofacial Growth
Figure 1. Patient exhibiting characteristics of “adenoid facies.”
Nordlund in 1918, and this concept is still considered valid by many
today.
At the turn of the century, Körner (1891) and Bentzen ('03) stated that
the detrimental effects of mouthbreathing were not limited to narrow
dental arches, but also included underdevelopment of the nasal cavity and
maxilla. They thought that the height of the palatal vault increased due to
inactivity, and this reduced growth of the nasal cavity. This theory of
inactivity is also mentioned by Nordlund (18) and, like the theory of
compression, is recognized by many today (e.g., Fränkel, '77).
A specific facial type, adenoid facies, has become associated with indi-
viduals who have a long history of mouthbreathing (Fig. 1). It is charac-
terized by an open-mouth posture, a nose that appears to be flattened,
nostrils that are small and poorly developed, a short upper lip, a volumi-
nous and pouting lower lip, and, as a result of the hanging posture of the
lower jaw, a vacant facial expression.
122




Linder-Aronson
Patients exhibiting “adenoid facies” often are typified by proclined
upper incisors, a narrow V-shaped upper jaw with a high palatal vault and
a Class II skeletal relationship. Woodside ('68) suggested that obstructed
nasal ventilation could, if present during a long period of time, act as an
etiological factor in the development of a Class II malocclusion. A change
in the rest position of the mandible to a more retrognathic posture could
also occur. Woodside ('68) described a neuromuscular Class II malocclu-
sion in which a change in the mode of breathing could lead to an altera-
tion in the neuromuscular reflexes controlling the rest position of the
mandible. Harvold and co-workers (Harvold et al., '73; Harvold, '75,
’79), experimenting on monkeys, found that a change from nose to
mouthbreathing led to a narrowing of the maxilla and to a posterior
rotation of the mandible. This also resulted in an increase in anterior
facial height.
In discussing the effects of adenoids on the development of the face
and dentition, it is important to note their influence on the mode of
breathing and to relate this to specific facial types and dentitions. It is
difficult otherwise to establish a direct relationship between the presence
of adenoid vegetations and specific dentitions.
A third group of investigators (Nordlund, '18; Brash et al., 29) has
argued that reduced nasal breathing is a direct result of the existing facial
and dental morphology. They observe that in cases with long narrow
faces, the nasopharynx is constricted and, consequently, nosebreathing is
more difficult. In examining the literature written on this subject over the
past 100 years, one has the feeling that these early, somewhat speculative
theories have gradually been accepted as fact without the presentation of
any conclusive evidence.
THE RELATIONSHIP BETWEEN REDUCED RESPIRATORY
FUNCTION AND FACIAL TYPE
In an earlier investigation (Linder-Aronson, '70), 26% of 81 mouth
breathers judged as needing adenoidectomies were classified as having
adenoid facies. Only 4% of a similar number of controls were found to
have this type of facial expression. The cases were reassessed, this time by
another orthodontist and an otologist. They were asked to examine photo-
graphs of each mouth breather needing an adenoidectomy and each con-
trol case, and select those who had adenoid facies. The orthodontist se-
lected 28 cases from the mouth breathers as having adenoid facies and the
otologist selected 25 cases. They were in agreement in 21 cases or 25.9% of
the mouth breather sample. Both observers found 3 cases in the control
group (4%). Since only 1/4 of the patients with enlarged adenoids were
Selected as having this type of face, and since it can also be found in
123
Naso-Respiratory Function and Craniofacial Growth
individuals who are nose breathers with good nasopharyngeal airways and
no adenoids, it cannot be labelled as a distinguishing characteristic of
reduced nasal respiratory function due to the presence of enlarged ade-
noids.
Whether reduced nasal breathing resulting from enlarged adenoidal
masses can cause the development of a specific facial type is still uncer-
tain. It has been established, however, that enlarged adenoid masses do
occur in conjunction with different facial types, and that reduced nasal
respiration is often associated with enlarged adenoids and long narrow
faces. In the present study, children with obstructed nasal breathing ex-
hibited increases in both the lower and total facial heights and a more
retrognathic maxilla and mandible compared to the control children. Fur-
thermore, the sagittal depth of the bony nasopharynx was less and the
tongue position was lower, a natural compensatory attempt to improve
the airway.
The Relationship Between Reduced Respiratory Function and the Dentition
The relationship between mouthbreathing and the dentition has been
described in the literature for many years. Chronic mouth breathers have
been characterized as having narrow V-shaped upper jaws, high palatal
vaults, proclined upper incisors and Class II occlusal relationships.
In a previous study (Linder-Aronson, '70), the following characteristics
were present in chronic mouth breathers: a narrow upper jaw, retroclined
upper and lower incisors, normal palatal vault height, a tendency to have
or the presence of a crossbite, a tendency to have an openbite and a
normal anteroposterior relationship between the upper and lower jaws.
The presence of a narrow upper jaw and/or a crossbite agrees with earlier
findings. However, the retroclined incisors, the lack of a Class II maloc-
clusion and normal palatal vault height contradict earlier findings. The
openbite tendency has seldom been mentioned. A dentition typical for a
mouth breather thus has retroclined incisors, a narrow upper jaw, a cross-
bite, incisor crowding, and a tendency towards or an open bite.
EFFECTS ON THE DENTITION AND FACIAL SKELETON OF A
CHANGE FROM MOUTH- TO NOSEBREATHING
A five year follow-up study (Linder-Aronson, '73) of children who had
received adenoidectomies to clear obstructed nasal passages was under-
taken. The purpose of the follow-up study was to examine the effects of a
change in the mode of breathing on:
1. upper and lower incisor inclination,
2. upper arch width,
124
Linder-Aronson
3. Sagittal depth of the nasopharynx,
4. anterior facial height and inclination of the mandible to the maxilla
(ML/NL angle).
The time interval necessary for such changes to become apparent was
also studied.
This study involved 41 children who had undergone adenoidectomies
and 54 children who were used as controls. In comparing the mean values
for both groups of children, only those children who changed from
mouth- to nosebreathing were included. The control children were
matched by sex and age with the operated children. The mean age for the
former group was 7.9 years and for the latter, 7.5 years. The control
children had no previous history of obstructed nasal breathing and had
never undergone adenoidectomy or orthodontic treatment. They were
also examined by an otorhinolaryngologist. All children from both groups
were reexamined one and five years postoperatively.
In the dentition, the following variables were examined: upper and
lower incisor inclination and the distance between the upper first molars.
In the facial skeleton, 12 variables were examined including the angle
formed by the mandibular plane and nasal plane, the angle formed by the
nasal plane and sella-nasion plane, and the depth of the bony nasopha-
rynx measured from the pterygomaxillary point to basion (Fig. 2). The
inclination of the upper incisors was measured in relation to the sella-
nasion plane, while the lower incisor inclination was measured in relation
to the mandibular plane. The arch width between the upper first molars
was measured using models. Comparison of mean values, correlation and
regression analyses, and stepwise regression analyses were then per-
formed.
The Effect of a Change to Nosebreathing on the Inclination of the Upper
Incisors
During the first year after adenoidectomy there was a change from
mouth- to nosebreathing which was accompanied by a relatively greater
increase in upper incisor inclination compared to that of the control chil-
dren (Fig. 3). The difference between the two groups was 3.5°. This was
found to be statistically significant. Between one and five years postop-
eratively the difference between the groups diminished. The children who
had adenoidectomies remained nose breathers, and there was a 2.3° in-
crease in incisor inclination in their group, with a corresponding increase
of 0.4° for the control children. This difference is only significant at the
0.05 level. It is striking that after five years the increase in incisor inclina-
tion for the children who had their adenoids removed was such that the
mean values were almost the same as those calculated for the control
125
Naso-Respiratory Function and Craniofacial Growth
NSL
Figure 2. Cephalometric planes used in this study.
children. It is, therefore, possible to say that following a change from
mouthbreathing to nosebreathing, a normalization of upper incisor incli-
nation, as measured to the sella-nasion plane, occurred during the five
year postoperative period.
The Effect of a Change to Nosebreathing on the Inclination of the Lower
Incisors
Figure 4 illustrates the effect of change in mode of breathing on the
inclination of the lower incisors to the mandibular plane. The greatest
change among the children who altered their mode of breathing following

126
Linder-Aronson
DE GREES
ILs/NSL
1O6- DIFF:23.
DIFF = O.5 - - - - - - - - * * *- :- m ºn tº ---------->
oal …---------. - - - - - - *** ** ars DIFF= O.4
DIFF = 4.O ......“
1O2– ..”
...' ------ 21 ADENOIDCASES
..” - - -36 CONTROLS
1OO- ..”
•”
98 — I —w- —w I
BEFORE 1 Nº EAR AFTER 5 YEARS AFTER
ADE NOIDECT ONAY ADENOIDECTONAY ADENJOIDECTONAS-
DIFFERENCE BETVVEEN DIFFERENCES FOR
ADENJOIDECTONAY-AND CONTROL CHILDREN

x x x
5.5
$1.9°
T--J
Figure 3. The effect of a change from mouth- to nosebreathing on the inclination
of the upper incisors. Means for inclination of upper incisor to sella-nasion plane.
adenoidectomy was seen during the first year postoperatively. During the
Subsequent four years, no significant difference could be found between
the two groups. This would suggest that a normalization of lower incisor
inclination occurred during the first year postoperatively, after which
both groups developed in a similar manner. The difference noted during
the first year was statistically significant.
The Effect of a Change to Nosebreathing on Arch Width
Figure 5 illustrates changes in arch width measured between the upper
first molars. Here again, the greatest change occurred during the first
year postoperatively following a return from mouth- to nosebreathing.
This change was only 0.4 mm. It was, however, statistically significant at
the 0.01 level. The increase of 0.5 mm for the control children during the
first year postoperative is in keeping with accepted norms for lateral arch
growth at that age. The average increase of 0.9 mm during the first year
postoperative for the children whose adenoids were removed was the
greatest yearly increase registered during the five year observation pe-
riod. Both groups had similar group averages at 5 years postoperative.
Thus, a normalization of arch width took place following adenoidectomy
and a change from mouth- to nosebreathing.
127
Naso-Respiratory Function and Craniofacial Growth
DEGREES
L/ML DIFF = 19.
Q6- ___---- TT
--tº- 2:- _ - - - T Pli: 18.
94: .............---------" "
DIFF-2 5.....----------" "
• * - - - - - - 21 ADENJOIDCASES
92- º - - -35C) CONJT ROLS
901– T -wr —y- —w— TI
BEFORE 1 Nº EAR POSTOP 5 NZEARS POSTOP

ADENOIDECTONAY
DIFFERENCE EETWEEN DIFFERENCES FOR
ADENOIDECTONAY AND CONTROL CH|{_DFEN

• 2- . x X
\be
wº- 203("**)
Figure 4. The effect of a change from mouth- to nosebreathing on the inclination
of the lower incisors. Means for inclination of lower incisor to mandibular plane.
NA-NA
|N NAN/A
47
DIFF-11.
- arº, 35
46 – _------.” ... • .
sº --~~~~... • * * *
DIFF = 93--... ...----
... T.----" "
45 _*...*DIFF-09 ------ 26 AD ENODCASES
ar ..” - - - 41 CONTROLS
• ‘’
44- I T —— y T
BEFORE 1 YEAR POSTOR 5 YEARS POSTOP
ADENODECTONAY
DIFFERENCE EETVVEEN DIFFERENCES FOR
ANDE-NOIDECTONAY-AJND CONTROL CHILDREN

O.Z."
yo," ")
Figure 5. The effect of a change from mouth- to nosebreathing on the arch width
between the upper first molars.
The Effect of a Change to Nosebreathing on the Nasopharynx
Figure 6 illustrates how the sagittal depth of the bony nasopharynx, as
measured from the pterygomaxillary point to basion, changed in the chil-
dren who became nose breathers after removal of their adenoids, as well
as that in the control children. The greatest change occurred during the
128
Linder-Aronson
PNA-BA
|N NANA
4.
17 - DIFF-24
*
_-T O
46- _--T ......”
-- T .... • * * DIFF = 2.6
_- - ... • * *
45- _-T ... • * *
... •T ... • * *
* ... • * *
_Pff-03-T .......”
44H "T. . . .......”
DIFF-19.--" ------ 354 ADENO DCASES
...” ---54 CONTROLS
45+ ...“
• ‘’
42 I I —r- T T I
BEFORE 1 YEANR POSTOP 5 YEARS PCST OF
ADENOIDECTONASr.’
DIFFERENCE EET\/\/EEN DIFFERENJCES FOR
ANDENJODECTON/Y-AJND CONTROL CHILDREN

`s ºr
yo 2(n-s)
wº-
Figure 6. The effect of a change from mouth- to nosebreathing on the depth of
the nasopharynx. Measured from pterygomaxillary point to basion.
first year postoperatively in the group of children whose adenoids had
been removed. This difference was statistically significant at the 0.01
level. During the subsequent four years, the increase in this group was
similar to that in the control group. Therefore, a normalization of the
depth of the nasopharynx occurs during the first year postoperatively,
after the alteration from mouth to nosebreathing has occurred.
Effect of Change to Nosebreathing on the Angle between the Mandibular
and Nasal Plane
Figure 7 illustrates how the angle between the mandibular plane and
the nasion plane changed due to change in mode of breathing. The actual
difference during the first year was 0.4°, which was not significant. During
the five year postoperative observation period, however, a greater change
in the ML/NL angle (significant at the 0.01 level) occurred in the group of
children who had had adenoidectomies than in the control group. It
would appear that a process of normalization continued throughout the
observation period. It is probable that the size of the ML/ NL angle, if
influenced by the mode of breathing, can decrease after a change from
mouth- to nosebreathing, thereby coming closer to normative values.
The size of the ML/NL angle is also related to changes in lower facial
129
Naso-Respiratory Function and Craniofacial Growth
DEGREES
MLNL
351
*..
°i _ _ "...... -----. 54 ADENOIDCASES
off-09 “...... ---54 CONTROLS
2G) - ""--..
***...
28 - “.....
27- * ~~ “... pHF- 35.
T-- ** = .
DIFF-05 ~~~~~ "---.
26 - T--~~~
T---INFF-18
25 T ~~e
I lſ I W I I
BEFORE 1 YEAR POSTOP 5 YEARS POSTOP
ADENODECTONAY
DIFFERENCE BETVVEEN DIFFERENCES FOR
ADENJODECTON/WY—AND CONTROL CHILDREN

*T- }oº
T- ºr
Figure 7. The effect of a change from mouth- to nosebreathing on the angle
between the mandibular and nasal planes.
height. A correlation analysis between reductions in the ML/NL angle
and changes in the lower facial height was found to be significant at the
0.001 level. The causal relationship between adenoid vegetations asso-
ciated with mouthbreathing and increased lower facial height may be due
to a rotation downwards and backwards of the mandibular symphysis.
In order to see whether the nasal plane is influenced in the same way as
is the mandibular plane, the angle between the nasal plane and the sella-
nasion plane was studied during the five year observation period. No
significant differences were found between the two groups (Fig. 8).
MECHANISMS BY WHICH CHANGES OCCUR IN THE DENTITION
AND FACIAL MORPHOLOGY
Changes in the dentition resulting from an altered mode of breathing
are thought to be influenced by the lip, cheek and tongue musculature.
Mouthbreathing due to obstructed nasal passages leads to a lowering of
tongue position (Subtelny, '54; Holik, '57; Ricketts, '58; Bushey, '65;
Linder-Aronson, '70; Yip and Cleall, '71). A change in the mode of
130
Linder-Aronson
DEGREES
NL/NSL) ------. $2 ADENOID-CASES
al - - - 544 CONTRON_S
DIFF-07.
7| QEE: of ................”
Plf-94––––––––––––––––––––––PR-9.
e — I T T I I
BEFORE 1 YEAR DOST OP 5 YEARS POSTCP

ADE NOIDECTONAY
DIFFERENCE BETWEEN DIFFERENCES FOR
ADENODECTONAY-AND CONTROLCHILDREN
T- yo-" " )
T- } o,(n-3)

Figure 8. The effect of a change from mouth- to nosebreathing on the angle
between the nasal plane and the sella-nasion plane.
breathing, furthermore, leads to a change in the balance between tongue
and cheek pressure surrounding the upper arch.
The lowered tongue position results in a reduction of buccally directed
pressure; and if, at the same time, the pressure from the cheek muscula-
ture remains unchanged, the upper premolars and molars will be influ-
enced in a palatal direction. Fränkel (77) uses this principal in reverse to
explain how expansion of the upper arch occurs when using the functional
regulator appliance. Pressure from the cheeks is inhibited so that the
tongue can exert an expanding pressure on the upper arch.
The change in incisor inclination due to the change to nosebreathing
can be interpreted partly as being caused by changes in orbicularis oris
pressure associated with the transition from an open to a closed mouth
posture. Since the position of the tongue is also affected, an alteration in
the balance between the pressures exerted by the lips and tongue on the
incisors occurs.
The findings from the above studies has led, in part, to the following
hypothesis. After there is an increase in the nasal airflow due to increased
Space, a change from mouth- to nosebreathing occurs. This results in a
raised resting position of the tongue and lips that can be held together,
thus promoting an increase in arch width. Furthermore, the inclination of
the upper and lower incisors increases, the lower facial height is reduced
(as expressed by the reduction in the angle between the mandibular and
nasal planes) and the depth of the bony nasopharynx increases.
131
Naso-Respiratory Function and Craniofacial Growth
Explanatory variable Partial corr. coeff.
Difference in size of adenoids —0.29
R* = 0.08;
Difference in size of adenoids —().05
Difference in mode of breathing —().31
R* = 0.17
Difference in size of adenoids –0.07
Difference in mode of breathing —0.33
Difference in tongue position –0.35
R2 = 0.27
Table 1. Stepwise regression analysis. Dependent variable: 1-year difference in
width of upper arch between first molars. Explanatory variables: 1-year differ-
ences in size of adenoids, mode of breathing and tongue position.
A stepwise regression analysis was done using 56 children who had
undergone adenoidectomy due to obstructed nose breathing and 56 con-
trol children of the same age. This analysis determined that a change in
arch width between the initial and first year registrations is the dependent
variable (Table 1).
The change in the amount of obstruction of the nasal airway, as mea-
sured preoperatively and one year postoperatively, was examined first in
order to estimate the effect of the change on arch width. The change in
size of the nasal airway explained only 8% of the change registered in
arch width. The partial correlation coefficient (-0.29) is moderate and
shows that large differences between the size of the adenoids initially and
after one year causes the greatest change in arch width.
When differences in the mode of breathing are introduced into the
analysis, it is interesting to note that the explanatory factor increases to
17%. Furthermore, the previously established relationship between dif-
ferences in the size of the adenoids and differences in arch width is now
dominated by the variable for differences in the mode of breathing. A
change in the mode of breathing has thus had greater value in explaining
differences in arch width than the size of the adenoids.
If the analysis is now supplemented by the variable for changes in
tongue position, it can be seen from the partial correlation coefficient that
the relationship between changes in arch width and altered mode of
breathing remains. A new correlation is introduced, however, between
differences in tongue position and differences in arch width. This can be
interpreted as meaning that both variables explain changes occurring in
132
Linder-Aronson
t-value Partial corr.
Regressor Std. error
Preop. airflow
after nose drops 0.05 –2.57* —0.20
Il-S 0.12 –3.51*** — 0.27
Height of upper
lip 0.16 3.69*** 0.28
Height of lower
lip 0.10 4.10% + + 0.31
SS-Il-SII] 0.16 4.99%++ 0.37
SS-n-ba 0.11 –4.20% + + —0.31
R* = 0.45
RSD = 4.19
Table 2. Regressand: angle between mandibular and nasal lines (ML/NL). Std.
error, level of significance (marked with asterisks), partial correlation coefficients,
the total correlation coefficient (R*), and the standard deviation of the residuals
(RSD), in an analysis of 32 regressors.
arch width, though in different ways. With regard to the change in mode
of breathing, it is the lip and cheek musculature which are the causal
factors, whereas it is the tongue musculature with regard to the change in
tongue position. The explanatory factor for the three variables combined
is 27%. This would appear to support the hypothesis mentioned above.
A change in the mode of breathing is thought to cause an alteration in
pressure of the lip and cheek musculature because whether the mouth is
held mostly open or closed depends on mode of breathing. It is possible
that the role of the muscular ring consisting of the orbicularis oris, the
buccinator muscle and the superior constrictor muscle is significant in this
respect.
Altered function (a change from mouth- to nosebreathing) due to in-
creased nasopharyngeal airflow may also be related to the growth of the
nasopharynx. This supposition is in agreement with the theories of Bosma
('63), Moss and Salentijn ('69) and Fränkel (77).
Using regression analyses (Table 2), it can be seen that reduced nasal
airflow explains the difference in size of the ML/NL angle. From this
regression analysis in which the ML/NL angle is the dependent variable,
the airflow, after using nose drops to decongest the nasal passage, is
found to be one of the explanatory variables. The negative sign shows
that nasal airflow is less in patients with a large ML/NL angle. This
reduced nasal airflow which causes mouthbreathing is, in turn, caused by
133
Naso-Respiratory Function and Craniofacial Growth
F---------------------- —l ------------- º F-------------- H
| |
| FREQUENT | NASAL SEPTAL | CONTRACTED |
| | | | | |
| RESPIRATORY INFECTION | DEVIATION | MAXILLARY ARCH
* = * = = <= = * = * = * * * = flººs º- * = * | !---— — — — — — — — — — — !----------------,
H
SWOLLEN
NASAL - |
MUCOSA REDUCED º
k-º-mºmºmº- DECREASE IN
W NASAL
NASAL W I DTH
e-| BREATH ING
ENLARGED
ADENO IDS
MOUTH
BREATH ING
| |
LOWERED TONGUE EXTENDED
POS IT ION HEAD POSTURE
LOWERED

MAND I BULAR POSTURE
Figure 9. Factors contributing to the alteration in the posture of the mandible
(angle between mandibular and nasal planes).
frequent respiratory infection, nasal septum deviation and a narrow max-
illary arch. Therefore, all these factors contribute to the alteration in the
postural position of the mandible (Fig. 9).
Changes in Head Posture
To what extent mouth breathers unconsciously maintain an extended or
upwardly rotated position of the head in order to improve the oropharyn-
geal airway, is as yet uncertain. In order to examine this question, the
head posture of 16 patients who had undergone adenoidectomies to im-
prove nasal airflow was studied and compared to that of a similar number
of controls of the same age. The inclination of the sella-nasion line (SN)
134
Linder-Aronson
CONTROL ( 16 cases ) NASAL OBSTRUCTION (16 cases)
i-89.sto. 9]
SQ
_^ |
N DIFFERENCE: 6.4°t 1.4°
T - VALUE . 4.5 xxx
Figure 10. Values for the SN/Vert. angle before adenoidectomy.
CONTROL 16 cases NASAL OBSTRUCTION (16 cases
-
x= 86.7°t 1.0°.
\º. oš
DIFFERENCE : 2,3 t 1.5
T–VALUE: 1.7 Ns
Figure 11. Values for the SN/Vert. angle one month postoperative.
was measured relative to a vertical reference line (Vert.) included in the
lateral skull radiographs. The SN/Vert. angle will be less in patients with
extended head posture than in those with normal posture.
Measurements were made before and one month after surgery was
performed. When cephalograms were taken, the patients were standing in
a relaxed position in front of a mirror placed outside of the cephalostat.
A lightcross as a reference was projected on the cheek of each patient. A
horizontal pencil mark following the horizontal line of the lightcross was
drawn. Then the patient’s head was placed in the cephalostat and orien-


135
Naso-Respiratory Function and Craniofacial Growth
2. ^ SN/VERT ! • 16 MOUTHBREATHERS
LL
à 95_ [T] | D 16 ContROLS
T l
Q-2 |
I O D t
C/D O
as [] | C
tº 90_ C
cº D e O
3; D
L1– [] C |
C/O D O
H. 85.1 – - - - - -D––––. - - - - - - - - - - - - - - - - - G-- - -O –––
§ O |
C |
| O
2 O | O
tº-sº | O
5: 8O_ O | CO
Lil |
> |
S
5
LL] | O
—l O
% 75_ | PERCENTILE FOR LOWER
º ; | ANTER I OR FACE HE I GHT
|
I —I-T- I I —I- I–I ASSESSED FROM CANAD I AN
H. 3 10 25 5O 75 90 97
POPULATION STANDARDS
Figure 12. Head posture of mouth breathers and controls relative to lower facial
height.
tated so that the pencil mark and the horizontal line of the lightcross were
superimposed. To minimize observer bias, the x-rays were taken by a
nurse who did not know to which group each patient had been assigned.
In spite of the small number of cases examined, a significant difference
in the size of SN/Vert. angle was found when comparing the two groups
before surgery was performed (Fig. 10). This difference could not be
found one month after adenoidectomy (Fig. 11).
Figures 12 and 13 illustrate the SN/Vert. for the mouth breathers and
controls relative to lower and upper facial height, respectively (norms for
facial height in the paper were taken from Canadian population stan-
dards). Most of the mouth breathers have a smaller SN/Vert. angle and a
larger value for lower facial height than do the controls (Fig. 12). There is
thus a significant difference in lower facial height between the mouth
breathers and the controls but no significant difference in upper facial
height (Fig. 13). It can be concluded from this study that head posture for
patients with obstructed nosebreathing seems to be somewhat more ex-
tended and that this can influence the position of the mandible.
Bosma ('63) has stated that one important function of head posture is
to maintain an adequate oronasopharyngeal airway. Therefore, patients
in which morphological disturbances impede nasal airflow should have
extended head posture as well. The Pierre Robin syndrome (Fig. 14) is an
136
Linder-Aronson
n
† SN/VERT • 16 MOUTHBREATHERs
Cr-
G 954 tº G 16 CONTROLS
T
G
5 D
- D
fi BC D D
35 90. D
D - -
3;
LL- D D
£ C
C
& 854? D C - - -
CD
LL -
c.
2. - -
- - -
H. -
É 80_ - - -
>
N-
~~
C/d
LL
G - -
# 75. PERCENTILE FOR UPPER
-
H ; ANTERIOR FACE HEIGHT
H. T-I T T T TT ASSESSED FROM CANAD I AN
3 10 25 50 75 90 97
POPULATION STANDARDS
Figure 13. Head posture of mouth breathers and controls relative to upper facial
height.
Figure 14. Pierre Robin syndrome in Figure 15. Lateral cephalogram of same
newborn. patient in Figure 14 at 11 years of age.
example of such a morphological disturbance. A lack of forward man-
dibular growth locates the tongue too far posteriorly, thus necessitating
mouthbreathing. Typical characteristics include very large SN/Vert, and
ML/NSL angles, a large ML/NL angle, a retrognathic maxilla and mandi-
ble, a very large gonial angle, and a distinct antegonial notch (Fig. 15).
137

Naso-Respiratory Function and Craniofacial Growth
Figure 16. Soft tissue-stretching and retrusive force on the facial complex due to
an extended head posture.
Due to the extended head posture, an increased stretching of the soft
tissue occurs and a subsequent retrusive force is generated against the
facial complex (Fig. 16).
Bushey ('74) found that a pair of monozygotic twins of 8.9 years of age
had different anterior facial heights and tongue posture. One of the twins
had had difficulty breathing through his nose for several years (Fig. 17).
In support of the above findings, I should like to present the case of a
12-year-old female patient who had a submucous cleft and associated
nasal speech. At this age the patient’s facial height was normal. It was
decided that a velopharyngeal flap operation was to be performed in
order to reduce the nasopharyngeal leakage and improve the patient’s
speech. This was done, and the patient was reexamined five years later.
At this stage, it was found that the velopharyngeal flap had been made
too wide, resulting in a change from nose- to mouthbreathing. There was
a marked opening of the bite compared with norms for 17 year old
females, and an increase in the lower facial height (Fig. 18). At 12 years
of age, lower facial height was 65 mm which is normal for that age. At 17
years of age she should have had a lower facial height of 72 mm but
instead hers was 82 mm. This may be correlated to a change in the
inclination of the mandible and an opening of the bite brought about by
the change from nose- to mouthbreathing.
Recently Subtelny and Nieto (78) reported the results of a longitudinal
study of maxillary and mandibular growth after pharyngeal flap surgery
on 24 children. The chin position was more downward and backward in
the group who had undergone surgery than in the control group. There
was no difference in the growth of the mandible itself between the two
138

Linder-Aronson
- - NORMAL
--- - OESTRUCTED
Figure 17. Difference in facial morphology of monozygotic twins, one of which
had obstructed nosebreathing capacity (courtesy of Dr. Robert Bushey).
groups. The increased lower facial height of these children can probably
be explained by reduced naso-respiratory function.
Warren ('75) showed that children with defects of the lip, jaw and
palate who were treated by velopharyngeal flap surgery had a greater
resistance to nosebreathing when compared to control children.
Figures 19 and 20 illustrate the case of a patient with a cleft lip and
palate who, as a result of surgery of the palate and the nose, had an
almost total obstruction of the nose during the growth period from 7-17
years of age. The lower anterior face height fell between 75%-90% of the
Canadian population standards at the ages of 7-12 years. After pubescent

139
Naso-Respiratory Function and Craniofacial Growth
Lower Face height 65.0mm 82.0mm
Gonial angle 126.0° 128.0°
Figure 18. The change in anterior facial height five years after a velopharyngeal
flap operation, and a subsequent change from nose- to mouthbreathing (from
Bushey, '74).
growth was finished, the patient’s nasal obstruction problems increased
and the lower face height did not channelize, so its increased value fell
between the 90-97 percentile at the age of 17 years (Fig. 21). The values
for upper face height were lower than the 3rd percentile during the whole
10 year period (Fig. 22).
The tracings of the profile of this patient at the ages of 7, 12 and 17
years are shown in Figure 23. Observe the increased vertical growth




140
Linder-Aronson
Figure 19. Lateral and anteroposterior cephalograms of a 7-year-old male with a
cleft lip and palate.
Figure 20. Lateral and anteroposterior cephalograms of the same patient seen in
Figure 19 at 17 years of age. Note the almost total nasal obstruction.
direction of the gnathion after puberty, at which point the patient com-
plained of increased nasal obstruction. The growth direction of subnasale
remained the same during the whole period.
In many studies of children with cleft lip and/or palate, it has been
shown that these children have increased facial heights compared to con-
trols. One of the possible explanations for this difference is the reduced
nasal respiratory function present in cleft lip and palate cases.
141


Naso-Respiratory Function and Craniofacial Growth
MM
85.
8O_
75.
7O.
65.
6O_
55.
50
45_
I
6 9
/
...--T
%
y-/
__*
1
O
_^
º
.3
2^
º
T
percentile

12 14 is is 20 Act
Figure 21. Individual growth curve for same patient seen in Figures 19 and 20 of
lower face height not channelizing, using Canadian population standards.
142
Linder-Aronson
MM
7O_
_* percentile
65_ 2^
/~~~ _ !!
/~ *
6O. / % ^ -- _ !!
%20–e
55 % %/ ~~~
e V_- tº-
% /...”
5O_ º,”
45. 2"
40_
35.
Z
I I
6 g 12 a 16 1820 age
Figure 22. Individual growth curve for same patient seen in Figures 19-21 of upper
face height channelizing, using Canadian population standards.

143
Naso-Respiratory Function and Craniofacial Growth

144
Linder-Aronson
Y
º
- º, ..", *
Preoperative year postop 5 years postop
Figure 24. Self-correction of unilateral crossbite due to adenoidectomy and resul-
tant change of mode of breathing from mouth to nose.
The results presented here clearly support the theory that disturbed
nasal respiration can affect both facial morphology and the dentition.
These findings would lend support to the concept that some facial charac-
teristics, previously thought to be strictly the consequence of a genetic
determination of skeletal form, may also be a product of environmental
influences. However, this statement does not imply that certain environ-
mental conditions are necessary prerequisites for excess lower anterior
face height. The ease with which the skeletal and occlusal changes re-
ferred to above can be initiated by chronic environmental impact, causing
an opening of the mandibular angle, and the complete or partial reversi-
bility of this change raises some interesting points relative to orthodontic
diagnosis and treatment planning. The use of mixed dentition and perma-
nent dentition analyses in the diagnosis and treatment planning of incisor
crowding may, therefore, not be an invalid procedure where environmen-
tal impact is the primary etiological factor. In such cases the arch width,
incisor inclinations, and incisor crowding may be significantly reestab-
lished if altered at a sufficiently early age and using such corrections as
eliminating nasal obstruction. Therefore, one can use a conservative
treatment approach rather than an extraction approach which is impor-
tant in patients with excess lower anterior face height. Thus, in certain
individual cases a retrognathic mandible, a vertical mandibular growth
direction, an open bite and a crossbite may be primarily due to such
chronic environmental factors as airway obstruction (Fig. 24).
145

Naso-Respiratory Function and Craniofacial Growth
In addition, such environmental disturbances may also be superim-
posed on an existing dysplasia or malocclusion. This concept requires a
new therapeutic approach. Instead of accepting the dysplasia and adapt-
ing the dentition accordingly, one should try to modify it by eliminating
or minimizing the environmental impact and its resultant effects on jaw
position, occlusion and tooth alignment.
Finally, orthodontic treatment can also be impeded by the functional
factors associated with abnormal nasal respiration. When treating chil-
dren who have an open bite, a crossbite, or cleft lip and/or palate, it is
especially important to ensure that a good nasal airway is present.
REFERENCES
Bentzen, S. Beitrage zur Aetiologi des hohen Gaumens. Archive Laryngology
and Rhinology, 14, 1903.
Bosma, J. F. Oral and pharyngeal development and function. J. Dent. Res.
42:375, 1963.
Brash, J. C., H. T. A. McKeag and J. H. Scott. The etiology of irregularity and
malocclusion of the teeth. Dent. Board U. Kingdom, 1929.
Bushey, R. S. Alterations in certain anatomical relations accompanying the
change from oral to nasal breathing. Master’s thesis. University of Illinois,
Chicago, 1965.
Bushey, R. S. Personal communication, 1974.
Fränkel, R. Personal communication, 1977.
Harvold, E. P., K. Vargervik and G. Chierici. Primate experiments on oral
sensation and dental malocclusions. Am. J. Orthodont. 63:494, 1973.
Harvold, E. P. Experiments on mandibular morphogenesis. In: Determinants of
Mandibular Form and Growth. J. A. McNamara, Jr. (ed.), Monograph No. 4,
Craniofacial Growth Series, Center for Human Growth and Development,
The University of Michigan, Ann Arbor, 1975.
Harvold, E. P. Neuromuscular and morphological adaptations in experimentally
induced oral respiration. In: Naso-Respiratory Function and Craniofacial
Growth. J. A. McNamara, Jr. (ed.), Monograph No. 9, Craniofacial Growth
Series, Center for Human Growth and Development, The University of Michi-
gan, Ann Arbor, 1979.
Holik, F. Relation between habitual breathing through the mouth and muscular
activity of the tongue. Ceskoslovenska Stomat. 57:170, 1957.
Korner, B. Einige Erfahrungen uber Hyperplasie der Rachentonsille. Zeitschrift
die Ohrenheilkunde. Ed. 21 (cit. Nordlund, H.), 1891.
Linder-Aronson, S. Adenoids - their effect on mode of breathing and nasal air-
flow and their relationship to characteristics of the facial skeleton and the
dentiton. Acta Otolaryng. Suppl. 265, 1970.
Linder-Aronson, S. Effects of adenoidectomy on the dentition and facial skeleton
over a period of five years. Trans. Third Int. Orthodont. Congress, p. 85,
1973.
146
Naso-Respiratory Function and Craniofacial Growth
Meyer, W. On adenoid vegetations in the nasopharyngeal cavity, their pathway,
diagnosis and treatment. Med. Chir. Trans. (1870), London, 1868.
Moss, M. L. and L. Salentijn. Functional matrices in facial growth. Am. J.
Orthodont. 55:566, 1969.
Nordlund, H. Ansiktsformens, spec. gomhojdens betydelse for uppkomsten av
kroniska otiter. Appelbergs Boktryckeri AB, Uppsala, 1918.
Ricketts, R. M. Respiratory obstructions and their relation to tongue posture.
Cleft Pal. Bull. 8:4-5, 1958.
Subtelny, J. D. The significance of adenoid tissue in orthodontia. Angle Ortho-
dont. 24:59, 1954.
Subtelny, J. D. and R. P. Nieto. A longitudinal study of maxillary growth follow-
ing pharyngeal-flap surgery. Cleft Pal. J. 15:118, 1978.
Tomes, C. S. On the developmental origin of the V-shaped contracted maxilla.
Month. Rev. Dent. Surg. 1:2, 1872.
Woodside, D. C. Personal communication, 1968.
Yip, A. S. C. and J. F. Cleall. Cinefluorographic study of velarpharyngeal func-
tion before and after removal of tonsils and adenoids. Angle Orthodont.
41:251, 1971.
147
NEUROMUSCULAR AND MORPHOLOGICAL
ADAPTATIONS IN EXPERIMENTALLY INDUCED
ORAL RESPIRATION
Egil P. Harvold, D.D.S., Ph.D., LL.D.
Center for Craniofacial Anomalies
University of California
Attempts to understand the function of the respiratory system and the
effects of nasal obstruction on facial morphology require confronting a
very complex set of interacting biologic processes or systems.
For a century oral respiration has been described in the dental litera-
ture as a causative factor of dental malocclusion. Animal experiments on
oral respiration began in 1879 when Ziem attempted to block the nasal
airway in order to study the effect. Employing the less sophisticated
techniques of that era, he placed cotton in one of the animal’s nostrils and
studied the asymmetric development of the face. In 1890, Talbot sug-
gested that there was an association between shape of the human palatal
vault and oral respiration. An updated review of these early experiments
was presented by Brash (54). Some adverse effects of nasal obstruction
have been delineated including those on speech and on the function of
the Eustachian tubes. The effect of nasal obstruction on craniofacial
growth, however, is not fully understood. We cannot predict with reason-
able accuracy the harmful effects of nasal airway restriction, nor the
potential improvements after clearing a restricted nasal airway.
The research design and execution of human studies of these problems
are extremely difficult. Animal experiments are usually simpler to con-
duct than clinical studies and often provide more definitive answers to the
questions posed. On the other hand, the experimental situation will never
be the same as the actual life circumstance. Furthermore, experimental
animals will always be different from the humans, whose problems we are
attempting to duplicate and analyze. Therefore, we must remain cogni-
Zant that monkeys are not humanoid even though many similarities may
be striking.
To conduct an experiment on oral respiration or on nasal airway re-
striction, we need (1) a theory which expresses our understanding, our
insight and bias, and (2) an experimental model whose characteristics
create a condition comparable to the human circumstances under investi-
149
Neuromuscular and Morphological Adaptions
gation. The design should permit an assessment of the significance of
pertinent factors and findings. An animal experiment without a strict
framework becomes merely a survey which will yield less information
than a direct appraisal of the group of children under study.
Our theory assumes that oral respiration is associated with the recruit-
ment of certain muscles of the orofacial system which are not usually used
for that purpose. The changed function of the musculature has an impact
on morphogenesis; it affects not only the musculature itself but also the
skeleton, including the position of the teeth and the occlusion. This the-
ory is based on the acceptance of the following three statements:
1. Muscle development depends, within certain limits, on the use of the
muscle. This, of course, refers to the fact that muscles undergo hypertro-
phy or hypotrophy, dependent upon their general activity or use.
2. Changes in 'bone morphology as well as in tooth position depend on
bone reorganization, and for this to occur there must be simultaneous
bone apposition and bone resorption. With only one of these processes
occurring, there is pathology in either ossification or bone resorption.
The live processes of bone morphogenesis and remodeling depend upon
apposition and resorption proceeding simultaneously within a restricted
aI Ca.
3. Interaction occurs between muscle function and bone development
as expressed by Wolff's Law. That this law applies to the orofacial region
was demonstrated in two experiments on rhesus monkeys (Harvold, '68).
It was substantiated that changes in the activity and position of the mus-
culature relative to bone have the potential to elicit simultaneous bone
apposition and resorption.
These three statements can now be combined into postulates. Changes
in muscle activity or use will alter the composite orofacial musculature as
well as bone morphology if the new muscle activity elicits simultaneous
bone apposition and resorption. Changes in muscle use or motor activity
will alter the composite orofacial musculature but will not necessarily
affect jaw morphology, dental arch form and tooth position. In other
words, a change in muscle function does not necessarily mean a change in
bone morphology.
The orofacial musculature is used for mastication, deglutition, facial
expression, respiration, sound production (speech) and maintenance of
posture. The relative significance of these functions for muscle use and
development is not known. Also, the relative importance of muscle re-
cruitment for respiration was unknown at the beginning of these experi-
ments. We had assumed that: (1) mastication would probably recruit the
largest muscle force for short periods with much fluctuation, while, on the
other hand, muscle activity related to postural maintenance could be low
level with little fluctuation occurring over extended periods of time; (2)
150
Harvold
muscle activity resulting from oral respiration would probably rank be-
tween that resulting from mastication and postural maintenance. The
question posed is: does this additional muscle recruitment for oral respi-
ration alter the musculature and induce some bone remodeling or changes
in growth pattern?
There are several significant aspects of the craniofacial anatomy which
should be mentioned. All major muscles serving the orofacial functions as
well as posture are attached to the mandible with the exception of the
palato-pharyngeal group and a few facial muscles. The masticatory
muscles tie the mandibular ramus to the zygomatic, temporal, frontal,
parietal and occipital bones, but not to the maxilla or premaxilla. Facial
muscles affix the body of the mandible to the maxilla and premaxilla.
Thus the maxilla and premaxilla belong to a muscle-bone system different
from the zygoma-temporal bone group. This should be considered when
we subsequently assess the experimental findings.
A distinction between gross morphologic changes in bone structure and
changes in muscle function should also be observed. Modifications in
bone morphology are slow processes relative to the rapidly fluctuating
alterations in muscle activity. Therefore, we can expect changes in bone
only when an altered muscle function is consistent and extends over a
period of time. On this basis a tentative hypothesis can be established:
Changes in muscle activity which are consistent, which show limited fluc-
tuation in intensity and which continue over a certain period of time, may
induce changes in bone morphology. The main variables, then, are muscle
activity, fluctuation and time.
Our hypothesis and Wolff's Law are based on the accepted concept
that within a system the muscle-bone interaction is highly integrated.
Supporting this concept is the observation that in the embryo, bone de-
velops in the connective tissue where muscle fibers enter an area adjacent
to more rigid tissue, such as a cartilage or a tooth bud. The bone tissue
undergoes remodeling as the structure grows, and eventually it develops
an architecture which corresponds to an expected stress distribution rela-
tive to adjacent muscles.
We may assume then, that if we could take an embryonic bone and
change its position, for example 45° relative to the musculature, it would
undergo additional remodeling until the architecture again corresponds to
the stress created by the musculature. It is generally recognized that after
bone fracture and healing with dislocation, a gradual bone remodeling
may occur. This remodeling may be a form of muscle-bone interaction
which occurs only in the embryo and under special traumatic conditions
after birth, or it may represent a basic principle which applies throughout
life.
If this form of muscle-bone interaction represents a basic principle, it
151
Neuromuscular and Morphological Adaptions
must be a very important mechanism in bone remodeling during growth
as well as in association with oral respiration. In this connection several
questions arise: (1) Can muscle activity be linked directly to bone forma-
tion? (2) Does the change from nasal to oral respiration have a significant
impact on the muscle activity? (3) Does the new muscle activity alter the
position of the mandible relative to the adjacent muscles and to the
maxilla? (4) Is the fluctuation of the new muscle activity within the criti-
cal limits? (5) Does it last long enough to effect bone remodeling and
direction of new bone growth?
An experimental model was designed to address questions concerning
the characteristics of muscle activity critical to new bone formation.
The model was a prepared site at the attachment of the temporal
muscle in rhesus monkeys. The coronal part of the temporal muscle was
exposed and a cut 1 cm long was made across the fibers close to the edge
of the attachment. Two parallel cuts 1.5 cm in length along the muscle
fibers produced a flap which was elevated from the bone. A bone graft
taken from a rib was placed on the parietal bone under the flap and
secured with steel ligatures. The muscle flap was placed over the graft
and tied down, with the muscle fibers ending over the groove formed by
the upper edge of the graft and the skull bone (Fig. 1).
It was expected that the blood clots formed in the groove around the
graft would be invaded by capillaries and replaced by connective tissues.
In the upper groove under the endings of the muscle fibers, however, we
could expect new bone formation if the activity in the muscle fibers had a
bone inducing effect. That is, osteoblasts would appear, and bone would
be formed and scattered between the capillaries until it was consolidated
in a process comparable to the early embryonic bone formation men-
tioned earlier. Biopsies taken four to six weeks after placement of the
graft showed that calcification and bone formation occurred in the crypt
area. New bone formation also was found in the space between the graft
and the skull (Fig. 2). This is not the type of bone formation which is
found when bone remodeling proceeds from the periosteum. Bone forma-
tion in the pacified zone at the end of the muscle fibers was scattered in
the connective tissue, and it appeared that a preosseous matrix had been
synthesized and had undergone calcification.
Biopsies taken 2 to 3 months after placement of the graft demonstrated
that after the hard tissue had formed, the bone underwent remodeling as
the graft was resorbing. The new bone gradually remodeled back to its
original shape, and one year later very little of it remained.
For the next experiments it was postulated that if the synthesis of the
preosseous matrix were dependent on the muscle fibers ending in rela-
tively stable connective tissue, then more vigorous muscle activity might
prevent bone formation. To test this possibility, a pacemaker was im-
152
Harvold
/* TEMPORAL
MUSCLE
Figure 1. (A) A flap is prepared in the temporal muscle. A bonegraft from the rib
is secured to the skull under the muscle flap and the wound in the scalp is closed.
(B) New bone will develop in the crypt X above the graft.




153
Neuromuscular and Morphological Adaptions
Figure 2. Biopsy of calvarium of a rhesus monkey taken 4-6 weeks after place-
ment of bone graft. (A) Biopsy taken at 4 weeks. (B) Biopsy taken at 6 weeks.
(1) parietal bone; (2) resorbing bonegraft; (3) muscle fibers; (4) bone formation
in the crypt between skull and graft. Note in (B) how the new bone has trans-
formed to lamellar bone.
154

Harvold
-
-
-
Figure 3. Biopsy of calvarium of a rhesus monkey in which a pacemaker had been
implanted in the temporal muscle. (1) skull; (2) bone graft; (3) muscle fibers; (4)
crypt between skull and graft. Note that no bone formation has occurred in the
Crypt.
planted which kept the temporal muscle contracting once per second. The
findings showed that the rhythmic motion disturbed the process of bone
formation, as there was no new bone at the end of the activated muscle
fibers (Fig. 3). -
It was apparent that muscle contractions caused by the pacemaker had
a disruptive effect on new bone formation at the end of the stimulated
muscle fibers. However, the effect of the induced muscle contraction and
movement was distributed over a wide area of the skull. Bone remodeling
Was observed at more distant sites, for instance, at the attachment of the
Sternocleidomastoid and digastric muscles on the opposite side of the
Skull. Alizarin staining also revealed that remodeling of the interior of the
mandible was very active.
It appears, then, that vigorous muscle activity may prevent bone remo-
deling at the attachment but induce bone formation and remodeling at
more distant sites. This may occur because the motion is changed or
dampened over a distance, or it may be due to altered activity of other
muscles in response to the stimulus. Thus the answer to the question
previously raised is that a linkage between muscle activity and bone for-
mation can be demonstrated.
155

Neuromuscular and Morphological Adaptions
º-
Figure 4. Radiographs of mandible of a teenage girl taken (A) a few weeks after
and (B) several months after placement of a bone graft which was modeled as a
normal section of the jaw and which extended from the first premolar to the
temporal region. Note in (B) the new bone extending from the premolar region to
the external pterygoid and to the temporal muscle. This new bone replaced the
resorbing graft.
The same principles of bone induction by muscle activity can be applied
to the restoration of a missing part of the facial skeleton. The radiographs
of the mandible belonging to a teen-aged girl may serve as an illustration
(Fig. 4). The right side of the mandible had been removed because of a
malignancy. The whole ramus and the body extending forward to the first
premolar were missing. The masseter, medial pterygoid and buccinator
muscles had also been removed. Only the temporal and the external
pterygoid muscles remained on that side, in addition to the muscles at-
tached to the front part of the mandible.
A bone graft extending from the front part of the mandible to the
free-ending temporal and external pterygoid muscles served to immobil-
ize the soft tissue. At the same time, special jaw orthopedic treatment
controlled the muscle activity, as described elsewhere (Harvold, 75).
Radiographs taken after a few weeks of treatment showed new bone
formation extending from the external pterygoid as well as from the
temporal muscle and from the anterior part of the mandible, where the
mylohyoid, digastric and platysma muscles are attached.
For several months both the resorbing graft and the new developing
bone could be followed radiographically until the new bone was clearly
visible and the graft, which was shaped like a normal ramus, had disap-
peared. The new mandibular bone had no protuberance at the gonial
region. If the masseter and medial pterygoid muscles had been intact, a
bony extension would have developed at the gonial angle.
When the observations mentioned above are considered relative to oral
respiration, the pertinent questions would be: does oral respiration re-
156

Harvold
quire a significantly different relation between the maxilla and the mandi-
ble, and is the new positioning sufficiently consistent to cause remodeling
of any bones?
Satisfied that muscle-bone interaction is a reality with regard to bone
induction and bone remodeling, we can look more closely at muscle
function in terms of consistency and fluctuation. Muscle function and
muscle recruitment for respiration have been discussed by Miller and
Vargervik (Miller, 78; Miller and Vargervik, '79). The hypothesis under
consideration here includes the vague terms “consistent”, “limited fluc-
tuation” and “a period of time.” In order to establish a more precise
concept of these variables relative to the recruitment of muscle function
for oral respiration, the following reasoning was applied. Muscle activity
is either voluntary or involuntary. Voluntary activity cannot be consistent
over an extended period of time. Although it may have an impact on
bone remodeling, we can assume that it will be a secondary factor. On
the other hand, involuntary activity, which is monitored by a sensory-
motor feedback system, may be repetitious over an extended period of
time and fall into the category which elicits bone remodeling.
In an earlier experiment (Harvold et al., 72), a plastic wedge was placed
in the palatal vault in a group of monkeys. The tongue sensed the plastic
and, in response, the experimental animal lowered its tongue and the
mandible. Within four to six months the experimental animals had devel-
oped severe open bites not found in the control animals. It was demon-
Strated that this consistent muscle activity indeed elicited bone remodeling
which could be quite extensive during a period of a few months.
On this basis the term “an extended period of time” would refer to
four to five months or more. “Consistent” and “limited fluctuation”
would apply when the sensory stimulus was stable and when a certain
muscle activity would serve to eliminate temporarily the sensory input.
We turn now to the animal experiments on nasal obstruction. The
assumption was made that the drive for adequate oxygen uptake presents
a “consistent” sensory stimulus which continues for an “extended period
of time.” The elicited muscle recruitment, on the other hand, may not
necessarily be consistent because a relieving oral airflow can be secured
through a variety of compensatory lip, tongue and jaw movements and
position. It was expected, however, that the experiments would demon-
strate whether or not this additional activity would have any impact on
orofacial muscle development; that is, can nasal obstruction and oral
respiration be disregarded as factors contributing to orofacial form devel-
opment? Furthermore, the experiments would disclose any preferred pat-
terns of muscle recruitment and offer an opportunity to trace the impact
on bone morphology and remodeling.
For the past several years, experiments on nasal airway restriction have
157
Neuromuscular and Morphological Adaptions
exº-
a to tº
Figure 5. Normal (A) facial appearance and (B) tongue of a rhesus monkey
(Macaca mulatta). The tongue maintains contact with the soft palate when the
mouth is wide open.
been conducted in our laboratory utilizing rhesus monkeys (Harvold et
al., '73). In the experimental design the animals were placed in pairs of
similar type, sex and age, with one of each pair designated as the experi-
mental animal. The observed intrapair and intergroup differences were
assessed by standard statistical methods. Photographs of face, tongue and
teeth, plaster casts of the dentition, cephalometric radiographs of the
skull in five projections, and electromyographic recordings were obtained
for each subject.
Although the facial appearance of healthy rhesus monkeys may vary
considerably, usually the animals keep their mouths closed (Fig. 5), al-
though occasionally the lips may separate. When the animal is under light
anesthesia, for example with ketamine, oral respiration may occur. How-
ever, all experimental animals with their nares blocked kept their mouths
open continuously (Figs. 6 and 7). The distinction between the control
and the experimental animals was easily observed. The electromy-
ographic recordings demonstrated that with oral respiration the upper lip
was elevated rhythmically. In most animals the upper lip gradually devel-
oped a notch in the middle (Fig. 6). When nasal respiration was restored,
the rhythmic elevation of the lips discontinued and the notch gradually
disappeared. Apparently the muscles of the lower lip were not engaged in
the respiratory function.
The tongue acquired a new shape in all experimental animals but the
particular shape varied. In general, it became more narrow and more
pointed. Most animals developed a groove along the midline of the
tongue which, with the palatal vault, formed a tube for airflow. Two
animals developed one such groove on each side of the tongue midline
158

Harvold
Figure 6. Young adult animal with (A)
normal occlusion and (B) normal
tongue position. (C) The tongue
moved forward in response to nasal ob-
struction. (D) Three years later an ef-
fective oral airway was well-estab-
lished. Six months after nasal respira-
tion was resumed (E) the lips and the
(F) tongue were again positioned nor-
mally. (G). The acquired dental maloc-
clusion, however, was retained.
- -



Neuromuscular and Morphological Adaptions
Figure 7. (A) This young adult monkey opened his mouth rhythmically for respi-
ration when the nose was obstructed. (B) Three years after the experiment had
begun, a notch in the lip and a groove in the tongue had formed to provide an
oral airway. (C) Six months after nasal respiration had resumed, the notch in the
lip had disappeared and (D) After 1 year the rhythmic advancement of the mandi-
ble moved the maxillary teeth forward and produced a dual bite which was re-
tained. Note (E) the retained acquired occlusion, and (F) the centric relation.
160

Harvold
Dimension Before Experiment Increments during experiment
Larger group 2 tailed P. larger group 2 tailed P
1. Sella-Nasion E. 0.25 C. 0.094
2. Sella-Prosthion E. 0.047 C. 0.218
3. T. M. - Prosthion E. 0.016 C. 0.078
4. T. M. - M. Symphysis E. 0.031 C. 1.000
5. Nasion - Palatal plane E. 0.44 E. 0.016.”
6. M. Symphysis - Palatal plane E. 0.094 E. 0.44
7. Nasion - M. symphysis E. 0.063 E. 0.031 *
8. Angle S-N, palat. plane E. 0.69 E. 0.031*
9. Angle S-N, Occlusal plane E. 0.43 E. 0.30
10. Angle S-N, lower Mand. Border C. 0.94 E. 0.016*
11. Angle post. ramus border, S-N E. 0.84 E. 0.38
12. Gonial angle C. 0.47 E. 0.031*
Table 1. Comparison of cephalometric measurement from the control and experi-
mental group in an experiment with 7 pairs of animals. Wilcoxon signed rank test.
E, experiment; C, control.
(Fig. 8). All animals demonstrated some rhythmic protrusion of the
tongue during oral respiration in which the genioglossus muscle was in-
volved (Miller, 78; Miller and Vargervik, '78). In some animals the ca-
nines moved and prevented the mandible from closing with the condyles
in their normal position. These animals developed a dual bite (Fig. 7).
The pertinent cephalometric findings are shown in Table 1. The dis-
tance from nasion to the chin increased significantly in the mouth
breathers. The distance from nasion to the hard palate also increased
significantly, but not the distance from the palate to the chin. This dem-
onstrates that the lowering of the mandible was followed by a downward
displacement of the maxilla. The lower border of the mandible took a
steeper inclination and the gonial angle increased in the mouth breathers.
Further, the maxillary incisors established a steeper inclination in the
mouth breathers. *
The mouth breathers demonstrated different patterns of adaptations to
nasal airway restriction. Those with a dual bite and rhythmic advance-
ment of the mandible also had a Class II malocclusion. The few that
established a tract for oral respiration and maintained a more stable low
position of the mandible developed a Class III malocclusion (Fig. 6). A
more detailed discussion of the malocclusions is in preparation.
The experiments demonstrated that the recruitment of orofacial
muscles for respiration had a significant effect on muscle development.
This, in turn, changed the morphology of the upper lip, the tongue and
161
Neuromuscular and Morphological Adaptions
Figure 8. This animal developed one air channel on each side of its tongue.
the oropharyngeal port. We may assume that other changes also oc-
curred, and a full survey will be made. The changes in lip and tongue
were followed by remodeling in the alveolar process and by changes in
the direction of tooth eruption, resulting in dental malocclusion. It is
likely that the change in tongue morphology is more significant for bone
remodeling than the rhythmic movement of the tongue.
The lowering and the rhythmic protrusion of the mandible may be
characterized as fluctuating and inconsistent movements. Yet remodeling
occurred, resulting in an open gonial angle. The changes in the mandible,
however, were associated with a downward displacement of the maxilla
which gradually restricted the mandibular upward movements. In the
human condition, tooth extrusion may be more significant than maxillary
displacement under similar circumstances. The most distinct remodeling
of the mandible occurred in the ramus, which retained its normal relation
to the skull when the chin assumed a lower position. This may indicate
that the masticatory muscles tying the ramus to the skull are practically
unaffected by the respiratory function and continue to remodel and shape
a normal ramus.
162


Harvold
SUMMARY
Certain functional and morphologic traits which developed in the rhe-
sus monkey in response to nasal airway restriction resemble familiar clini-
cal conditions. We may assume, therefore, that these experimental find-
ings have some clinical relevance. The morphologic changes were not
uniform among the animals, but varied depending on the preferred posi-
tioning and movements of the tongue and mandible to accommodate oral
respiration. The more significant changes were associated with changes in
positioning rather than the rhythmic movements. The experimental ap-
proach may help to expose, if not clarify, certain cause and effect rela-
tionships in the developmental process which should be recognized in
diagnosis and treatment.
ACKNOWLEDGEMENTS
This project was supported by NIH Grant No. 5 R01 DE02739.
REFERENCES
Brash, J. C. The etiology of irregularity and malocclusion of teeth. The Dental
Board of the United Kingdom, 1956.
Harvold, E. P. The role of function in the etiology and treatment of malocclusion.
Am. J. Orthodont. 54:883-898, 1968.
Harvold, E. P. New treatment principles for mandibular malformations. Trans.
3rd Int. Orthodont. Cong. Crosby, Lockwood and Staples, pp. 148-154, 1975.
Harvold, E. P., G. Chierici and K. Vargervik. Experiments on the development
of dental malocclusions. Am. J. Orthodont. 61:38-44, 1972.
Harvold, E. P., K. Vargervik and G. Chierici. Primate experiments on oral
Sensation and dental malocclusion. Am. J. Orthodont. 63:494-508, 1973.
Linder-Aronson, S. Naso-respiratory function and craniofacial growth. In: Naso-
Respiratory Function and Craniofacial Growth. J. A. McNamara, Jr. (ed.),
Monograph No. 9, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, 1979.
Linder-Aronson, S. and D. G. Woodside. The growth in the sagittal depth of the
bony nasopharynx in relation to some other facial variables. In: Naso-
Respiratory Function and Craniofacial Growth. J. A. McNamara, Jr. (ed.),
Monograph No. 9, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, 1979.
Miller, A. J. Electromyography of craniofacial musculature during oral respira-
tion in the rhesus monkey (Macaca mulatta). Arch. Oral Biol. 23:145-152,
1978.
Miller, A. J. and K. Vargervik. Neural control of oral respiration in the rhesus
monkey. In: Muscle Adaptation in the Craniofacial Region. D. S. Carlson and
J. A. McNamara, Jr. (eds.), Monograph No. 8, Craniofacial Growth Series,
163
Neuromuscular and Morphological Adaptions
Center for Human Growth and Development, The University of Michigan,
Ann Arbor, 1978.
Miller, A. J. and K. Vargervik. Neuromuscular changes during long-term adapta-
tion of the rhesus monkey to oral respiration. In: Naso-Respiratory Function
and Craniofacial Growth. J. A. McNamara, Jr. (ed.), Monograph No. 9, Cra-
niofacial Growth Series, Center for Human Growth and Development, The
University of Michigan, Ann Arbor, 1979.
164
THE INTERDEPENDENCE OF THE NASAL AND
ORAL CAPSULES
Robert M. Ricketts, D.D.S., M.S.
Department of Orthodontics
Loma Linda University
The relationship between the development of occlusion and naso-
respiratory function has been debated for at least a century. Prior to
1930, many individuals were convinced that mouthbreathing affected the
development of the oral apparatus (Catline, 25; Price, '42). However,
during the 1930's and 1940’s, the serial studies of Broadbent (37, 41) and
Brodie (38) suggested “constancy” of the growth pattern, providing a
theory of facial growth strongly influenced by genetic factors. The work
of Lundstrom ('55) and Goldstein (53) further implicated the role of
heredity and the pendulum swung from theories of environmentally influ-
enced patterns of facial growth to the immutability of genetically deter-
mined growth patterns. That there is a relationship between the nose and
the mouth would seem obvious on both a functional and neurologic basis
(Moss, '62). The nasal and oral regions are supplied by divisions of the
same fifth cranial nerve, as both respiration and mastication evolved si-
multaneously from the branchial arch system. Both oxygen and food are
basic necessities of survival, with oxygen being the more critical short-
term need. -
Adenoid facies and, more recently, the long face syndrome are con-
sidered distinct clinical entities. Most orthodontists recognize the prob-
lems associated with retaining results in treated open-bite and posterior
lingual crossbite cases. Most contemporary orthodontists have employed
rapid separation of the midpalatal suture, often in the hope of increasing
the nasal airway (Wertz and Dreskin, '76). It is, therefore, timely that the
diagnosis and prognosis of abnormal conditions in the nasal cavity be
updated, together with a reevaluation of its possible implications on total
facial growth and total patient welfare.
HYPERNASALITY
In order to provide a background for this subject, we will first consider
a series of investigations by the author and others. The first of these
Studies was aimed at understanding the structural differences in the cra-
165
Nasal and Oral Capsules



Figure 1. Tracing of midsagittal laminagraph showing bony nasopharyngeal space
and airway in an adult male.
niofacial region of cleft palate patients. Since differences in nasality occur
in apparently similar cleft patients, the nasal chamber was studied from
both lateral and frontal laminagraphic sections (Ricketts, '56). Studies of
those patients with incompetence in nasopharyngeal function indicated
that one of the variations present in these patients was in the cranial base
region (Figs. 1 and 2). Wide angles (nasion-sella-basion) or obtuse rela-
tionships between the anterior and posterior regions of the cranial base
seemed to be consistent with excessive nasopharyngeal space. Speech
bulbs placed posterior and superior to the soft palate led to remarkable
improvement in speech quality. Some of these patients had greater diffi-
culty in speech following adenoidectomy because they apparently had
taken advantage of the adenoidal tissue to help valve the airway (Fig. 3).
From these investigations, the author reached the conclusion that five
factors contribute to hypernasality: (1) abnormal form or shape of the
166
Ricketts
M BC
T7 ACUTE CRANIAL BASE
M Bd
T (5 OBTUSE CRANIAL BASE
Figure 2. Variation in cranial base in midsagittal orientated from Nasion-Sella-
Basion-Opisthiom (N-S-Ba-M). .
cranial base, (2) true submucous cleft, (3) vomerine or septal defects, (4)
restriction of movement of the palate due to neuromotor problems or
Scarring of the pillars following tonsillectomy, and (5) possible deficiency
of tissue in the soft palate or anterior displacement of the maxillary
complex (Fig. 4).
HYPONASALITY
If the above hypothesis is true, is the opposite also true? Is there a
dichotomy? Instead of excessive nasopharyngeal space, could there be
too little space caused by the opposite of the factors listed above? To
answer this question, additional investigations were carried out in which
the relationship between the soft tissues in the nasopharynx and available
Skeletal space were examined (Fig. 5). An analysis of subjects with hypo-


167
Nasal and Oral Capsules
SUPERIOR – INFERIOR NASOPHARYNGEAL
SOS – IN
Figure 3. Extremes of bony nasopharynx variation vertically in twenty subjects at
pubertal ages.
Figure 4. Ten-year-old male subject with severe nasality and cleft palate speech.
Note obtuse cranial base angle (144°) and small and restricted palate carried
forward by position of the skeletal midface.


168
Ricketts
Figure 5. Blockage of airway by adenoid in a 17-year-old male subject. Ninety
percent of the nasopharyngeal space is occluded.
nasality and respiratory limitations was undertaken. Findings revealed not
Only differences in hard and soft tissue morphology, but also remarkable
differences in functional patterns of posture and speech (Fig. 6). This
Work was the basis for the later nasopharyngeal analysis using lateral and
frontal headfilms (Fig. 7). Hypernasality and hyponasality were discussed
in an earlier paper (Ricketts, '58a) which included conditions of craniody-
Sostosis and other cervical dysplasias (Figs. 8 and 9).
TONSILLECTOMY AND/OR ADENOIDECTOMY
Keeping in mind the possible influences on craniofacial growth of con-
ditions within the nasopharynx, observations were made before and after
Surgery of patients with enlarged tonsils and/or adenoids, many of whom
also had unilateral or bilateral lingual crossbites (Fig. 5). Some patients
also exhibited displacement of the mandibular condyle in the glenoid
fossa.
Twenty-five patients from three to twelve years of age (18 females and

169
Nasal and Oral Capsules
Figure 6. Function during speech in patient seen in Figure 5. Note the forward
thrust of mandible in contrast to usual straight downward movements of parts.
17 males; Fig. 10) were studied. An attempt was made to take T2 head-
films of these patients about 2 months after the surgical procedure, but
the interval ranged from from 2 months to 6 months postoperatively.
Tracings of the pre- and postoperative headfilms were compared in
order to determine tongue height relative to the palate, postural altera-
tion of the soft palate, positional changes of the hyoid bone and changes
in head posture.
Both functional and postural changes were observed when the two sets
of films were compared. The tongue and hyoid bone elevated in a major-
ity of cases and the soft palate tended to raise during rest. However, the
point of greatest interest was the resting posture of the whole head. It

170
Ricketts
PT V P |One
(4)
(AE)
Figure 7. Method of study of nasopharyngeal-cervical conditions. A, cranial base
Saddle angle (N-S-Ba); B, nasopharyngeal angle (Ba-S-PNS); C, space for airway
from pterygoid vertical plane (less than 5 min is critical); D, vertical location of
hyoid relative to E (PNS); F, menton; G, CV4 and horizontal location of hyoid to
PTV plane (is typically on plane).
tipped downward a mean of 2°. Six patients exhibited a dramatic change
in head posture as well as a change in facial expression (the correction of
facial ptosis associated with prolonged mouthbreathing). In these six pa-
tients there was a change in the relationship between tongue and palate.
This was generally not a consequence of marked tongue elevation.
Rather, as the downward-tipping posture of the head lowered the palate,
the upper arch moved downward over the tongue (Fig. 11). This study
was reported in preliminary form in 1958 (Ricketts, '58b) but was never
completed due to the uncertainty of positioning in the cephalometer.

171
Nasal and Oral Capsules
SN BO CN
19 - O 12Oo
Figure 8. Illustration of 19-year-old female (who still has deciduous teeth) with
craniodysostosis. Note the forward position of cervical vertebrae, failure of verti-
cal growth of palate, precipitous droop of soft palate and low tongue position.
The vertical line is perpendicular to the true horizontal posture of the head as the
head is tilted upward.
The above findings led to an hypothesis of a possible alteration in the
entire postural kinetic chain of the head resulting from blockage of the
nasopharynx. It was further hypothesized that likely changes in mandibu-
lar position could be associated with failure of adenoidal and tonsillar
involution. The fact that not all patients responded in the same way
following adenoidectomy and/or tonsillectomy led to further investigation
of other factors involved in respiratory obstruction. These included (1)
enlargement of the turbinates or presence of polyps, (2) factors involved
in the deviation of the septum including sinus infections, (3) allergic
manifestations, (4) chronic rhinitis, (5) partial nasal bony atresia, (6) the
Small nasal cavity or microrhino dysplasia, and finally (7) foreign body
obstruction (one patient had put a bean in the nose, another had lodged a

172
Ricketts
Figure 9. Pierre Robin Syndrome in a 6-year-old male who, due to posterior cleft
repair, suffered fibroses of nasopharynx. Notice head posture and sustainment of
large oral airway, as well as fusion of cervical vertebrae and lack of posterior arch
of atlas. Vertical line is perpendicular to the true horizontal.
rubber eraser in the nose for several months and yet another had snuffed
a lead weight from a fishing box which ended up in the frontal sinus).
THE RESPIRATORY OBSTRUCTION THEORY
During the 1950's most workers became aware of the problems in
“tongue thrust” resulting in an open bite. Because tongue posture had
been associated already with conditions of the nasopharnx (Ricketts, ’54),
and because changes in the nasopharyngeal space had resulted in accompa-
nying changes in tongue position (Ricketts, '58b), it was also theorized that
certain physiologic demands could be primary to problems in deglutition
and even in mandibular rest position (Ricketts, ’52). Therefore, a study
was conducted in 1960 to determine possible interactions in the physiology
associated with speech, breathing, deglutition and malocclusion.

173
Nasal and Oral Capsules
Figure 10. Method employed for study of changes associated with removal of
adenoids and/or tonsils. Note N-S-CV IV for head posture change. Dotted area
illustrates excessive adenoid mass. Hatched area is soft palate with line drawn
through long axis to facilitate study of palatal changes. Dots show tongue and
pharyngeal distances. Hyoid and tongue may be related to cervical vertebrae and
posterior throat wall.
Twenty patients were selected from the private practice of the author.
Fifteen of the patients had tongue problems and the other five were used
as controls. In conjunction with the Speech Department and the Depart-
ment of Radiology at the University of California, Los Angeles, speech
and deglutition were studied cineradiographically (including barium Swal-
lows) and cinematographically.
The results of the study confirmed that there was a relationship be-
tween the factors associated with problems in tongue posture and degluti-
tion. The normal swallow was described radiographically and three types
of tongue behavior were identified: adaptive tongue behavior was secon-
dary behavior resulting from other primary problems (Fig. 12); transitory
tongue behavior was associated with glossoptosis (Fig. 13); and habitual
tongue behavior was characterized by atavistic conditions of failure of a

174
Ricketts
6–8 to 6- . O
Figure 11. Six-year, 8-month-old female subject before (solid line) and 2 months
after (dashed line) removal of tonsils and adenoids. Hatched area indicates remo-
Val of tonsils and adenoids. Blackened area indicates elevation of soft palate and
tongue. Note the downward change in tilt of head after surgery.
natural lowering of the pharyngeal apparatus (Fig. 14; Ricketts, '62). Later
work further confirmed the different patterns of hyoid bone behavior in a
45 patient sample studied cinefluororadiographically (Sloan et al., '67).
Extremes of craniofacial form were also described in a discussion of the
relationship between environment and esthetics (Ricketts, '68a).
Continued cephalometric observation of untreated patients followed
Serially and of patients treated clinically for certain malocclusions led to
the description of the respiratory obstruction syndrome (Ricketts, '68b). It
included the following characteristics: (1) primary unilateral or bilateral
lingual crossbite, (2) functional unilateral crossbite with mandibular de-
flection - mesial on one side and distal on the other, (3) presence of large
adenoids or tonsils or history of same, (4) open bite, (5) lowered tongue
position, (6) tongue thrust, (7) narrowed upper arch, (8) chronic mouth-
breathing with variations of adenoid facies (9) secondary problems in
temporomandibular joint and maxilla, (10) pseudo Class I condition in

175
Nasal and Oral Capsules
7 – 1 O
Figure 12. Tracing from lateral headfilm of 7-year-old male subject with adaptive
tongue thrust secondary to large tonsils. Tongue is thought to be factor in anterior
crossbite but not Class III malocclusion.
bilateral crossbites with a deflection of the mandible anteriorly, (11) head
tipped backward on cervical column (face raised), (12) palatal plane
tipped upward anteriorly in thumb suckers and backward in ordinary
mouth breathers, (13) narrow nasal cavity, and (14) possible opening of
the mandibular angle.
This syndrome seemed to be verified as improvements in arch develop-
ment took place in some patients without orthodontic therapy when nor-
mal respiratory function was restored.

176
Ricketts
W
Figure 13. Note glossoptosis and hyoidptosis of 9-year-old female (note space
above tongue). Clinically the patient was still a chronic tongue thruster (transitory
type of thrust; note the open bite). No adenoid was present in this patient.
NORMAL AND ABNORMAL GROWTH OF THE NASAL CAPSULE
Work with the computer was started in 1965. By 1968 frontal and
lateral cephalograms had been collected on forty untreated subjects who
had been followed for at least 5 years. Twenty of the subjects were
Studied for 8 years from ages 5 to 13 years. Data from dried skulls of
younger individuals were used for the period from birth to 3 years, and
Samples of older subjects were used for maturing developmental data
(Figs. 15, 16, 17).
The findings of Brodie that the craniofacial complex grows in a down-
ward and forward manner when superimposition is made along the sella-
nasion plane at sella were reconfirmed in the lateral headfilms in this
Study. But our data showed even better orderliness of growth when the

177
Nasal and Oral Capsules
7-O
º *
C)|Y
C)
Figure 14. Lateral headfilm of 7-year-old female with an unusually high habitual
type tongue thrust with atavistic condition. Note the hyoid bone (falling between
cervical vertabraes II and III), short neck and normal airway. Contrast with
female in Figure 13.
nasal cavity was related to the basion- nasion (BaN) plane or the basi-
cranial axis (Figs. 18-21). These studies also included development of the
bony pharynx and cervical vertebrae (Fig. 22).
Data regarding the development of the face in the frontal dimension
was lacking until the time this study was performed. The growth of the
nasal region, as indicated in the serial frontal headfilms, appeared to
follow the same general somatic course, starting with a nasal cavity at
birth of about 10 mm which by 3 years of age was about 16 mm. By age 8
years the nasal width was radiographically measured at 25 mm (+2 mm).
In adult males the width reached 31.5 mm (+1.5 mm). This is a

178
Ricketts

_*
24
/
C
L/
/*
J/
|
(
Ş
\
AZ
WX
7 Nº
• Nº.
ſ
L^2
|
2-
\
*~sº
*
J.--T
Figure 15. Method of orientation of head plate tracing for description of hard and
Soft tissue anatomy. A coordinate grid is constructed from Frankfort (horizontal)
and a perpendicular at the posterior margin of pterygopalatine fossa (vertical).
This is called the pterygoid vertical plane and the crossing is the zero point on the
coordinate. Note darkened airway. -
yearly increase of only about 0.6 mm per year in nasal width after age 8
(Fig. 23; Ricketts, '72). The polar grid (Fig. 17) applied to the frontal
headfilm suggested a bipolar behavior originating from the regions of the
foramen rotundum.
The foregoing work led to the development of standards of normal nasal
cavity and orocervical physiology to which abnormal development could be
compared (Fig. 24A, B, C). In the lateral view it was also found that the
palate (oriented along the palatal plane) displayed a cant of 7 degrees
(+2.5) relative to the sella-nasion and almost parallel orientation to the
Frankfort plane. Palates tilted superiorly were considered abnormal.
179
Nasal and Oral Capsules
§ 3; # 33 3; # 3; # # 3; ; ;
A.//
4-9 ya
23O-57

Figure 16. Same head plate seen in Figure 15 of 4-year, 9-month-old female
subject oriented on polar grid at “center of growth on the face.” Anatomical
points tend to follow grid lines in normal growth (on average).
Correction of obstructed airway conditions is possible by orthopedic
orthodontic procedures, and nasal cavity growth can be influenced by
mechanical intervention. Note the change in the female patient seen in
Figure 25A. Treatment consisted of removal of adenoids, palatal widen-
ing, and placement of extraoral orthopedic traction appliances on the
upper molar. When the palate was widened, the airway was also widened
and the tongue moved upward, returning to a normal rest position. The
results of this treatment have remained stable to age 13 years (Fig. 25B).
The nasal cavity width increased from 24 mm to 30 mm by age 10 years
and 2 months, a distance of 6 mm where only 1.5 mm normally would
have been expected in a 2.5 year growth period (Fig. 25C). The width
between the upper molars was increased from 46 mm (see crossbite in
Fig. 24C) to 62 mm in the same period. No increase in molar width would
have occurred without intervention.
We will now consider craniofacial growth in patients who were treated
by orthodontic therapy alone. In many patients with respiratory obstruc-
180
Ricketts

AGA 3
Figure 17. A frontal tracing oriented from two centers — one for each half of the
face near region of foramen rotundum at base of sphenoid (darkened area).
Points tend to follow bipolar phenomenon in normal growth.
tion, orthodontic treatment may not, in itself, be adequate to resolve the
patient’s problem. For example, in Figure 26 compare serial tracings of a
male patient with severe denasality, an abnormally restricted upper nasal
cavity and infected sinuses (Figs. 26A, B) with those of a short lower facial
height patient (Fig. 26C). The orthodontic result was not stable, as indi-
cated by the cephalometric tracings of the same patient taken 11 years later
(Fig. 26D). The facial axis opened 4°, indicating a continued abnormal
Vertical growth in this patient (the facial axis does not normally open or
close appreciably during growth; see Fig. 32 for an illustration of the nor-
181
Nasal and Oral Capsules
Figure 18. Illustration of growth of nasal cavity (palate) from birth to 18 years as
Oriented from basion to nasion at nasion. Note parallelism of palate -- no change
in point A (SD + 1.0 in ten years).
mal development of the oral capsule). The case seen in Figure 26 illustrates
the need for a complete physiologic approach to orthodontic treatment.
WORK OF OTHERS
This paper has focused thus far on a series of studies of the author. It is
important, however, to consider these studies in the light of the work of
others. Subtelny (54) cephalometrically studied the growth of the airway
space. He concluded that about 4 mm of airway space was critical to
normal function. He also suggested that nosebreathing was important to
the normal development of the dentition. Bushey ('73) tested the rela-
tionship between conditions in the nasopharynx and the actual airway.
After adenoidectomy, three groups were identified: those that improved,
those that partially improved and those with little improvement. Those
that improved tended to be more brachyfacial while those improving less
were more vertical in facial pattern.
Behavior of the nasopharyngeal space was studied by Pruzansky (75).
He suggested that tonsillar and adenoidal lymphoid tissues do not neces-
Sarily involute simultaneously and that the adenoids may begin to shrink
before the onset of puberty. He also stated that Scammon's curve of
lymphoid behavior may not apply in all cases.

182
Ricketts
Birth
3
8
13
18
Figure 19. Illustration of growth of nasal cavity (palate) from birth to 18 years
oriented on Frankfort horizontal plane as seen in Figure 15. Note near 90° rela-
tion and same constancy as observed in Figure 18.
Linder-Aronson's ('70) cross-sectional and longitudinal work is also
significant. In a comparison of patients with and without respiratory ob-
struction, he observed differences in morphology of the facial bones,
including the mandible. His 5-year follow-up study of the patients above
produced further evidence that lack of normal nasal respiration effects
the morphology of the face adversely, and that attainment of normal
nasal respiration can result in attainment of normal facial morphology.
Quinn ('78) associated nasal airway to various kinds of facial problems
including asymmetrical and vertical growth patterns.
In animal studies Harvold ('73) showed changes associated with in-
duced mouthbreathing after gradually blocking the nasal airway. After
the monkeys became mouth breathers, gradual alterations in the form of
the symphysis and changes in occlusion became evident.
CONTEMPORARY VIEWS FROM RELATED DISCIPLINES
Many of the concerns regarding naso-respiratory function of those from
Other disciplines (e.g., pediatrics, otorhinolaryngology) have been some-

183
Nasal and Oral Capsules
Figure 20. Lateral view of serial samples age 5 to 13 years oriented at foramen
rotundum (Pt point) and showing gnomic nature of growth of nasal capsule (in
lateral view).
what different in the past from those of orthodontists. Of primary con-
cern to the physician (Steele, '68) are patients exhibiting repeated tonsilli-
tis, hypertrophy of adenoid tissue to the extent that the Eustacian tube is
blocked, and chronic nasopharyngeal infection that does not respond to
drug therapy. Growth of the midface and development of occlusion has
not been, as a rule, the concern of the physician. Another major concern
of the physician is the function of immunoglobulins which are, in part,
produced by lymphoid tissue (Fairchild, '68). However, no data has been
offered regarding the dependence of this antigen or globulin role on the
adenoids.
Ogura and colleagues ('68) studied pulmonary function and found an
association between it and upper airway obstruction. The nasal cavity is
thought to induce a reflex to the general soma and this may work both
ways.
There are other problems related to the function of the nasal airway.
Gray ('76), a rhinologist, detailed twenty functions of the nose. He also
described racial types. Gray showed that each side of the nose is indepen-
dent and is associated with a separate half of the brain and a separate lung,
the air is warmed, humidified, and put under presure in the nasal cavity;
nerves go directly from the nose to the hypothalmus; hormonal changes


184
Ricketts
Figure 21. Superimposed tracings of an individual from birth through 13 years
Showing a pattern of integration of sphenoid growth with the maxilla from a
Frankfort plane-pterygoid vertical orientation.
affect nasal function. He suggested that one should begin to monitor ade-
noids and method of breathing in children by three years of age.
Other individuals have suggested alternate causes for naso-respiratory
problems. Marks ('65), a pediatric allergist, is firm in his belief that
respiration can be restricted due to infant sensitivity to cow's milk. Fur-
ther, he connected this allergy to venostasis and probable alteration in the
nasal capsule.
If the foregoing conclusions of Marks are true, and considering the
findings of Harvold ('73) in mouthbreathing monkeys, it would seem
likely that early swelling of the nasal passages could indeed be a tenable
explanation for many crib deaths.
Smith (79) studied hyperkinetic children and found that allergies and
diet were basic contributory factors effecting a neurochemical phenome-
non which affects the child’s ability to discern his environment. He de-
Scribed the child who could not determine whether or not his own nose
was clogged. This hyperkinetic condition is linked to neurophenephrin,

185
Nasal and Oral Capsules

3

0

M
º
Figure 22. Illustration of growth of oropharynx boundary, Basion (Ba), posterior
nasal spine (PNS), lower pharynx hyoid bone (H), and third cervical vertebrae
(CV3). Note general consistency with menton (M).
an enzyme. He also stated that the majority of cases of otitis media are
caused by milk allergies. Diet control is more essential than ever con-
sidered previously, and Smith suggests massive doses of vitamins to break
chronic physiologic conditions.
Many of the mouth-breathing conditions were described by Kahn in
1939.
186
Ricketts
4 to 13 Y
& g;
© A tº
Figure 23. Illustration of frontal growth of nasal cavity from age 4 to 13 years, as
viewed from Frankfort and midsagittal planes. Mean nasal width (NC) increase
was 0.6 mm per year after age 5 years. Note relation of developing canines to
Widest outline of nasal cavity where measurements are taken.
GENERAL GROWTH OF FACIAL CAVITIES
It would appear from cephalometric studies, especially those using im-
plants, that the maxilla and nasal cavity grow in two ways: (1) growth at
Sutures and (2) localized bony remodeling. Ricketts compared 3 skulls
(newborn, 5-year-old and adult female) radiographed from three direc-

187
Nasal and Oral Capsules
Figure 24. (A) tracing of female patient
age 7 years, 8 months with respiratory
obstruction caused by the adenoid.
Note the low anterior elevation of
tongue and palate. (B) Same patient il- \
lustrating an open mouth rest position
as a result of the need to create an oral kº ----T— a 5.
airway. Note the space between the (? & N 27°
tongue and palate and the parted lips. ſº Nſ)
(C) Note the severe bilateral lingual º ſº Hº
crossbite of upper molars and asymme- º
try of nasal cavity in frontal view. /7 (Nº.
QºS /\ gº
tions (Figs. 27-29). Tracing the outline of the nasal cavity and superim-
posing all three showed an approximation of the growth of the nasal
cavity in three dimensions (Figs. 30–32; Ricketts, '76). As with the orbital
and oral cavities, growth of the nasal cavity seems to be related to the
distribution of the fifth cranial nerve. This suggests neurotrophic influ-
ences in normal development.
DISCUSSION
Evidence has mounted that the adenoid is an important, but not the
only, factor leading to naso-respiratory obstruction. In addition, other oral
problems invite prolonged breathing through the mouth. The mouth-
breathing child has a dull facial expression, an open mouth and a narrow
and often turned-up nose. There is a flat, toneless speech quality, and the
tongue often protrudes between the teeth as the lower lip is tightened in

188
Ricketts
Figure 25. (A) Same patient as seen in \0
Figure 24 now age 10 years, 2 months
or 2.5 years later. Note clear airway.
Note tilted palate has been corrected to
parallel to Frankfort. Note normal !-
tongue position. (B) Same patient at 12 \ |\ C
years and 10 months of age. Adenoids ~ /|\
have not grown back and the results of 2-SN== Sºl_Z–Y
treatment remain stable. (C) Frontal \? () () ſ
view of this patient reveals dramatic \ tº 2A
changes produced by orthodontic treat- Nº SA
ment: the nasal cavity has increased 6 Ç {| ſº
mm (or three times that which nor- QC J. CYº
mally occurs) and molar width has in- º/ UDſ 2
creased 15 mm where no increase was W |
expected without treatment. Compare
to Figure 24C.
the act of swallowing. The tongue at rest is positioned downward and
forward to provide space between it and the soft palate for an oral airway.
There are other collateral findings related to mouthbreathing which
seem to have a bearing on the overall welfare of the child. He is often
restless in sleep, complains of being tired, does poorly in school, often
has a poor appetite and may be undernourished, is often tormented and
at home may be hyperkinetic when not resting.
The dentition is often characterized by a crossbite or generalized nar-
rowness of the dental arches. A high arched palate is seen in extreme
cases, the hyoid bone may be lowered to create an oral airway and the
head may be tilted backward to assist oral breathing.
When it became obvious that the condition of the airway should be

189
Nasal and Oral Capsules
Figure 26. (A) This patient had a severe open bite, retrognathic chin, nasal
impairment causing mouthbreathing, an oral gnomic angle of 62° (ANS-Xi-Prm; it
should be 45°) and palate tipped upward. Compare this to (C); a patient with a
oral gnomic angle of 32°. Note in (B) a deviation of the septum, radiopacity in left
sinus, and constriction high up in nasal cavity. Note asymmetry in nasal floor. The
patient’s malocclusion was corrected with orthopedic treatment and vertical direc-
tional extraoral therapy. Treatment was finished by the time the patient was 11
years old. He suffered a steady relapse and (D) by 19 years of age had a 78° facial
axis (normal is 90°), a 67° oral gnomic angle, an even greater open bite and severe
tongue thrust. Relapse occurred despite attempts at additional treatment (my-
ofunctional therapy).
considered a basic factor in diagnosis, research was undertaken by the
Foundation for Orthodontic Research with several of the study sections
contributing. This gave rise to a critical analysis which was adopted for
computerization as a separate entity (Schulhof, '78). Nasal width seemed
to be important at the level of 2 standard deviation dysplasia. Using this
method to test the material of Bushey, diagnosis of patients who stand to
be improved was 80%. This is a remarkable finding because cases se-
lected at random stand only a 50% chance.

190
Ricketts
Figure 27. Tracings of the newborn skull in the lateral, frontal and basal view. All
are oriented using the Frankfort plane. Note the basion-nasion axis in the lateral
view.
SUMMARY
Respiration and mastication are biologically inseparable. The nose is a
regulator, a heater, a humidifier, a vacuum cleaner, a sterilizer and a
primary sensory organ. The nasal cavity just happens to be formed by
essentially the two parts of the maxilla which also happen to be the basal
Structure for the upper teeth and most of the upper jaw. The lower limits
of the nasal cavity also happen to be the upper limits of the oral cavity.
What affects one affects the other. It would appear that normal nasal

191
Nasal and Oral Capsules
Figure 28. Tracings of an approximately 3-year-old skull with a complete decidu-
ous dentition oriented on Frankfort horizontal plane. Notice the dominance of the
brain case. In the basilar view the transverse line is at PT point.
breathing is conducive to normal growth of the maxilla and normal devel-
opment of the occlusion of the teeth. The well-being of the whole child
may be involved where mouthbreathing is concerned, and the clinician
dealing with conditions related to mouthbreathing must look not only at
the specific condition he is being asked to treat, but at all related condi-
tions as well. Therefore, it would seem that the time has come for this
problem to be subjected to a multidisciplined team of clinicians who can,
as a team, treat the whole child.

192
Ricketts
Figure 29. An adult female skull, again radiographed on the three different views
of Frankfort horizontal orientation and traced accordingly.

193
Nasal and Oral Capsules
Figure 30. The same specimen as seen in Figure 29 demonstrating the general
characteristics of the growth of the nasal cavity as viewed from all three direc-
tions. A dominant amount of growth occurred after age 3 years. Notice square
allometric shape in the lateral view, the periform shape in the frontal view and
oval shape in the basillar view.

194
Ricketts
()
ºme eme * - - - - - -
tº
W sº
W. § § *\\
A
\ §
{}
Figure 31. Comparison of orbital cavities from Figures 27, 28 and 29. The devel-
opment of the orbit is viewed in three planes of space and superimposed at the
approximate area of the ophthalmic division of the fifth nerve (V1). Notice the
allometric type growth in all three views and dominance of early eye growth
(which is neural in type).















195
Nasal and Oral Capsules
Figure 32. Tracings superimposed and oriented on Xi point. This represents the
entrance of the mandibular division of the fifth nerve (V3) into the mandible.
Notice the development of lower facial height and the gnomic nature of growth in
the lateral view (above). Notice in the frontal view (center) the organization of
growth upward and outward for the condyle, and downward and outward on the
gonial angle. Notice in the basilar view (below) the organization of growth of the
mandible for the condyle and the mental foramina areas. Note all three of the
illustrations in this figure would tend to support the neurotrophic theory in that
the cavities tend to be oriented to the location of nerves.

196
Ricketts
REFERENCES
Broadbent, B. H. Ontogenetic development of occlusion. In: Development of
Occlusion, pp. 31-48, Philadelphia, Univ. Penn. Press, 1941.
Broadbent, B. H. The face of the normal child: Bolton standards and technique.
Angle Orthodont. 7:183-233, 1937.
Brodie, A. G., W. Downs, A. Goldstein and E. Myer. Cephalometric appraisal
of orthodontic results. Angle Orthodont. 8:261-265, 1938.
Bushey, R. Recent research findings relating nasopharyngeal function to oral
physiology and craniofacial development. Proc. Found. for Orthodont. Res.
pp. 17-63, 1973.
Catline, G. The Breath of Life. New York, John Wiley, 1861. Foreword by
Edward H. Angle, 1925.
Fairchild, R. C. A pediatrician views the tonsil and adenoid problem. Forum on
the tonsil and adenoid problem in orthodontics. Am. J. Orthodont.
54:491-494, 1968.
Gray, V. The challenge for an interdisciplinary approach to structural and patho-
physiologic problems of external and nasal septal deformities as related to
orthodontics. Presentation to Edward H. Angle Southern California Ortho-
dontic Society, 1976.
Goldstein, A. The dominance of the morphological pattern: Implications for
treatment. Angle Orthodont. 23:187-195, 1953.
Harvold, E. P. Relapse in the light of animal experiments on muscle function and
dental occlusion. Proc. Found. Orthodont. Res. pp. 64-107, 1973.
Kahn, F. Man in Structure and Function. New York, Alfred A. Knopf, 1939.
Linder-Aronson, S. Adenoids: Their effect on mode of breathing and nasal inflow
and their relationship to characteristics of the facial skeleton and the dentition.
Acta Oto-Laryngologica, Supplementum 265, 1970.
Linder-Aronson, S. Effects of adenoidectomy on the dentition and facial skeleton
over a period of five years. Trans. 3rd Int. Orthodont. Cong., pp. 85-100,
1975.
Lundstrom, A. The significance of genetic and non-genetic factors in the profile
of the facial skeleton. Am. J. Orthodont. 41:819-826, 1955.
Marks, M. B. Allergy in relation to orofacial dental deformities in children, a
review. J. Allerg. 3:293-302, 1965.
Moss, M. L. The functional matrix. In: Vistas in Orthodontics, B. S. Kraus and R.
A. Riedel (eds.), Lea and Febiger, Philadelphia, 1962.
Price, W. A. Nutrition and physical degeneration. The Academy of Applied Nutri-
tion, Los Angeles, 1942.
Pruzansky, S. Roengencephalometric studies of tonsils and adenoids in normal
and pathological states. Ann. Oto, Rhino Laryng. 84(Suppl. 19):55, 1975.
Ogura, J. H., T. Unno and J. R. Nelson. Nasal surgery: physiological considera-
tions of nasal obstruction. Arch. Otolaryng. 88:288, 1968.
Quinn, G. W. Airway interference and its effect upon the growth and develop-
ment of the face, jaws, dentition and associated parts. N. Carolina Den. J.
60:28-31, 1978.
197
Nasal and Oral Capsules
Ricketts, R. M. Various conditions of the temporomandibular joint as revealed
by cephalometric laminagraphy. Angle Orthodont. 22:98-115, 1952.
Ricketts, R. M. The cranial base and soft structures in cleft palate speech and
breathing. Plast. Recon. Surg. 14:47-61, 1954.
Ricketts, R. M. Present status of knowledge concerning the cleft palate child.
Angle Orthodont. 26:10–21, 1956.
Ricketts, R. M. The functional diagnosis of malocclusion. Trans. Europ. Ortho-
dont. Soc. pp. 1-21, 1958a.
Ricketts, R. M. Respiratory obstructions and their relation to tongue posture.
Cleft Palate Bull. 8:3, 1958b.
Ricketts, R. M. Clinical research in orthodontics. In...: Vistas in Orthodontics, B.
S. Kraus and R. A. Riedel (eds.), Lea and Febiger, Philadelphia, 1962.
Ricketts, R. M. Esthetics, environment and the law of lip relation. Am. J. Ortho-
dont. 54:272-289, 1968.
Ricketts, R. M. Respiratory obstruction syndrome. Am. J. Orthodont.
54:485-514, 1968.
Ricketts, R. M. Introducing computerized cephalometrics. Rocky Mt. Com.
Denver, 1969.
Ricketts, R. M., M. R. Bench, J. Hilgers and R. Schulhof. An overview of
computerized cephalometrics. Am. J. Orthodont. 61:1-28, 1972.
Ricketts, R. M. New perspectives on orientation and their benefits to clinical
orthodontics -- Part I. Angle Orthodont. 45:4, 1975.
Ricketts, R. M. New perspectives on orientation and their benefits to clinical
orthodontics -- Part II. Angle Orthodont. 46:1, 1976.
Schulhof, R. J. Consideration of airway in orthodontics. J. Clin. Orthodont.
12:440-444, 1978.
Sloan, R., R. Bench, J. Mulick, R. Ricketts, S. Brummet and J. Westover. The
application of cephalometrics to cinefluorography: Comparative analysis of
hyoid movement patterns during deglutition in Class I and Class II orthodontic
patients. Angle Orthodont. 37:26-34. 1967.
Smith, L. Personal communication, 1979.
Steele, C. H. An otolaryngologist views the tonsil and adenoid problem. Forum
on the tonsil and adenoid problem in orthodontics. Am. J. Orthodont.
54:485-491, 1968.
Subtelny, J. The significance of adenoid tissue in orthodontia. Angle Orthodont.
24:59-69, 1954.
Wertz, R. and M. Dreskin. Midpalatal suture opening: A normative study. Proc.
Found. for Orthodont. Res. 1976.
198
ADENOID OBSTRUCTION OF THE
NASOPHARYNX
Robert S. Bushey, D.D.S., M.S.
Department of Orthodontics
University of Colorado
The interest of orthodontists in nasopharyngeal airway obstruction may
be attributed to the need to better understand:
1. the growing individual’s ability to maintain normal lip posture;
2. the cause for the protrusion of maxillary incisors;
3. optimal tongue position and adequate dental arch expansion;
4. the individual’s ability to posture the mandible in a normal “rest”
position with centric occlusion and centric relation being concomitant
with effective incisal guidance without molar fulcruming; and finally,
5. all factors which may adversely influence facial growth in recognition
that in non-growing individuals the most extreme facial forms, e.g., the
long face syndrome, can be corrected only by orthognathic surgery.
All five of the above concerns have been associated with the untoward
influence of enlarged lymphoid tissue in the oropharynx, and Linder-
Aronson ('70) has developed the following working hypothesis to evalu-
ate this influence:
1. Enlarged adenoids obstruct the oropharyngeal airway causing
mouthbreathing.
2. Mouthbreathing leads to changes in tongue and lip postures.
3. Such changes in the soft tissue balance of the oral cavity produce
variations in dentitional relationships.
4. Any combination of the above may lead to a change in the develop-
ing facial form.
A careful examination of each part of the four part hypothesis reveals
that the cause and effect relationship may be absolute or only partial. The
strength of each causal relationship will influence the next portion of the
“causal chain”, and thus ultimately influence the final effect. Each part of
the hypothesis could be the subject of extensive discussion.
The purpose of this presentation, however, is:
1. to develop an appreciation for conflicting opinions in the interpreta-
tion of oropharyngeal obstructions that are relevant to orthodontics by
reviewing the literature; and
2. to identify craniofacial characteristics of mouth breathers by review-
199
Adenoid Obstruction of the Nasopharynx
ing the findings of a University of Illinois study of adenoidectomy
patients.
REVIEW OF THE LITERATURE
Much of the confusion associated with the effects of enlarged tonsils
and adenoids on dentofacial development today is the result of both
misinformation and misinterpretation of the findings and opinions of
others. In an effort to avoid repetition of this error, the review will be
focused on three separate hypotheses proposed by Linder-Aronson ('70).
These are:
1. Adenoid enlargement leading to mouthbreathing results in a particu-
lar type of facial form and dentition.
2. Conversely, enlarged adenoids leading to mouthbreathing do not
influence facial form and type of dentition.
3. Enlarged adenoids in certain types of faces and dentitions lead to
mouthbreathing.
Hypothesis I: Adenoid Enlargement Leading to Mouthbreathing Results in
a Particular Type of Facial Form and Dentition
A positive causal relationship between adenoids and mouthbreathing
leading to dental and facial changes was the basis for the earliest explana-
tions of the etiology of malocclusion and the “adenoid facies.” These
explanations have been divided into the following three general catego-
ries, each describing a mechanism by which the adenoid-mouthbreathing
relationship influences the etiology of facial form and dentition; 1) com-
pression, 2) disuse atrophy, and 3) altered air pressure.
Compression. The classical compression theory was first proposed by
Tomes in 1872. He reported that children with enlarged adenoids usually
displayed V-shaped dental arches. This characteristic narrowing in the
upper arch was the result of an unbalanced musculature composed of a
low tongue position, excessive compressive force on the maxillary arch
buccal segments, and an atrophic lip development caused by mouth-
breathing. Many others have also cited atypical tongue and lip function as
causative factors in maxillary alveolar change (Angle, '07; Subtelny, '54;
Moyers, '63).
Woodside ('68) listed six different etiologic possibilities for the origin of
Class II, Division 1 malocclusions. The last of these he describes as a
Class II, Division 1 malocclusion in which the midfacial area and the
mandible were harmoniously related until permanent alteration in the
rest position of the mandible occurred, as happens in chronic nasal ob-
200
Bushey
struction when the mandible assumes an environmentally created retrog-
nathic position. This represents a neuromuscular malocclusion, since its
origin involves the alteration of some very basic neuromuscular reflexes.
In the area of naso-respiratory allergy, Marks ('65) has reported on
dental and facial features typical of such patients, although enlarged ton-
sils and adenoids may not be directly implicated as the source of mouth-
breathing.
It should be noted that all of the authors cited above have described
clinical entities without attempting to measure difference in characteristic
relationships. Eastman ('63), however, in measuring resting tongue pos-
tures cephalometrically, found that individuals with seasonal nasal al-
lergies had significantly lower and more retracted tongue postures than
the normal sample.
Harvold ('68, '72) has provided additional documented support for the
compression theory. The placing of an acrylic block in the palate to
permanently depress the tongue in experimental animals resulted in in-
creased lower facial height and Class II malocclusions.
Disuse Atrophy. The second mechanism said to cause an alteration in
the maxillary arch is that of inactivity of the nasal cavity. Nordlund (18)
Stated that obstruction of nasal respiration due to adenoids causes the
nasal cavity to undergo disuse atrophy. This results in the relative eleva-
tion of the palatal vault as the alveolar process grow downward. More
recently, Bimler ('65) described a “microrhino dysplasia” syndrome with
characteristic tipping up of the anterior portion of the palatal plane and
nasal floor to parallel the sella-nasion plane. Because of the upturning of
the small nose, the nares are directly visible when viewed from the front.
Moss’ “primacy of the functional matrix in orofacial growth” ('68)
further supports the idea of inactivity as a mechanism by which mouth-
breathing could alter dentofacial form. He states that, in the case where
congenital bilateral choanal atresia causes an absence of naso- respiratory
function, marked underdevelopment of the functional space occurs.
Altered Air Pressure. An explanation of a third mechanism by which
adenoids and mouthbreathing effect dentofacial form lies in the fact that
air pressure within the nasal and oral cavities is altered. The excavation
theory proposed by Bloch ('03) and Michel ('08) states that the upward
stream of oral airflow presses on the palate leading to a higher palatal
vault. The air pressure theory described by Kantorowicz (16) and James
and Hastings (32) holds that a change to mouthbreathing causes the
normal negative pressure in the anteriorly sealed oral cavity produced by
nasal respiration to be lost, and the palate thus is not carried downward
with the growth of the maxillary alveolar process. It should be noted that
201
Adenoid Obstruction of the Nasopharynx
the above reports were descriptive in nature: the authors did not directly
measure the amount of airflow or directly view (radiographically) the
nasopharyngeal area.
Hypothesis II: Enlarged Adenoids Leading to Mouthbreathing do Not
Influence Facial Form and Type of Dentition
The second major hypothesis regarding the influence of adenoidal ob-
struction is essentially a negative premise. The controversial nature of the
airway problem has persisted since the 19th century. Kingsley (1888)
stated that the V-shaped form of the palate was an inherited feature and,
therefore, not related to mouthbreathing. In a much-quoted study by
Howard (32), histories of 500 patients with tonsillar problems were re-
viewed for incidence of mouthbreathing and the patients were examined
for malocclusion distribution. Of the supposed 32% mouth breathers,
only 14% (or 4.5% of the total sample) had Class II, Division 1 malocclu-
sions. Huber and Reynolds (46), using questionnaires gathered from 500
college-age students determined that only 5.4% had “breathing difficul-
ties.” As in Howard’s study, dental examinations of the students revealed
a normal malocclusion distribution in those with breathing problems. It
should be noted, however, that by the time the subjects had reached the
age of 20 years (the mean age of the sample), the lymphoid tissue leading
to mouthbreathing would have long since atrophied.
Humphreys and Leighton ('50) examined the mode of breathing in a
sample of over 1,000 children, 2.5 years to 5 years of age. By observing
condensation on a cold metal tongue blade held under the nose, they
found only 6 children who were totally mouth breathers. Almost 50% of
the 500 Class II subjects in the sample had their mouths habitually open
but breathed exclusively through their noses.
A more detailed study was performed by Leech ('58), who examined
500 patients in an upper respiratory clinic. Using the metal tongue blade
technique, he found that 19% of the sample were mouth breathers (13%
due to enlarged adenoids and 6% due to nasal obstruction). Interestingly,
he found that Class II, Division 2 malocclusions were more often asso-
ciated with the presence of enlarged adenoids than Class II, Division 1
malocclusions.
Based on a review of the non-airflow literature, the following state-
ments appear to be justified:
1. Mouthbreathing can be caused by a variety of obstructions in the
nose and nasopharynx. By far, the greatest single source of obstruction
has been attributed to adenoids.
2. Mouthbreathing has been associated with all types of malocclusions
as well as normal occlusions (Howard, 32; Humphreys and Leighton, '50;
Wallis, ’53; Leech, '58).
202
Bushey
3. A distinction needs to be made between true mouthbreathing and
merely a separation of the lips (Humphreys and Leighton, '50; Ballard,
'52; Ballard and Gwyne-Evans, '58).
4. Use of the lateral roentgencephalometric film has been demon-
strated as a valid technique in relating oropharyngeal function to its skele-
tal environment (Ricketts, '54; Subtelny, '54).
5. Studies employing the lateral cephalometric film have revealed a
functional relationship between adenoidal obstruction of the airway and
the posture of the tongue (Subtelny, '54; Ricketts, '54, '58; Yip and
Cleall, '71).
6. The size of the adenoid mass is a function of both age and infectious
irritation (Epstein, 37; Subtelny, '54; Pruzansky, '75; Handelman and
Osborne, '76).
7. That there is a stereotype called adenoid facies is a matter of record,
but whether it predisposes toward mouthbreathing remains to be demon-
strated (Robert, 1843; Meyer, 1872; Angle, '07; Duke, '30; Massler and
Schour, '48).
Linder-Aronson and Backstrom ('60) provided the first published re-
port on relative nasal respiratory resistance in a study of 297 patients.
Although increased nasal resistance was found in patients with long, nar-
row faces, enlarged adenoids were found in patients with both broad and
narrow faces and palates.
Two additional airflow studies subsequent to that of Linder-Aronson
and Backstrom have sought to test the skeletal and dental portions of
Hypothesis II mentioned above. Watson and colleagues ('68) measured
nasal resistance (pressure) with transducers on 51 subjects, ages 9 to 17
years. It should be noted that with this technique the subject creates a lip
Seal around an oral catheter which measures oral respiratory resistance
(pressure to airflow). The skeletal classification was based on the angular
measurement of AB differences to the Frankfort horizontal plane. No
positive correlation could be shown between arbitrary determinations of
Class I, II and III and the degree of measured nasal resistance.
A second airflow study by Rasmus and Jacobs ('69) of the University of
Iowa sought to test the relationship between respiratory velocity (i.e.,
mode of respiration) as measured by thermistors on 30 subjects age 9.5 to
15.5 years. The subjects were evenly divided between Class I occlusions
and Class II, Division 1 malocclusions. Again, no correlations could be
shown between the dental classifications and respiratory velocities. It
should be noted that there was no breakdown of the Class II, Division 1
malocclusions into the six etiologic subsets described by Woodside ('68).
The relationship of naso-respiratory obstruction to mouthbreathing was
further examined by Mergen and Jacobs ('70). Their cephalometric study
was designed to test the relationship of the variables (1) nasopharyngeal
203
Adenoid Obstruction of the Nasopharynx
depth, (2) nasopharyngeal area, (3) the area of convexity of the posterior
pharyngeal wall, (4) facial convexity and, (5) depth of the midface. Their
sample consisted of 20 subjects with Class I normal occlusions and 20
subjects with Class II malocclusions, all age 13 years + 4 months. They
found that nasopharyngeal depth and area were significantly greater for
subjects with normal occlusions than for those with Class II malocclu-
sions. Posterior pharyngeal wall convexity was more than twice as preva-
lent in the Class II group as in the Class I group. The authors concluded
that the size of the nasopharyngeal area is not significantly related to
anterior bony facial convexity. It should be noted, again, that there was
no distinction of subsets within the Class II group, and there was no
determination as to the relationship between the size of the oropharyn-
geal airway and the mode of respiration.
A review of the literature for investigations supporting the second hy-
pothesis that enlarged adenoids related to mouthbreathing do not influ-
ence facial form and type of dentition, would be incomplete without
considering tongue posture and posterior crossbite investigations. There
is a paucity of recent literature dealing directly with the question of
tongue posture. Yip and Cleall ('71) reported on a cineflourographic
study of velopharyngeal function before and after removal of tonsils and
adenoids which, although designed to focus primarily on deglutition and
speech, provided several interesting findings associated with the nasal
obstruction-tongue posture aspect of this second, working hypothesis.
The separation of the dorsum of the tongue from the velum prior to the
tonsillectomy was noted. Twenty of the 28 subjects showed a lack of
posterior seal preoperatively. Postoperatively 50% of the subgroup
showed an elevation of the tongue which put it into contact with the
velum, and another 14.3% demonstrated tongue elevation. Because in-
flamed tonsils have been implicated by Truesdell and Truesdell (37) and
Rix (’46) as the cause for the teeth-apart swallow, it was most interesting
that only 2 subjects, or 10% of the subgroup of 20 subjects with this
characteristic preoperatively, changed to a teeth-together Swallow postop-
eratively. It should be noted that no reference is made to either the
change in the mode of respiration pre- or postoperatively or the malocclu-
sion incidence in the study.
There also is a paucity of studies assessing the relationship between
posterior crossbite development and mouthbreathing. The most recent
comprehensive buccal crossbite study was reported by Day and Foster
('71) in which they examined 2,752 patients in an orthodontic department
and 965 school children, all of whom were 11 and 12 years old. The
frequency of buccal crossbites in the orthodontic patient sample was 16%
as compared to 12.6% for the school children sample. The distribution of
etiologic factors was: 11% of the group was associated with anterior
204
Bushey
crossbite (often one tooth with a functional shift), almost all unilateral;
35% were related to skeletal Class III relationships; and 50% were asso-
ciated with digital sucking and tooth-apart swallowing. Again it should be
noted that no reference is made to mode of respiration.
In an effort to extend the investigation of posterior crossbite etiology,
the author (Bushey, '77) first compared the dental, skeletal and asymme-
try characteristics of 59 orthodontic patients undergoing maxillary expan-
sion. Measurements of transverse, anteroposterior, and vertical dimen-
Sions were made from lateral and frontal cephalometric roentgenograms
taken before treatment, immediately after expansion, after all expansion
support was removed and when active treatment was terminated. A perti-
nent finding was that symmetrical (bilateral) posterior crossbites are asso-
ciated more often with Class III skeletal and dental characteristics,
whereas asymmetrical (unilateral) crossbites are associated more often
with Class II skeletal features.
A second portion of the author’s investigation dealt with a comparison
of 23 crossbite characterists of extreme horizontally growing Class III and
15 extreme vertically growing Class III individuals. The severity of the
Class III features can be recognized when it is noted that the 38 subjects
were drawn from a sample of 6500 cases consecutively processed at a
national computer center. Although the subject's records did not reveal
mode of respiration, the strong association of posterior crossbite with
Class III (skeletal) facial morphology was demonstrated by the presence
of crossbites in 87% of the horizontal Class III subjects and in 66% of the
vertical Class III subjects. An upward deflection of the anterior cranial
base and forward positioning of the glenoid fossae proved to be common
anatomical characteristics for subjects with Class III skeletal facial form
and posterior crossbites. Asymmetrical (unilateral) posterior crossbites
were associated with the 15 vertical Class III subjects.
Hypothesis III: Enlarged Adenoids in Certain Types of Faces and
Dentitions Lead to Mouthbreathing
The controversy concerning the effect of nasopharyngeal volume on the
impact of the adenoid mass dates back to 1897. After extensive measure-
ment, Siebenmann (1897) maintained that a high palate was commonly
found in individuals with a narrow nose and small nasopharyngeal vol-
ume. Therefore, adenoids often caused mouthbreathing in these individu-
als. Ricketts ('54) also demonstrated that the absolute size of the adenoid
mass was not as significant as its size relative to the size of the nasopha-
rynx. Subtelny (54) found, in a longitudinal study on the change in
configuration of the adenoids with age, that adenoids do not cause
mouthbreathing unless they occupy a major portion of the nasopharynx.
205
Adenoid Obstruction of the Nasopharynx
Lubarth ('60) made the observation that children often have small na-
Sopharynxes so that nasal breathing may be impeded by even a small
adenoid mass.
In his comprehensive study of adenoidectomy patients, Linder-
Aronson ('70) made use of an otolaryngologic evaluation, a cephalomet-
ric analysis of lateral and frontal headfilms, a dentition analysis and mea-
surements of nasal resistance. There were 131 variables measured. The
sample consisted of 81 children who had adenoidectomies performed and
81 control children. The average age of the children was 8 years and all
attended the Otolaryngologic Department of the Orebro Regional Hospi-
tal. The sample was divided into 5 groups.
The control subjects were divided into 3 groups: Group I (37 children
of whom 3% were mouth breathers) had no adenoids; Group 2 (33 chil-
dren of whom 5% were mouth breathers) had small or moderate ade-
noids; and Group 3 (11 children of whom 9% were mouth breathers) had
large adenoids. No significant otolaryngologic symptoms were noted in
any of the 3 groups.
The experimental subjects were divided into 2 groups: in Group 4,
adenoidectomy was performed for recurrent otitis media (21 children); in
Group 5, adenoidectomy was performed for obstructed nasal breathing
(60 children).
Group differences are summarized as follows:
1. Group 1 had the greatest upper-to-lower arch width. Groups 3 and 5
had the least molar arch widths.
2. Group 5 had a significantly higher occlusal-to-mandibular plane
angle and interincisal angle.
3. Groups 3, 4 and 5 could not be distinguished by the ratios of adenoid
area to pharyngeal area.
4. Groups 3 and 5 had similar readings for nasal airflow; i.e., increased
resistance to nasal respiration, although Group 3 showed no symptomatic
discomfort. Group 4 had no airway problems and, thus, showed a more
normal level of nasal respiratory resistance.
5. Group 3 had the greatest and Group 5 had the smallest facial widths;
the converse was true for facial heights.
6. Group 5 had a lower tongue position than Group 1 (tongue position
was not measured in the other groups).
The basic conclusions that can be drawn from the Linder-Aronson
study are:
1. Adenoids relatively large when compared to the epipharyngeal space
they occupy, as seen in the lateral headfilm, do cause a restricted airway
(as in Groups 3 and 5).
2. The enlarged adenoid restriction of the airway will result in mouth-
breathing if the individual has a high narrow face.
206
Bushey
3. The presence of enlarged adenoids can contribute to buccal crossbite
of the molars with or without mouthbreathing. It should be noted that
those subjects who compensated for large adenoids by mouthbreathing
(Group 5) had a more normal dentition, judged by molar relation hori-
zontally and overbite vertically, than those subjects with large adenoids
who did not mouthbreath due to their broad facial dimensions (Group 3).
4. Although a positive relationship can be demonstrated between the
presence of large adenoids and low tongue position, tongue position
could not be linked directly to width variables of the molars.
The last conclusion underscores the difficulty in interpreting the effect
of enlarged faucial tonsils on tongue position and arch width. Enlarged
tonsils were present in only 20% of those subjects who underwent adenoi-
dectomy for airway obstruction (Group 5) and were correlated weakly to
lower lip length, lower face height and the facial height to width ratio.
In 1974 Linder-Aronson reported on changes occurring in adenoidec-
tomy subjects (Group 5) during a five year postsurgical period. The great-
est increases in the dentition variables of incisor inclination and upper
arch width occurred during the first year postoperatively, as did the great-
est increase in the bony sagittal depth of the nasopharynx. Lower face
height and the angulation of the mandibular plane to the palatal plane
both decreased during the entire five year postoperative period. Linder-
Aronson described these changes as a “normalization” of the dentofacial
complex resulting from a change from oral to normal nasal respiration.
In the light of the above review of the literature, the original University
of Illinois study (Bushey, '65) can be critically assessed and compared to
the studies of Linder-Aronson ('70, '74). This will then serve as the
foundation for a classification of nasopharyngeal airway obstruction and
aberrant tongue posture cases relative to orthodontic diagnosis and treat-
ment which will be discussed in the second part of this presentation, i.e.,
the paper entitled, “Diagnosis and Treatment Planning of Nasopharyn-
geal Obstruction” appearing later in this book.
CRANIOFACIAL CHARACTERISTICS OF MOUTH BREATHERS
Original Evaluation of University of Illinois Study (Bushey, '65)
Material. The sample consisted of a group of 41 patients being treated
at the Eye and Ear Infirmary, Department of Otolaryngology, School of
Medicine, University of Illinois (Bushey, '65). These patients had been
Selected for tonsillectomy and adenoidectomy on the basis of ear, nose
and throat examinations. The chief reasons cited for surgical correction
were recurrent sore throats (15 patients), otitis media (13 patients), hy-
pertrophied tonsils and adenoids (10 patients), tonsillitis (4 patients),
207
Adenoid Obstruction of the Nasopharynx
allergic rhinitis (3 patients) and nasal obstruction (2 patients). Several
patients had more than one symptom. The ages of the subjects ranged
from 4.5 to 14.5 years with a bimodal frequency distribution at ages 6 and
10 years. There were 25 females and 16 males; 23 Caucasians and 18
Blacks.
Method. Otolaryngologic, respiratory and cephalometric examinations
were performed and the resulting data analyzed. Records were made
approximately 10 days preoperatively and from 4 to 6 months postopera-
tively when it was deemed that all postsurgical edema had dissipated and
Some scar tissue resolution had occurred.
1. Clinical Examination. This involved the use of a standard T and A
(tonsil and adenoid) examination form for an otolaryngological evalua-
tion of (a) individual morphological variation in nasal and pharyngeal
structures, (b) the patient’s history of ear, nose and throat symptoms and
(c) the chief problem leading to surgical correction by tonsillectomy and/
or adenoidectomy. A dental examination was also performed to deter-
mine malocclusion classification, presence of crossbite and presence of
tongue and lip habits.
2. Respiratory Examination. Respiratory readings for relative amounts
of oral and nasal airflow were made on each patient to assess the physio-
logic impact of oropharyngeal obstruction. Separate masks were placed
over the nose and mouth simultaneously and the airflow valves were
gradually adjusted to divert the airflow through the apparatus until con-
sistent, measurable recordings were being made. .
At the end of each patient’s recording, the apparatus was calibrated at
0.5, 1.0, 1.5 and 2.0 centimeters of water on a manometric scale to
compensate for daily variations in tambour tension, style pressure, etc.
Inspiration and expiration wave amplitudes were then measured and con-
verted to absolute manometric pressure values. A pilot study was con-
ducted on a small sample to test the validity of taking single pre- and
postsurgical respiratory recordings. Three separate sets of records were
made on individuals of varying modes of respiration and no significant
differences were found between pairs of readings.
3. Cephalometric Examination. One frontal headfilm with the dentition
in occlusion and two lateral headfilms, one in physiologic rest position
and the other with the dentition in occlusion, were taken before and after
Surgery. Barium sulfate paste was used as a disclosing agent on the dor-
sum of the tongue and Iodochlora was used in the nose.
- Analysis of the Material. Examination of the preoperative respiratory
recordings revealed that the 41 subjects could be divided into three
208
Bushey
groups: complete mouth breathers (6 subjects), partial mouth breathers
(29 subjects) and complete nose breathers (6 subjects). The malocclusion
distribution, determined from individual dental models, then was tabu-
lated with the three modes of respiration.
Next, lip separation was recorded by examining the preoperative lateral
headfilms of the rest position and this, in turn, was tabulated with the
three respiratory function groups.
In order to compare the mode of respiration with the morphology of
the airway, the otolaryngologic findings from the T & A examination
form were also tabulated with the respiratory function groups.
In the assessment of the tonsil and adenoid morphology, the author
desired to compare the findings of the direct visual examination with
those from the lateral cephalometric films. Thus, the lateral headfilms
were examined for (a) types of tonsil images and (b) the degree of ob-
struction caused by the adenoid mass as it impinged on the velum or
partially closed the epipharyngeal airway (within approximately 3-4 mm
of velum contact).
The postoperative analysis of the material required the quantitative
comparison of pre- and postoperative respiratory recordings. This was
accomplished by converting the absolute amounts of postoperative oral
and nasal respiration as determined by the manometric recordings into
the relative percentage of nasal respiration. The change in the group of
complete mouth breathers to a high degree of postoperative nasal breath-
ing was quite apparent. However, the partially mouthbreathing group was
divided into those subjects showing a substantial increase in nasal breath-
ing and those showing only a relatively small increase (or even a de-
crease) in nasal breathing. The group with complete nasal breathing be-
fore surgery showed no respiratory changes after surgery.
The author then sought to relate the changes in respiration to surgically
induced alterations in the epipharyngeal airway (as observed on the lat-
eral headfilm). This analysis was divided into a series of pre- and postop-
erative measurements of the square areas of both the adenoid tissue and
the epipharynx (by means of a compensating polar planimetry), and a
Series of linear and angular measurements of the anatomical parts bound-
ing the functional areas. The planimetry technique was derived from the
earlier work of Brader ('57) with the exception that the head films taken
in the rest position were used for pre- and postoperative superpositioning
in lieu of the occlusal series. This was done because of the frequency of
gagging and the abnormal positions of the tongue, velum and mandible in
the occluded position.
The skeletal and soft tissue landmarks in the master tracing are illus-
trated in Figure 1, and are defined as follows:
209
Adenoid Obstruction of the Nasopharynx
/*
efº/\ * <-2
2-p
*—sº
|
Figure 1. Skeletal and soft tissue landmarks used in University of Illinois study
(Bushey, '65). The cross-hatched area below AT (adenoid tissue) depicts tissue
reduction by adenoidectomy clearing the epipharyngeal airway obstruction. The
cross-hatched area below V (velum) depicts the typical location of the faucial
tonsil masses. Note the separation of the velum and the dorsum of the tongue
caused by the tonsil masses presurgically.
Points
S (sella) is the point representing the center of sella turcica.
AA is the most anterior point of the anterior arch of the atlas.
PMF (pterygomaxillary fissure) is the point of intersection of the pte-
rygomaxillary fissure and the palatal plane (comparable to the posterior
nasal spine).
H (hyoid bone) is the most anterior and superior point on the body of
the hyoid bone.
N (nasion) is the anterior point of the juncture between the frontal and
nasal bones.
Ba (basion) is the most anterior and inferior point on the anterior
margin of the foramen magnum.



210
Bushey
Areas
AT (adenoid tissue) is bounded anteriorly by the rostrum of the sphe-
noid, posteriorly by line S-AA-H, and anteriorly by line S-PMF.
EP (epipharynx) is bounded superiorly by the inferior surface of AT,
posteriorly by line S-AA, inferiorly by line AA-PMF and anteriorly by
line S-PMF.
OP (oropharynx) is the entire area beneath the adenoid tissue and
above the dorsum of the tongue and bounded by lines S-AA-H and
S-PMF-H.
The epipharyngeal depth was measured linearly from point AA to
point PMF. The angles formed by lines AA-S-PMF and Ba-S-PMF were
also measured. The epipharyngeal height was measured anteriorly from
point S to point PMF, and posteriorly from point S to points AA and Ba,
respectively. The angles formed by lines S-AA-PMF and S-Ba-PMF were
also calculated. Sphenoid body thickness was measured along line S-H
from point A to the rostrum. Adenoid tissue (AT) thickness was mea-
sured along line S-H from the rostrum to the inferior border of the
postoperative adenoid mass.
Functional changes were measured in the following manner: tongue
elevation was measured along line S-H from the preoperative to the
postoperative levels; hyoid elevation was measured along the line S-H
from the preoperative to the postoperative levels.
The analysis of the postoperative findings employed the ranges, means
and standard deviations for the morphologic variations for each respira-
tory group. Group comparisons for mean differences were tested for
significance using the t-test for nonpaired experiments.
Because of the wide range of variation for each variable within each
group, correlation coefficients were used to measure the concomitant
variations between variables. Specifically, comparisons of the correlations
for pre- and postoperative findings in the mouth breathers were made in
order to demonstrate which dimensions were more critical for improved
nasal breathing. Thus, those complete and partial mouth breathers who
showed substantial improvement in nasal respiration postoperatively were
compared to those partial mouth breathers that evidenced little or no
improvement.
Findings and Discussion. A comparison of the quantitative assessment of
mouthbreathing as measured manometrically to the subjective interpreta-
tion as recorded in patient histories indicated a disparity of 17% of partial
mouth breathers with no history of obstruction and 66.6% of the complete
nasal breathers with histories of mouthbreathing. The difference in range
of mouthbreathing frequency between that determined by using the cold,
metal tongue blade (Humphreys and Leighton, '50; Leech, '58) and that
211
Adenoid Obstruction of the Nasopharynx
reported in patient histories (Howard, 32; Huber and Reynolds, '46)
varied from 0.06% to 19% using the first method and 5.4% to 31% using
the second. The relatively high percent (85%) of measured mouth
breathers in the present study is attributed to the selectiveness of the
sample; i.e., all subjects had medical indications sufficiently severe to war-
rant having tonsillectomies and adenoidectomies. However, the inability to
control additional, intermittent and seasonal changes in respiration caused
by variation in posture, room temperature and seasonal allergies tempers
the findings of all mouth-breathing investigations.
The malocclusion distribution for the sample was as follows: all six
complete mouth breathers had Class I malocclusions, of the 29 partial
mouth breathers, 21 had Class I occlusions, five had Class II, division 1
malocclusions, two had Class II, division 2 malocclusions and one had a
Class III malocclusion; of the six complete nasal breathers, five had Class
I occlusions ànd one had a Class II, division 2 malocclusion. The maloc-
clusion distribution in the 35 measured mouth breathers is similar to three
large samples reviewed by Reidel ('63).
Although Linder-Aronson ('70) concluded that adenoids can affect the
mode of breathing, which in turn influences the individual’s dentition, he
did not find significant correlations between mouthbreathing and inter-
molar widths and interincisal angulation of the anterior teeth unless cor-
related to other factors as well.
Twenty-three percent of the mouth breathers had molar crossbites,
whereas none of the nose breathers had molar crossbites. Similar results
were reported by Linder-Aronson ('70). -
It was also noted that lip separation was evident in 40 of the 41 subjects
prior to surgery, including 5 of the 6 complete nose breathers. As sug-
gested by Humphreys and Leighton ('50), lip separation per se is not a
reliable indication of mouthbreathing.
A comparison of the mode of respiration with a number of characteris-
tics in airway morphology was carried out by the otolaryngology staff.
There is a significant disparity between the clinical and radiographic eval-
uations of the tonsil and adenoid morphologies. Clinical examination of
the oropharynx presents the difficulties associated with both indirect visu-
alization and the quantification of subjective observations. Likewise, ra-
diographic interpretation of tonsillar size and position is limited by the
lack of image definition of the smaller and less dense masses and the
absence of the width dimension on the lateral headfilm. Recognizing the
limitation of each technique, the examiner must combine the advantages
of both in order to make a complete evaluation of the airway morphology
for each individual.
Table 1 shows group changes in mode of respiration. Group I (preop-
erative mouth breathers) showed the greatest increase in nasal respira-
212
#
GROUP I
RESPIRATORY GROUPS
GROUP IIA
GROUP IIB
GROUP III
Preoperative Mouth
Breathers Who Showed
a Postoperative
Increase in Nasal
Preoperative Partial
Mouth Breathers Who
Showed a Postopera-
tive Increase in
Preoperative Partial
Mouth Breathers Who
Showed No Postopera-
tive Increase in
Nasal Respiration
Preoperative Nose
Breathers
Respiration Nasal Respiration
Percentage (N=6) (N=17) (N=12)
Nasal
Respiration Range Mean S.D. Range Mean S.D. Range Mean S.D. Range Mean S.D.
Preoperative 0 0 0 11–16 34.8 + 16.1 30–57 42.3 + 9.2 0 100 0
Postoperative 63–100 89.2 + 17.3 62–100 94.6 + 13.4 21–62 45.7 -- 11.2 0 100 0
Increase 63–100 89.2 + 17.3 40–89 59.7 -- 15.2 – 15 to —20 3.4 + 11.8 0 0 0
Table 1. Subjects grouped together according to postoperative respiratory changes.
:
Adenoid Obstruction of the Nasopharynx
Figure 2. Pre- and post-adenoidectomy changes are compared for Surgical results.
(A) Unfavorable surgical result seen when adenotome is used to clip posterior
and inferior adenoid tissue leaving obstructive anterior and superior tissue. (B)
Preferred surgical result depicts significant tissue removed superior to the velum
and in approximation to the posterior choanae more anteriorly.
tion. Table 2 illustrates the amount of adenoidal tissue removed and
resulting epipharyngeal space increase as measured in area by a compen-
sating polar planimetry. It should be noted that there were no statistically
significant differences between the Groups IIA and B (preoperative par-
tial mouth breathers who did and did not show, respectively, an increase
in nasal respiration postoperatively).
The lack of a linear relationship between nasal respiration and size of
the epipharyngeal airway has been reconciled by several hypotheses. The
location of the excised adenoid tissue is one explanation (Fig. 2). The
epipharyngeal airway is not significantly increased if adenoid tissue is only
excised from the more inferior and posterior portion of the adenoid con-
tour. Bosma ('63) underscored the primacy of respiration in the newborn
by describing the extreme muscular and postural accomodations that oc-
cur in an infant’s effort to breathe. It follows that a threshold, or critical
set of dimensions, develops for each individual which may not have a
proportionate relationship to the amount of nasal and/or oral respiration.
The disproportionate influence of infection is another possible explana-
tion for the lack of a form-function relationship of the airway before
surgery for all mouth-breather groups and after surgery for the unim-
proved partial mouth breathers (Group IIB). Epstein (37) proposed that

214
#
GROUP IIB GROUP III
Preoperative Partial Mouth
Breathers Who Showed No
Increase in Postoperative Preoperative Nose
Epipharyngeal In Nasal Respiration Nasal Respiration Nasal Respiration Breathers Significant
Airway and (N=6) (N=17) (N=12) (N=6) Differences
Adenoid Tissue Between
Area Range Mean S.D. Range Mean S.D. Range Mean S.D. Range Mean S.D. Group Means
*
0.44– 0.97 0.62 + 0.15 0.46— 0.84 0.61 + 0.13 I:IIA*, I:IIB”
I: III*
0.22– 0.78 0.42 + 0.16 0.22– 0.47 0.31 + 0.09 I:IIA***, I:IIB*
I: III***
+0.01 – 0.41 0.20 + 0.11 0.20– 0.38 0.30 + 0.08 IIB:III*
+ 1.59–56.90 31.60 + 17.70 36.70–61. 10 51.80 + 8.50 I:IIA
0.10– 0.40 0.25 + 0.09 0.10– 0.37 0.24 + 0.14 I:IIA*, I:IIB”
0.23– 0.58 0.41 + 0.12 0.21– 0.73 0.50 + 0.22 I:IIA***, I:IIB*
I: III*
—0.03– 0.31 0.17 ± 0.10 0.16— 0.34 0.26 + 0.07
— 13.40–73.30 37.20 + 23.20 39.70–76.20 54.20 + 14.30
RESPIRATORY GROUPS
GROUP I
GROUP IIA
Preoperative Mouth
Breathers Who Showed
a Postoperative Increase
Preoperative Partial Mouth
Breathers Who Showed a
Postoperative Increase in
Adenoid Tissue Area (square inches)
Preoperative 0.65– 0.98 0.78 + 0.15
Postoperative 0.46— 0.78 0.59 + 0.14
Net Decrease +0.01– 0.34 0.19 + 0.11
% Decrease + 1.30–36.60 24.80 + 12.70
Epipharyngeal Airway Area (square inches)
Preoperative 0.00– 0.34 0.11 + 0.13
Postoperative 0.11— 0.39 0.21 + 0.11
Net Increase –0.04– 0.25 0.10 + 0.10
% Increase –36.4— 0.00 49.60 +51.50
0.23– 0.83 0.62 + 0.17
0.16— 0.48 0.35 + 0.09
+ 0.04– 0.48 0.27 = 0.12
+ 17.40–60.90 40.90 + 17.30
0.10— 0.43 0.24 + 0.11
0.31 – 0.68 0.45 + 0.09
0.02– 0.42 0.20 + 0.09
4.40–73.70 47.50 + 8.70
*Significant at 0.05
**Significant at 0.01
***Significant at 0.001
Table 2. Amount of adenoid tissue removed and increase in epipharyngeal space.
§
Adenoid Obstruction of the Nasopharynx
PMF
!)
Figure 3. A comparison of differences in angular height of the epipharynx (S-AA-
PMF) when the adenoid mass area is the same. (A) The more obtuse epipharyn-
geal angular height is often associated with a more adequate airway. (B) The
more acute epipharyngeal angular height is associated with more obtuse cranial
base angulations and a tendency to epipharyngeal airway obstruction.
a small amount of adenoid tissue with no apparent obstructing qualities
may still cause mouthbreathing by acting as a focus of infection for the
nasal airway.
Table 3 compares the linear and angular dimensions of the epipharynx
of the four respiratory groups. Note the importance of linear depth AA-
PMF. This has been previously suggested by Ricketts ('54) to be the
critical dimension of the oropharynx. The means for the four groups
range only from 34.2 to 35.5 mm, which closely approximates the clinical
norm of 34.5 + 3.5 of the master study of Rocky Mountain Data Systems
(Ricketts, '69). Angular height appears to be a more discriminating factor
as described by the angle S-AA-PMF (Fig. 3). Group I had the smallest
angular depth and Group IIA the largest, there being a statistically sig-
nificant difference between these two groups. Additional angular and



216
#
Significant
IIA IIB III Differences
Between
Range X SD Range X SD Range X SD Range X SD Group Means
Depth
AA-S-PMF (°) 45.0–54.0 48.8 +3.3 33.5–52.0 44.4 +5.0 29.0–58.5 43.8 + 8.3 42.5–55.5 48.0 +5.4 I:IIA*
Ba-S-PMF (°) 56.0–68.0 63.3 + 4.0 52.0–70.5 62.0 +5.6 55.5–71.5 63.0 +5.2 57.0–70.5 62.5 +5.7
AA-PMF (mm) 31.9–37.0 35.5 + 1.9 29.3–41.5 34.2 +3.9 28.0–40.7 34.4 +4.2 31.5–40.4 34.3 + 4.0
Anterior Height
S-AA-PMF (°) 50.0–70.0 60.3 +6.9 55.0–77.0 65.5 +6.1 60.0–75.0 66.5 +4.8 58.5–71.0 64.0 +4.8 I:IIB”
S-BA-PMF (°) 51.0–63.5 56.3 +4.5 55.0–68.0 59.6 +3.7 52.0—68.0 59.8 +4.7 55.0–65.5 60.2 +3.6
PMF-S (mm) 36.3—46.5 40.9 +3.6 36.1–52.4 44.0 +4.1 39.7–48.4 44.5 +3.6 35.4–44.5 41.4 +3.5 I:IIB”
Posterior Height
BA-S (mm) 38.1–46.6 42.5 +3.5 34.6–47.9 43.1 +3.1 37.9–50.0 43.1 +4.2 33.0–44.2 40.0 +4.7
AA-S (mm) 40.5–47.4 44.2 + 2.5 35.4–50.7 45.1 +4.1 38.7–53.2 45.0 +4.4 35.6–48.4 42.6 +4.5
Cranial Base Angulation
BA-S-N (*) 133–147 137.2 —5.1 125–142 133.1 +4.9 125–142 131.1 +5.1 127–139 134.5 +5.0 I:IIB”
Measured Along Line S-H
Sphenoid body III:IIA***
thickness (mm) 16.4—20.0 18.0 — 1.5 15.5–24.8 19.7 +2.4 16.6–23.5 19.1 + 1.9 13.5–18.6 16.3 + 1.7 III:IIB^*
tongue eleva-
tion (mm) –2.5–7.2 3.4” —3.3 0–9.3 4.1 ** +2.6 – 5.5–5.5 1.3 +3.3 0–7.7 3.5* +3.2 IIA:IIB”
Hyoid eleva-
tion (mm) –2.0–8.1 4.8° —3.6 – 2.5–9.6 3.0°." -- 3.7 – 7.0–9.9 0.7 -E4.7 —5.0–8.0 1.0% +4.2
Respiratory Groups
*Significant at 0.05
**Significant at 0.01
***Significant at 0.001
Table 3. Respiratory group comparisons based on linear and angular dimensions of the epipharynx
§
Adenoid Obstruction of the Nasopharynx
linear relationships are compared in Table 3. The cranial base angulation
means are well above the normative value of 129° (Ricketts, '69) for all
groups except Group IIB; with Group I showing a mean value of 137°.
Table 3 further illustrates that accompanying an increase in nasal respira-
tion for all improved groups are elevations of both the tongue and hyoid
bone, as previously reported by Subtelny (54) and Ricketts ('58).
Table 4 shows the grouping of certain morphologic features correlated
to respiratory response. That is, the size of the airway appears to bear a
reciprocal relationship to the size of the adenoid in those subjects whose
epipharyngeal dimensions are similarly combined. Small airways are
found to be associated with smaller anterior heights; larger angular depth,
a result of the linear depth remaining relatively constant which results in a
higher level of the floor of the epipharynx (AA-PMF); relatively larger
adenoid masses; and more obtuse cranial base angulations.
Reevaluation of Data from the University of Illinois Study
A second statistical analysis was conducted on the data from Bushey’s
study ('65), using a more comprehensive six part series of variables to
demonstrate the following relationships: dental, skeletal, skeletodental,
lip, craniofacial and deep structure (Bushey, '72; ’74)
Findings and Discussion. The findings of the first evaluation of the data
from the 1965 study were limited to the dimensions of the epipharynx,
and tongue and hyoid positional changes. It was felt, however, that an
explanation for the poor response of Group IIB (unimproved partial
mouth breathers) might be found in a more comprehensive facial analy-
sis. Portions of the dental, skeletodental, craniofacial and deep structure
Segment of the reevaluation of the data (Bushey, '72) are presented as a
partial analysis of the 51 variables actually measured.
Table 5 shows that, although the entire sample had larger than average
lower anterior facial heights, that of the unimproved mouth breathers
(Group IIB) was extreme. In addition, the relationship of the occlusal
plane to the ramus shows an elevation of the posterior portion of the
occlusal plane for the improved mouth breathers (Groups I, IIA) but a
lower than average posterior position for the unchanged groups (IIB,
III). The difference in occlusal plane orientation takes on additional sig-
nificance because of the smaller facial axis (Ba-N to facial axis) and facial
taper (Go-Gn to N-Po) values for Group IIB. These variables indicate
that the Group IIB subjects are more retrognathic and have a steeper
mandibular plane, in spite of the SNA and SNB values which are remar-
kably similar to those of Groups I and IIA.
This finding underscores the fallacy of making a “skeletal assessment”
based only on the relationships of points A and B as advocated by Wat-
218
Bushey
son and colleagues ('68). Craniofacial variables of maxillary depth and
maxillary height suggest a superior directed deflection of the anterior
cranial base at nasion, which could account for the lower than average
values of the palatal plane to SN relationship. Hence, if the “microrhino
dysplasia syndrome” described by Bimler ('65) is pertinent, it would have
to be shown that nasion was related in an “average position”, and not
show this above-average elevation. Further, the obtuseness of the cranial
base angle (described in the earlier study, Bushey, '65) could account for
the higher location of nasion. It is interesting to note that this same
upward deflection of the anterior cranial base described by Schulhof and
colleagues ('77) as a predictor for a Class III growth pattern, was also
found to be one of the common characteristics of severe posterior cross-
bite, even those found in Class II subjects (Bushey, "77). Thus, there is a
potential in the cranial base morphology of mouth breathers for an inhe-
rent tendency to develop a posterior crossbite which goes beyond mere
tongue height (posture) relative to the posterior segments.
Deep structure variables (Table 5) provides an explanation for the
unimproved mouthbreathing of Group IIB individuals, showing the ret-
rognathic features of a large increase in lower facial height by document-
ing the obtuseness of the gonial angles of these subjects. The mandibular
arc (defined as the divergent angle formed between the corpus axis and
the condylar axis which bears an inverse relationship to the gonial angle)
values for Group IIB show a marked contrast to those of Group I as
illustrated in Figure 4.
The facial form analysis of the data (Bushey, '72) described above was
extended again by the author (Bushey, '74) by comparing the 1965 Uni-
versity of Illinois mouth breathers with those described by Linder-Aron-
Son ('60). Table 6 presents the findings for nasopharyngeal linear depth
dimensions of PNS-Ba and angular depth of Ba-S-PMF. It is noteworthy
that in spite of the approximately 6,000 miles between the Swedish and
American mouth-breather samples, the mean linear depth differences are
less than 1.0 mm and mean angular depth differences are less than 2.1°
for groups 5 and I, IIA, and IIB. A further comparison of nasopharyn-
geal sagittal depth is shown in Table 7. The group means for linear depth
measured from the anterior arch of the atlas (AA) to the posterior nasal
spine (PNS) of the mouth-breather groups I, IIA and IIB (Bushey, '65)
range from 34.2 to 35.5 mm and are remarkably similar to the “normal”
means of 34.5 mm for subjects approximately 8.5 years of age in Ricketts’
1969 baseline sample. The normal mean for subjects approximately 13.5
years of age (Ricketts, '69) indicates growth increments of 0.39 mm per
year. The similarity of normal and mouth-breather means for linear depth
is reinforced by a corresponding similarity of angular depth (Ba-S-PNS)
means of 62° versus 62° - 63.3° respectively. As discussed earlier (Table
219
AIRWAY DIMENSIONS
AREAS
Adenoid Epipharynx Depth Anterior Height Posterior Height Postop Cranial
Com- Sphenoid Adenoid Base
Preop Postop Preop Postop bined PMF-S-AA PMF-S-Ba AA-PMF S-Ba-PMF S-AA-PMF PMF-S Ba-S AA-S Body Thickness Angle
Nasal Respiration
Preoperative —0.395t 0.334 –0.164 –0.397 –0.292 —0.236 0.304 0.144 0.151 0.001 0.136 0.245 —0.513
—0.512* * 0.205 –0.275 –0.369 –0.307 –0.574* 0.435 0.621 * 0.059 –0.223 –0.1.18 –0.345 –0. 160
Postoperative –0.598°* 0.521* –0.151 –0.314 —0.269 –0.268 0.122 —0.34] —0.126 –0. 129 0.362 0.267 – 0.508 –0.559
0.438 –0.039 0.559 0.227 0.019 0.369 —0.125 –0. 175 0.244 0.345 ().274 –0.1 12 0.176 0.024
Adenoid Area
Preoperative 0.745*** –0.622 0.581** 0.258 0.097 ().511 * –0.041 0.152 0.287 0.406 (). 117 –0.16() 0.194
0.754 –0.376 0.498 0.044 –0.057 0.494 –0.089 –0. 157 0.385 0.494 ().372 (). 124
Postoperative —0.702*** 0.467* 0.467* 0.170 0.494* —0.191 0.033 ().082 ().238 –().084 0.029 0.847 0.502*
–0.679* 0.705” ().076 –0.049 0.524 –0.026 –0.351 ().516 ().771 * * ().629 ().318 ().823 (). 156
Epipharynx Area
Preoperative 0.694 0.217 –0.169 –0.179 0.038 0.324 (). 118 ().329 (). 183 ().248 0.359 —(). 183
0.550 0.589* 0.240 –0.096 0.330 0.221 –0.022 ().374 (). 119 0.281 (). 174 — 0.245
Postoperative 0.302 —0.346 —0.188 0.088 0.342 (). 121 ().417* ().322 (). 45.4° ().424* –0.743*** –0.421*
0.041 0.163 —0.117 0.024 0.428 ().274 —().013 –().422 –().208 0.029 –0.839*** –0.363
Combined
Adenoid & 0.192 0.003 0.769*** 0.171 (). 193 0.628*** ().717*** (). 454* (). 141 0.211 0.144
0.261 —0.181 0.690* 0.056 —().213 (),69()* 0.641 * ().655* (). 462 ().075 –0.137
Epipharynx
§
#
—0.397 —0.349 –0.561 ** 0.546**
–0.432 –0. 106 —0.218 –0.391
—0.360 —0.433 –0.715*** –0.587°
—0.765 –0.444 –0.686* —0.563
0.300 0.322 0.107 –0.006
0.081 0.207 0.062 0.052
0.749*** 0.280 0.356 0.653***
0.557* —0.184 0.144 0.206
0.725*** 0.233 –0.241 0.265
0.336 —0.289 — 0.098 –0.014
0.729*** 0.447* 0.613°."
0.678.* 0.846*** 0.723**
0.724*** 0.440
0.910*** 0.678*
0.566**
0.753**
0.247
–0.293
0.127
–0.276
0.170
–0.008
—0.158
–0. 145
0.064
–0.108
0.012
0.475
0.144
0.715**
–0.102
0.624*
—0.292
0.283
0.754* * *
0.395
–0.672***
0.770°-
0.392
0.335
–0.689***
—0.659
–0.217
—0.304
–0.413*
—0.533
—0.191
–0. 138
—0,461 *
—0,466
–0.624**
–0.475
Airway Dimensions—Depth
PMF-S-AA 0.748***
0.598*
PMF-S-Ba
AA-PMF
Airway Dimensions—Height
S-Ba-PMF
S-AA-PMF -
PMF-S
Ba-S
AA-S
Sphenoid Thickness
0.634*
0.567
0.339
0.501
—0.603
—0.535
–0.634**
–0.695*
—0.110
–0.372
—0.210
–0.635*
0.043
—0.549
0.007
—0.532
0.595*
0.864*
*Significant at 0.05
**Significant at 0.01
***Significant at 0.001
*, Upper values represent Group I and Group IIA.
, Lower values represent Group IIB.
Table 4. Comparisons of correlations between respiration, epipharyngeal areas and dimensions.
§
Rocky Mt. Data
Group I Group IIA Group IIB Group III System Norms Total
Mean S.D. Mean S.D. Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Dental
Lower anterior
facial height 50.6 7.0 50.6 3.6 53.3% 2.8 51.9 2.6 47.0 3.0 51.59 3.94
Skeletodental
Occlusal Plane-
Ramus 2.6* 0.5 2.1 2.9 0.9 4.9 0.6 4.1 1.0 *m. 1.31 3.2
SNA 80.0 6.3 81.1 3.5 81.9 4.6 80.8 4.7 81.0 3.0 81. 12 4.32
SNB 76.2 4.7 76.1 3.8 76.6 4.4 75.6 4.9 79.0 3.0 76.22 4.09
Craniofacial
Facial Axis
(Ba-N to
Facial Axis) 87.72 4.2 87.3 4.3 85.6* 3.1 85.2 2.3 90.0 3.5 86.63 3.77
Facial Taper
(Go-Gn to N-Po) 65.7 6.5 64.8% 3.1 62.8° 3.5 63.5 3.7 68.0 3.5 64. 18 3.94
Maxillary Depth
(F.H. to NA) 92.5 5.5 92.0 3.5 92.7 3.3 93.0 2.7 90.0 3.0 92.47 3.57
Palatal Plane
(to SN) —6.9° 3.0 –7.1* 3.4 –6.8% 3.5 –6.5* 4.5 4.0–0.5/yr 3.5 —6.95 3.45
Deep Structure
Cranial
Deflection 28.83 2.1 29.4% 1.8 29.8% 2.4 30.6 1.4 27.0 3.0 29.64 2.01
Mandibular
Arc 28.89 6.9 25.0 4.9 21.5% 5.3 25, 1 2.2 26-0.5/yr 4.0 24.58 5.43
Table 5. University of Illinois study, 1972.
§
Bushey
|
Group IIA-Improved—t
Group IIB-Unimproved-
Figure 4. Comparison of composite tracings of improved partial mouth breathers,
Group IIA (Solid lines), and unimproved partial mouth breathers, Group IIB
(broken lines), from University of Illinois study (Bushey, '72). Note that the
unimproved mouth breathers had the less favorable skeletal characteristics of a
Smaller (more negative) facial axis, greater divergence of the mandibular and
nasal (palatal) planes, and a more obtuse gonial angle of the mandible.
3), the sagittal height in mouth-breather groups may be a more significant
factor in restricting epipharyngeal space for the adenoid than Sagittal
depth (Fig. 3). Table 7 presents a comparison of the normal, mean angu-
lar nasopharyngeal height of 61.9° to 63.4° (Ricketts, '69) to that of the
mouth breathers of Group I, IIA and IIB of 56.3° to 59.8° (Bushey, '65).
The adverse influence of an increased cranial base angulation in mouth
breathers suggests that the correlated decrease in angular height results



223
Adenoid Obstruction of the Nasopharynx
PNS-Ba (mm) Ba-S-PMF ()
Mean S.D. Mean S.D.
Linder-Aronson 1970 (N=162)
Group 1 (N=37) 44.72 3.25 63.47 4.57
Controls
No adenoids
Group 2 (N=33) 43.21 2.09 63.80 4.32
Controls
Small adenoids
Group 3 (N=11) 43.65 3.08 66.36 2.78
Controls
Large adenoids
Group 4 (N=21) 43.82 3.65 62.71 5.81
Adenoidectomy
Otitis media
Group 5 (N=60) 42.39 3.51 60.90 5.74
Adenoidectomy
Nasal obstruction
Total (N=162) 43.36 3.29 62.69 5.26
Bushey 1965 (N=41)
Group I (N=6) 42.13 2.37 63.30 4.00
Tonsil- & adenoidectomy
Complete nasal obstruction
Group IIA (N=17) 42.96 3.55 62.00 5.60
Tonsil- & adenoidectomy
Partial nasal obstruction
Improved
Group. IIB (N=12) 43.07 2.41 63.00 5.20
Tonsil- & adenoidectomy
Partial nasal obstruction
Unimproved
Group III (N=6) 40.20 2.65 62.50 5.70
Tonsil- & adenoidectomy
No nasal obstruction
Total (N=41) 42.46 3.04 62.74 4.99
Table 6. Nasopharyngeal sagittal depth (linear and angular)
224
#
Depth Height Cranial Base
AA-PNS (mm) Ba-S-PNS (°) S-Ba-PNS (°) Ba-S-N (°)
Study Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Ricketts
1954 (N=20) 42.0 33,0–55.0" 61.0 52.0–69.0 63.0 54.0–71.0° 130.0 121.0–141.0°
Subjects 8.5 years old 34.5 3.5 62.0 4.0 61.9 4.0 129.0 3.0
Subjects 13.5 years old 36.3 3.5 60.2 5.2 63.4 4.5 129.4 4.4
1969 (N=40) 0.395 /yr —0.39 0.7/yr 0.3 0.68/yr 0.025 0.43/yr
Bushey—1965
Group I (N=6) 35.5 1.9 63.3 4.0 56.3 4.5 137.2 5.1
Group IIA (N=17) 34.2 3.9 62.0 5.6 59.6 3.7 133.1 4.9
Group IIB (N=12) 34.4 4.2 63.0 5.2 59.8 4.7 131.1 5.1
Group III (N=6) 34.3 4.0 62.5 5.7 60.2 3.6 134.5 5.0
1969 (N=40)
1969 (N=40)
* , indicates range.
Table 7. Nasopharyngeal sagittal dimensions.
§
Adenoid Obstruction of the Nasopharynx
from the closer approximation of the posterior nasal spine to the rostrum
of the sphenoid body, thus shortening the posterior choanal height.
The second mouth breather sample comparison was that of lower face
height dimensions illustrated in Table 8. The divergence of the palatal
and mandibular planes is again remarkably similar for both groups of
mouth breathers who had significantly improved nasal respiration follow-
ing adenoidectomy (Group 5, Group I, IIA). Mouth breathers were thus
found to have angular lower face heights which were more than 1 stan-
dard deviation above the mean for nose breathers, as illustrated by the
Swedish control group mean of 26.54°. It is also noteworthy, however,
that the unimproved mouth breathers (Group IIB) had a significantly
greater lower face height (the mean of 34.13° is two standard deviations
above the normative value). To test the various measures of lower face
height in the American sample, a comparison of angular and linear
heights was made and is shown in Table 9. The oral gnomic angle of
ANS-Xi-Po developed by Rocky Mountain Data Systems has a normative
value of 47°, with a standard deviation of 3°, and parallels the increased
mandibular plane-palatal plane divergence of one standard deviation in-
crease for improved mouth breathers (Group I mean of 50.75° and Group
IIA mean of 50.58°) and two standard deviations for unimproved mouth
breathers (Group IIB mean of 53.31°). The linear lower face height mea-
surement techniques of Harvold ('71) and Linder-Aronson ('70) were
compared to the linear percentage technique in the second section of
Table 9 and illustrates that group linear comparisons are less precise
unless adjusted for the individual patient’s age as recommended by Har-
vold ('71) and Linder-Aronson and Woodside (Linder-Aronson, '74;
Linder-Aronson and Woodside, '79). The finding of an increased man-
dibular arc for mouth breathers (Bushey, '72) was further borne out by
the abnormally higher means for the gonial angle of the mandible. The
last finding suggests a significant contribution of mandibular morphology
to the increased lower face height in the mouth breather groups. The
cause of the difference in the gonial angle for mouth breathers who
respond to adenoidectomy (Groups I, IIA) and unimproved mouth
breathers (Group IIB) is the subject of much interest (Koski and Lahde-
maki, '75). Figure 4 illustrates group differences in composite tracings for
Groups IIA and IIB.
Table 9 again underscores that whereas the angular lower face height
(ML/PL) of the Swedish and American mouth-breather samples showed
great concordance, the linear comparisons illustrate that Group I (com-
plete mouth breathers) represented the lower age range of the American
sample (age 6 years) and had lower linear lower face height mean values
than the Swedish subjects (Group 5, age 8 years), while older (age 10
years), partial mouth breathers (Groups IIA and B) represented the
226
Bushey
ML-NL
Linder-Aronson 1970 (N=162)
Group 1 (N=37)
Controls
No adenoids
Group 2 (N=33)
Controls
Small adenoids
Group 3 (N=11)
Controls
Large adenoids
Group 4 (N=21)
Adenoidectomy
Otitis media
Group 5 (n=60)
Adenoidectomy
Nasal obstruction
Total (n=162)
Bushey 1965 (N=41)
Group I (N=6)
Tonsil- & adenoidectomy
Complete nasal obstruction
Group IIA (N=17)
Tonsil- & adenoidectomy
Partial nasal obstruction
Improved
Group IIB (N=12)
Tonsil- & adenoidectomy
Partial nasal obstruction
Unimproved
Group III (N=6)
Tonsil- & adenoidectomy
No nasal obstruction
Total (N=41)
sp-gn (mm)
Mean S.D. Mean S.D.
58.71 7.31 26.54 3.56
56.49 4.03 28.67 4.86
55.58 4.15 26.95 3.72
57.18 2.88 27.50 3.31
60.3 4.10 31.23 6.16
58.37 5.10 28.86 5.24
58.80 3.28 31.16 5.27
62.50 5.98 31.07 3.44
63.58 6.47 34.13 4.61
59.37 5.27 32.25 8.09
61.82 5.83 32.15 4.90
Table 8. Comparison of skeletal variables in lower face height
Group IIA
Group I Group IIB Group III
Variable Mean S.D. Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Angular
ANS-Xi-PO 50.75 6.92 50.58 3.58 53.31 2.81 51.87 2.59 51.59 3.94
Palatal plane
Mandibular plane 31.16 5.27 31.07 3.44 34.13 4.61 32.25 8.09 32.15 4.90
Linear
ANS'-Gn
(Harvold) 58.31 3.87 61.19 6.19 62.02 6.43 58.13 5.39 60.56 5.89
Sp'-Gn -
(Linder-Aronson) 58.80 3.28 62.50 5.98 63.58 6.47 59.37 5.27 61.82 5.83
% Total face
height 56.48 1.75 56.88 2.22 57.76 2.89 56.58 2.44 57.03 2.37
Gonial Angle 127.66 6.14 129.58 5.07 135.5 6.77 127.67 2.34 130.76 6.21
Table 9. University of Illinois study (Bushey 1965). Comparison of skeletal variables in lower face height.
§
Bushey
higher linear values for lower face height. From the 1974 analysis dis-
cussed above the author has concluded that:
1. The sagittal dimensions of nasopharynx are only diagnostically sig-
nificant when found to be extremely small and must be corrected to the
Subject’s age.
2. Angular measures of nasopharyngeal height and depth appear to be
more significant than linear measures but are even more greatly influ-
enced by the cranial base angulation and the relative mass of the adenoids
which occupy a given epipharyngeal dimension.
3. Increased lower face height is a significant facial feature of mouth
breathers and may best be interpreted by the angular divergence of the
mandibular and palatal planes, unless individual linear heights are ad-
justed for age.
4. Increased obtuseness of the gonial angle contributes significantly to
the increase in lower face height in mouth-breather groups. In its extreme
form, the gonial angle obtuseness may approach such a degree of skeletal
openbite that the increase in the airway produced by adenoidectomy may
not improve occlusal relationships.
SUMMARY AND CONCLUSIONS
This presentation has sought to critically review the conflicting litera-
ture on nasopharyngeal airway obstruction, and to present additional data
from the University of Illinois mouth-breather study. We may conclude
that:
1. The literature review underscores the need for the use of a four-part
hypothesis when evaluating investigations linking airway obstruction to
dentofacial changes.
2. The University of Illinois study reveals that because naso-respiratory
obstruction may be partial or complete, mouthbreathing may also be
partial or complete, and thus offers a continuum of physiologic adapta-
tion related to a number of morphologic variations of the craniofacial
complex.
3. A comparison of Swedish and American mouth-breather groups sug-
gests that there are common craniofacial characteristics for those subjects
who responded favorably to adenoidectomy by significantly altering their
respiratory pattern.
REFERENCES
Angle, E. H. Malocclusion of the Teeth. S. S. White Dental Manufacturing Co.,
1907. -
Ballard, C. F. Adenoidal facies and mouthbreathing: A clinical analysis. Med.
Press 228:347-351, 1952.
229
Adenoid Obstruction of the Nasopharynx
Ballard, C. F. and E. Gwynne-Evans. Mouthbreathing, discussion on the mouth-
breather. Proc. Roy. Soc. Med. Press 228:347, 1958.
Bimler, H. P. Uber die Microrhine Dysplasie. Fort. Kiererorthopadie 26:4, 1965.
Bloch, E. Die Hohe Gaumen. A. Ohrenheilk. 44, 1903.
Brader, A. C. A cephalometric X-ray appraisal of morphological variation in
cranial base and associated pharyngeal structures: Implications in cleft palate
therapy. Angle Orthodont. 27:179-195, 1957.
Bushey, R. S. Alterations in certain anatomical relations accompanying the
change from oral to nasal breathing. Master's Thesis, University of Illinois,
1965.
Bushey, R. S. Recent research findings relating nasopharyngeal function to oral
physiology and craniofacial development. Proc. Found. Orthodont. Res.
April, 1972.
Bushey, R. S. The relationship of nasopharyngeal airway obstruction to dentofa-
cial development and its implications for orthodontic treatment. Angle Soc.
Pap. 1974. ,
Bushey, R. S. Posterior crossbite: A four-dimensional assessment. Angle Soc.
Pap. 1977.
Day, A. J. W. and T. D. Foster. An investigation into the prevalence of molar
crossbite and some aetiological conditions. Dent. Pract. 21:402-410, July, 1971.
Duke, W. W. Deformity of the face caused by nasal allergy in childhood. Arch.
Otolaryngol. 12:493, 1930.
Eastman, G. A cephalometric study of tongue posture in individuals with nasal
allergies. Master's Thesis, University of Michigan, 1963.
Epstein, I. M. Factors influencing the results of tonsillectomy and adenoidec-
tomy. Am. J. Dis. Child. 53:1503, 1937.
Handelman, C. S. and G. Osborne. Growth of the nasopharynx and adenoid
development from one to eighteen years. Angle Orthodont. 46(3):243-259,
1976.
Harvold, E. P. The role of function in the etiology and treatment of malocclusion.
Am. J. Orthodont. 54:883-898, 1968.
Harvold, E. P. Personal communication. 1971.
Harvold, E. P. Experiments on development of dental malocclusion. Am. J.
Orthodont. 61:38-44, 1972.
Howard, C. C. Inherent growth and its influence on malocclusion. J. Am. Dent.
Assoc. 19:642–651, 1932.
Huber, R. E. and J. W. Reynolds. A dentofacial study of male student at the
University of Michigan in the physical hardening program. Am. J. Orthodont.
Oral Surg. 32(1):1, 1946.
Humphreys, J. F. and B. D. Leighton. A survey of anteroposterior abnormalities
of the jaws of children between the ages of two and five and one-half years of
age. Brit. Dent. J. 88:3, 1950.
James, W. W. and S. Hastings. Discussion on mouthbreathing and nasal obstruc-
tion. Proc. Roy. Soc. Med. 25:1343, 1932.
Kantorowicz, A. Uber den Mechanismus der Kieferdeformierung bei behin-
derter. Atmung. Dtsch. Mschr. Zahnheilk. 34:225, 1916.
230
Bushey
Kingsley, N. W. A treatise on oral deformities as a branch of mechanical surgery.
(Cit. Brash, J.) D. Appleton Co., New York, p. 10, 1888.
Koski, K. and P. Lahdemaki. Adaptation of the mandible in children with ade-
noids. Am. J. Orthodont. 68:660-665, 1975.
Leech, H. L. A clinical analysis of orofacial morphology and behavior of 500
patients attending an upper respiratory clinic. Dent. Prac. 9:57-68, 1958.
Linder-Aronson, S. Adenoids: Their effect on mode of breathing and nasal air-
flow and their relationship to characteristics of the facial skeleton and the
dentition. Acta Oto-Laryng. Supplementum 265:3-132, 1970.
Linder-Aronson, S. Effects of adenoidectomy on dentition and nasopharynx. Am.
J. Orthodont. 65:1-15, 1974.
Linder-Aronson, S. Personal communication, 1974.
Linder-Aronson, S. and A. Backstrom. A comparison between mouth and nose
breathers with respect to occlusion and facial dimensions. Odont. Revy.
11:343, 1960.
Linder-Aronson, S. and D. Woodside. The channelization of upper and lower
anterior face heights compared to population standard in males between ages 6
to 20 years. Europ. J. Orthodont. 1:25-40, 1979.
Lubarth, J. The adenoid problem. Arch. Pediat. 77:491, 1960.
Marks, M. B. Allergy in relation to orofacial dental deformities in children: A
review. J. Allergy, 36:293-302, 1965.
Massler, M. and I. Schour. The effect of mouthbreathing. In: The Atlas of the
Mouth, Plate 29. Am. Dent. Assoc. Chicago, 1948.
Mergen, D. C. and R. M. Jacobs. The size of nasopharynx associated with normal
occlusion and Class II malocclusion. Angle Orthodont. 40:342-346, 1970.
Meyer, W. On adenoid vegetations in the nasopharyngeal cavity: Their pathol-
ogy, diagnosis and treatment. Med. Chirurg. Trans. (London), 53:191, 1872.
Michel, A. Lippen-, Wangen-, Zungendruck. Dtsch, Mschr. Zahnheilk. 26:7,
1908
Moss, M. L. Primacy of functional matrices in orofacial growth. Dent. Pract.
19:63-73, 1968. -
Moyers, R. E. Handbook of Orthodontics, 2nd ed., Year Book Medical Pub-
lishers, Chicago, 1963.
Nordlund, H. Ansiktsformens, spec. gomhojdens betyselse for uppkomsten av
kronsika otiter. Appelbergs Boktryckeri AB, Uppsala, 1918.
Pruzansky, S. Roentgencephalometric studies of tonsils and adenoids in normal
and pathological states. Ann. Otol. Rhinol. Laryngol. 84:2, 1975.
Rasmus, R. L. and R. M. Jacobs. Mouthbreathing and malocclusion: Quantita-
tive technique for measurement of oral and nasal airflow velocities. Angle
Orthodont. 39:296, 1969.
Reidel, R. A. Diagnosis and treatment planning in orthodontics. Dent. Clin. N.
Am. 1:175-187, March, 1963.
Ricketts, R. M. The cranial base and soft structures in cleft palate speech and
breathing. Plast. Reconst. Surg. 14:47-61, 1954.
Ricketts, R. M. Respiratory obstructions and their relation to tongue posture.
Cleft Pal. Bull. 8(3):4, 1958.
231
Adenoid Obstruction of the Nasopharynx
Ricketts, R. H. Personal communication, 1969.
Rix, R. E. Deglutition and the teeth. Dent. Rec. 66:103-108, 1946.
Robert, A. Memoire sur le Gonflement Chronique des Anygdales cez les En-
fants. Bull. Gen. De Therap. 24:343-351, 1843.
Schulhof, R. J., S. Nakamura and W. V. Williamson. Prediction of abnormal
growth in Class III malocclusion. Am. J. Orthodont. 71:421-430, 1977.
Siebenmann. Uber adenoide Habitus und Leptoprosopie, sowie uber das kurze
Septum der Chamaeprosopen. Much. Med. Wschr. (cit. Nordlund, H.), 1897.
Subtelny, J. D. The significance of adenoid tissue in orthodontia. Angle Ortho-
dont. 24:59–69, 1954.
Tomes, C. S. On the developmental origin of the v-shaped contracted maxilla.
Month. Rev. Dent. Surg. 1:2, 1872.
Truesdale, B. and F. B. Truesdale. Deglutition with special reference to normal
function and the diagnosis, analysis, and correction of abnormalities. Angle
Orthodont. 7:90-99, 1937.
Wallis, H. R. E. Medical aspects of malocclusion. Dent. Rec. 73:519, 1953.
Watson, R. M., Jr., E. W. Warren and N. D. Fischer. Nasal resistance, skeletal
classification and mouthbreathing in orthodontic patients. Am. J. Orthodont.
54:367-379, 1968.
Woodside, D. G. The present role of the general practitioner in orthodontics.
Dent. Clin. N. Am. 3:483-508, July, 1968.
Yip, A. S. G. and J. F. Cleall. Cinefluorographic study of velopharyngeal func-
tion before and after removal of tonsils and adenoids. Angle Orthodont.
24:59-69, 1971.
232
RESPIRATORY MODE AND MORPHOLOGICAL
TYPES: SOME THOUGHTS AND PRELIMINARY
CONCLUSIONS
Peter S. Vig, B.D.S., Ph.D.
Department of Orthodontics
The University of North Carolina
What determines craniofacial morphology? The debate between protago-
nists of the genetic hypothesis and those in favor of environmental expla-
nations is both old and unresolved. Observation of current trends, both in
research and clinical thinking, reveal a strong resurgence of interest in the
influence of environment or function on the orofacial complex. Explana-
tions for abnormal growth and development are held by some in spite of
the questionable validity of the observations on which some of these
views are based.
Understandably, clinicians are attracted to the possibility of an environ-
mentally controlled and, therefore controllable, growth mechanism,
which dominates or supercedes a rigid genetic blueprint. The confirma-
tion and elucidation of the means by which function regulates form would
offer at least two significant advances in everyday clinical terms. Therapy
would no longer be determined by symptomatology and early control of
the significant environmental factors would truly intercept unfavorable
development. -
A review of the orthodontic literature reveals that these ideas are far
from new. Each generation seems to rediscover and restate such con-
cepts. Today’s interest in muscle re-education (myofunctional therapy),
gnathology, diet and mouthbreathing are all part of this.
It is exactly fifty years since Brash (29), the celebrated English anato-
mist, delivered his Dental Board Lectures, subsequently published under
the title “The Aetiology of Irregularity and Malocclusion of the Teeth.”
This work was the first “state-of-the-art” review on craniofacial develop-
ment as it relates to orthodontics. In summing up the association between
adenoids, mouthbreathing and malocclusion, he recalls that this idea
dates back to Meyer of Copenhagen (1868). Brash concludes that:
“Indeed, it was so frequently reiterated, and the truth of the supposed causal
relation between mouthbreathing and narrow jaws so constantly assumed in
233
Respiratory Mode and Morphological Types
innumerable reports that at one time it was commonly stated as if it were an
aetiological fact.”
He was doubtlessly referring to Bloch's ('03) assertions that mouth-
breathing can cause a failure of descent of the anterior palate and a
buckling of the nasal septum. Bloch likened air currents passing through
the mouth leading to the high arched palate seen in mouth breathers to
water wearing away stone.
More than seventy-five years later Quinn ('78) reiterated that “ . . .
Mouthbreathing is one of the early symptoms of improper or unnatural
acts of breathing . . . .” and that “ . . . Dramatic deformities of the face,
jaws, and dentition can be caused by the inability to breathe through the
nose properly.”
When a respected clinician such as Ricketts (79) states that “when we
observe a lack of function in the nose, we know there can be growth
inhibition” and that “under normal function in breathing, . . . a pressure
develops. Perhaps in the abnormal, this pressure is changed to a vacuum
and the maxillary complex is sucked inward, restricting the basal cone.”
The indication is clear for studies to examine such propositions.
What then is the basis for theories that link impaired nasal respiration
to craniofacial deformity? Proponents of the idea that mouthbreathing is
a major etiologic factor base their opinion on the following:
Clinical Impressions
1. A high proportion of the children seen by orthodontists, have incom-
petent lips and admit to mouthbreathing.
2. Cephalometric radiographs frequently reveal enlarged adenoids
which in the midsagittal plane seem to occupy a significant portion of the
nasopharynx and are assumed to cause physiologically significant obstruc-
tion
3. Patients with the long-face syndrome, adenoid facies, or microrhino
dysplasia have incompetent lips, frequently also a history of allergies and
possibly nasal obstruction as suggested by inspection of their anterior
nasal cavities where turbinates or deviations of the septum may be seen
and assumed to block the air passage. This chain of clinical impressions
and untested assumptions forms the basis of most theories and some
clinical practices.
Animal Studies
The classic experiments of Harvold ('73), in which nasal obstructions
were created in growing monkeys, revealed that nasal obstruction had a
profound effect on skeletodental growth. The combination of these obser-
vations has led to the following assumptions:
234
Vig
LIP INCOMPETENCE DEFICIENT MAXILLA
`Mouth GROWTH –º-HIGH NARROW VAULT
BREATHINGT MODIFICATION Tºe OPEN BITE
NASAL OBSTRUCTION \ LONG FACE SYNDROME
A natural corrollary to such an assumed link of relationships is seen in
the increased efforts to intervene by adenoidectomy, surgery for septal
defects, turbinate removal or attempts at lip exercises to modify respira-
tory behavior which many clinicians now enthusiastically recommend.
The theoretical basis for such procedures and indeed for the selection
of patients who may benefit, remains doubtful at best. Assuming that the
above growth modifications do result from mouthbreathing, is it not
equally logical to encourage nasal obstruction in the patient with develop-
ing “short face syndrome?”
QUESTIONS RAISED BY PREVIOUS RESEARCH
Extensive literature exists on the possible association between respira-
tion and oral and facial form. Papers range from anecdotal case reports to
epidemiological surveys and more recently include aerodynamic studies
on the mechanics of respiration. The evidence is far from strong for
causal associations between morphology and respiratory mode. No clear-
cut explanations have emerged of precisely how, or if at all, growth and
development are modified by variations in airflow in humans.
The fundamental problem which characterizes previous work, is a lack
of definition as to precisely what constitutes mouthbreathing or, for that
matter, impaired nasal respiration. Most observers have resorted to crude
and possibly unreliable means of identifying respiratory mode such as
asking subjects if they breathe through their mouth or nose, equating lips
apart posture (lip incompetence) with mouthbreathing, placing a cold
mirror under the subject’s nose, placing cotton wool under the subject’s
nose and assuming that a subject is a mouth breather if direct or radio-
graphic inspection of nose or nasopharynx reveals that the air passage is
obstructed or partially obliterated.
Therefore, while exercising some caution in interpretation, it is still of
interest to consider some of the findings. Morrison (31) found associa-
tions between nasal obstruction and the shape of the palatal vault. On the
other hand, McKenzie ('09) notes that some children exhibiting “adenoi-
dal facies” never developed adenoids. Humphreys and Leighton ('50)
failed to find significant evidence of a relationship between skeletodental
trends and mouthbreathing or a higher percentage of mouth breathers
among Class II individuals than in the general population.
Hastings and James (32) looked at 53 infants who had a “lips apart”
235
Respiratory Mode and Morphological Types
posture and found that all were nose breathers. Likewise, Leech ('58)
working in an upper respiratory clinic noted that fewer than one-third of
a group of lip-incompetent individuals he tested with a cold mirror could
be classified as mouth breathers. He also estimated that only 20% of the
adenoids he examined in this group of lip-incompetent individuals could
be indicted as causing mouthbreathing.
In more recent times, the necessity for objective data on respiratory
function has been recognized. Wertz ('68) used a warm-air anamometer
to record nasal airflow (velocity) and calculated the volume per breath by
using a planimeter to measure the area under the curve which was de-
rived by plotting flowrate against time. He compared nasal airflow of
individuals before and after rapid maxillary expansion and this produced
some interesting results. There was no significant difference in nasal air-
flow during resting respiration, but during mild exercise, nasal airflow
increased in 60% of the patients and decreased in 40% of the patients.
During maximal respiration, all subjects showed a greater volume of air
passing through the nose after maxillary expansion.
Rasmus and Jacobs ('69) appear to be the first to use thermistors to
study nasal airflow. They evaluated nasal breathing by recording peak
airflow velocity and applying the cold mirror test. In their opinion a
clinical impression of mouthbreathing does not correlate necessarily with
nasal airflow records. Nor did they find any correlation between mouth-
breathing and malocclusion.
Adopting a different approach, Watson and colleagues ('68) studied
nasal resistance to airflow. They determined a critical resistance value
below which nasal resistance is compatible with nasal airflow. It was their
clinical impression that of the individuals they clinically examined, 60%
breathed through the nose while 40% breathed through the mouth. How-
ever, when they compared the skeletal patterns of high versus low nasal
resistance groups cephalometrically, they found no significant difference
between the groups in terms of anteroposterior jaw relationship.
Such equivocal results do not support a direct causal relationship be-
tween airflow (either in terms of velocity or volume) and craniofacial
morphology.
The studies of Linder-Aronson ('70) on post-adenoidectomy changes
reveal definite skeletodental adaptations. Although these changes are
generally small, they do exhibit a general trend for craniofacial morphol-
ogy to return to the more normal control group values. Linder-Aronson
suggests that postural changes, possibly of the lips but not the tongue,
may be responsible for some of the observed dental adaptations after
removal of adenoids. The relationship between adenoidectomy and lip
posture is not clear.
Involution of lymphoid tissues such as tonsils and adenoids is a sponta-
236
Vig
neous process that occurs during normal maturation. This process usually
correlates with skeletal and muscular development as depicted on the
classical Scammon's Curves. However, it is conceivable that there are
those in whom lymphoid tissue involution is delayed or out of synchrony
with other aspects of maturation. If “enlarged adenoids” are thought to
be harmful, presumably these individuals would form a significant pro-
portion of adenoidectomy candidates. Delayed maturation in a patient
who has an adenoidectomy and subsequently has a growth spurt could
give a false impression of causality between treatment and post-treatment
changes. It should be noted that in this context, the maximum size of
adenoids may be attained as late as 14 years of age (Subtelny, '54).
From this discussion, it is clear that the key issues in this controversy
concerning form, function and what constitutes appropriate treatment
remain unresolved. It is by no means clear to what extent craniofacial
morphology is influenced by respiratory mode. Nor do we have reliable
data on the impact of variations in airway resistance and the precise
nature of adaptations in respiratory mode.
CURRENT STUDIES - A PRELIMINARY REPORT
During the past few years, a series of interrelated studies conducted in
the Orthodontic Department at the University of North Carolina have
focussed on the morphologic correlates of adaptive behavior. We are
currently conducting a prospective study of the factors influencing stabil-
ity in orthognathic surgery patients. It includes the evaluation of cranio-
cervical posture, muscle pressures on teeth, vertical or occlusally directed
forces, speech production and respiratory behavior. The airflow dynamics
studies are being carried out in close collaboration with the group headed
by Dr. Donald Warren ('79). .
The findings from one preliminary experiment only will be discussed
here. The objectives of this experiment were to answer the following
questions:
1. Is orofacial morphology a reliable indicator of breathing pattern?
Specifically, does lip incompetence or “long-face” type signify mouth-
breathing? &
2. How well do individuals judge if they are oral or nasal breathers?
3. How easily can individuals modify their mode of respiration?
This experiment is still in progress with over forty data-gathering ses-
Sions completed. Since modification in both instrumentation and compu-
terized analysis of data are still in progress, a statistical presentation of
the entire study will be postponed. The early results obtained to date,
however, are such as to warrant this report.
Subjects comprise three broad categories of morphologic types: nor-
237
Respiratory Mode and Morphological Types
mal, lip incompetent without long face, and lip incompetent with long
face. Each subject’s respiration is monitored through two types of face
mask. The first is a full face mask and records the total airflow from both
the mouth and nose. A second mask which leaves the mouth free is used
to monitor nasal respiration only. Instrumentation described by Watson
and colleagues ('68) is used to obtain nasal resistance, nasal airflow and
total (mouth and nose) airflow.
Subjects are asked to breathe normally while wearing both masks. To
ensure that respiratory behavior is normal, the subject's attention is dis-
tracted from the act of breathing by having them read. After the subject's
normal mode of breathing has been evaluated, the subject is asked to
deliberately mouthbreathe and, if possible, to prevent any air from pass-
ing through the nasal passage. This effort is monitored with the subject
wearing the nasal mask.
The subjects are given time to get used to the masks and when their
respiration reaches a regular, steady state as seen on the oscilloscope
monitor, a 25 second segment of breathing pattern is recorded and stored
in a computer file.
On completion of these studies, various parameters will be analyzed.
These will include respiratory rate, duration of inspiration and expiration
and volume per respiratory cycle, and nasal resistance.
For the present, however, peak airflow data obtained during expiration
from the first 15 subjects is shown in Figures 1 and 2. These 15 subjects
included 5 normal, 5 lip incompetent and 5 long-faced/lip-incompetent
morphologic types. The preliminary trends, which later data seem to
confirm, is summarized as follows:
1. All adult subjects studied to date have a nasal component to their
respiration.
2. Neither lip incompetence nor long-faced morphology can be as-
sumed to indicate mouthbreathing.
3. While nasal airflow does occur in the long-faced lip incompetents,
peak nasal airflow velocity appears to be less than that of the other two
grOups.
4. When asked to deliberately mouth breathe, only three of the fifteen
subjects could prevent all nasal respiration (four of the first twenty-five in
this series.).
5. When asked before the experiment how they normally breathe, all
the long-faced and nearly all the lip incompetent adults claimed to be
mouth breathers.
SOME TENTATIVE CONCLUSIONS
While it is obviously premature to make definitive statements, it does
seem appropriate to venture some conclusions at this time.
238
Vig
Peak Airflow During Expiration Comparing Nasal and Total Flows
CCS. / S e C.
500- (ccs./sec.)
O
[]
400- D
D
D [] O O
_ 300–
º A
O
Z A
200-
A
A
O
100– O
A
O—
T | | | TI
O 100 200 300 400 500
Total
D Normal
O Lip Incompetent
A Long Face and lip In competent
Figure 1. The distribution of peak expiratory airflow values measured through
nasal and total face masks. Note that all subjects demonstrate a nasal component
of respiration. -
The term mouthbreathing with its connotation of non-nasal respiration
is misleading. If that is what it means, we have yet to see a subject who is
a mouth breather. We have even found a nasal respiratory component in
two individuals who had histories of chronic allergies, who were com-
plaining of severe colds during the examination and who were long-faced,
lip incompetent morphologic types! It will probably prove more meaning-
ful in future work to consider each individual’s mode of respiration as
oronasal, with the degree of oral and nasal components varying. We
intend to develop an oronasal ratio (or percentage nasal) based on flow
rates and volume, to characterize individual variation in respiratory
mode. It is conceivable that some critical values of such a ratio would
correlate more closely with specific morphologic features than the previ-
ously used mouthbreathing/nosebreathing, all or nothing distinction.
239
Respiratory Mode and Morphological Types

500-
N
ºr N
+ T * T
– 400- T N
i. IN T
* T N + T, N r 1 TN
3 - 300– N | TN I. D
-S2 c - T
* 3 T i N
2 3 lo -
* 3. + T LD + T + T
# 5200-
Ul- D T - N + N
—x.
; -l-D D - D
N
Ch- 100- + N —l-D
D
O-- - - - - - - - - - -P-- -------- Q_1D tº-e E- ºr - E- ºr - E-e ‘º º-ºº º -º º º
'' NORMAL'' SUBJECTS L|P INCOMPETENT LONG FACE
L|P INCOMPETENT
T= Total Face Mask, Total Flow
N= No sol Mask, Nasal Flow Only
D= Deliberate Mouth Bred thing, Nasal Flow.
Figure 2. The grouping of subjects of three morphologic types showing peak
expiratory flow rates. Only three subjects (where D = 0) could deliberately
mouth breathe.
It is clear that a clinical examination of patients’ facial types or their lip
posture is not an adequate diagnostic criterion to determine the absence
of nasal respiration. Neither is the patient’s own evaluation of how he
normally breathes reliable.
The surprising inability of most people to change from nasal to purely
oral respiration voluntarily, seems to indicate that nasal respiration is the
more natural of the two modes. It is well known that infants born with
choanal atresia may die rather than adapt to mouthbreathing. However,
it was thought that adults with more refined neuromotor development
and skills would find it less difficult to adapt. It would appear that motor
behavior determining both posture and activity associated with respira-
tion is firmly established and resists change. It is highly questionable that
muscles can be re-educated to permanently maintain major alterations in
such basic activities as respiration.
Reports which occasionally state that lip incompetence improves fol-
lowing some effort at therapy are not at all surprising but mean little. A
recently published serial study by Vig and Cohen ('79) shows that lip
incompetence diminishes with age in the absence of any treatment and
irrespective of skeletal type.
How effective then are the currently popular operations to improve the
nasal airflow? Without quantitative data on oronasal airflow, it is impossi-
240
Vig



JG ,
9 12.
2. §§
6.
10. 13,
3.
7.
14.
11.
4.
8. C3-1





Figure 3. Tracings of cross-sections of nasal cavity air space made from computed
tomography pictures. Sections are from #1 at the back to #14 at the front of nose
and are made at 4 mm distance apart. Areas were measured by planimetry.
ble to answer this question. However, it is fair to say that the onus of
proof lies on those who prescribe such treatment.
It should be mentioned here that the removal of nasal turbinates may
prove to be a futile gesture in some cases. This view is based on studies
(Montgomery et al., '79) of the dimensions of the nasal air passages.
Using computed tomography (better known as CAT-SCAN), the area of
the nasal air passages was calculated at intervals of 4 mm from the front
to the back of the nose. The area in which the turbinates are found is the
front half of the nasal cavity and this area was not always the site of the
Smallest aperture. More commonly, the smallest dimensions were found
in the posterior third of the nose. Thus, removal of the turbinates in such
cases would not increase the minimum aperture size of the nasal airway
(Fig. 3).
So much for the removal of turbinates, but what about rapid maxillary
expansion? The effect of palate splitting, viewed on conventional frontal
view headplates, shows an obvious increase in the width of the pyriform
aperture of the bony nose. This has generally been assumed to indicate
that a more or less uniform increase in the dimensions of the bony nose
241
Respiratory Mode and Morphological Types
occurs throughout its entire length. However, the study mentioned
above, using computed tomography, shows that a variable dimensional
change has occurred (Fig. 4). While anteriorly the post-expansion dimen-
Sions may be somewhat larger than pretreatment dimensions, the change
in dimension is progressively less towards the back of the nose. In fact, in
the case illustrated, we found that 4 cm posterior to the anterior nasal
spine, the size of the nasal wall area was actually less after treatment than
before. Such effects on airway size which previously could not be ob-
served may explain the paradoxical results of Wertz ('68), who found no
increase in nasal airflow during resting respiration in subjects after maxil-
lary expansion.
POSSIBLE SIGNIFICANCE OF RESPIRATORY MODE ON
CRANIOFACIAL GROWTH
The Invisible Activator Hypothesis
The common practice of calling all functional appliances “activators” is
unfortunate. It leads to false assumptions, particularly in the minds of
those unfamiliar with the historic development and the differences be-
tween different appliance systems. For many years, American orthodont-
ists shunned the use of appliances based on the Andresen monobloc which
they felt to be inferior to the multibanded techniques for controlled tooth
movement. Today, an appreciation of the orthopedic possibilities of cer-
tain functional appliances attracts adherents who have realized the limita-
tions of routine orthodontics in controlling skeletal pattern during growth.
We believe the new generation of “activators” or functional appliances
is designed to act predominantly on the neuromuscular system. It is the
resulting effects of muscles acting in a modified way on the developing
skeletodental structures which results in altered orofacial relations. Thus,
therapeutic activators may be regarded as a highly visible means of induc-
ing muscle adaptation with ultimate morphologic change as the ultimate
goal.
The following argument is presented to support the idea that, in fact,
nature may have been using an invisible activator to produce morpho-
logic variations long before the clinician thought of functional appli-
ances. The possibility exists that respiratory requirements dictate neuro-
muscular adaptations which act in very much the same way as do func-
tional appliances.
In the experimentally induced mouthbreathing monkeys of Harvold
and colleagues ('73), dramatic changes occurred in the space of one
year. Although all the animals developed an anterior open bite, the
changes in mandibular morphology were varied. Differences in the
242
Vig
NASAL WALL AND AIR SPACE AREAS MEASURED ON TOMOGRAMS

|300-
1200-
noo: NASAL WALL AREA
|OOO -
CN
9
O
O
*
sº
800 -
700-
:
600- © AFTER MAXILLARY EXPANSION
tºº O BEFORE MAXILLARY EXPANSION
500-
sº
400T
200+
º
100 -
I I
I - I -
I I-I
O l 2
T I
3 4 5
DISTANCE FROM ANTERIOR NASAL SPINE IN cm.
Figure 4. Changes in nasal wall and air-space areas in a case before and after
rapid maxillary expansion. Note that increased dimensions are mainly in the front
of the nose.
change in mandibular form were consistent with the various mechanisms
which these animals used to adapt to mouthbreathing to compensate for
nasal obstruction. These differences were evident in the way in which the
tongue and mandible were used to maintain an oral airway. Harvold (75)
describes both the development in some animals of a prominent chin (not
usually seen in monkeys) and some marked changes in the gonial region.
The bone apposition at the chin occurred as the mandible assumed a
lower postural position in order for a monkey to mouth breathe. His
theoretical explanation proposed that altered muscle activity produces a
stable tension in the periosteal tissue and that such biophysical stimuli will
extend the perimeter of bone until the architecture is in balance with the
physical requirements.
It should be noted, however, that in these experiments total or nearly
complete nasal obstruction was obtained by occlusion of the nares. From
our present studies, it would seem that the mouthbreathing of these ani-
243
Respiratory Mode and Morphological Types
mals is not completely analogous to that of humans with increased nasal
air resistance to airflow. Another factor which should be considered when
extrapolating to the human situation is the anatomic differences (both
neuromuscular and dentoskeletal) between monkeys and humans which
would result in differences both in adaptation and, therefore, in the resul-
tant effects on morphology. Nevertheless, the principles operating may be
expected to be similar.
It is interesting to compare these studies of Harvold with observations
made by Linder-Aronson ('70, '79) on the effects of adenoidectomy. As
would be expected, the human post-adenoidectomy morphologic changes
are less dramatic and generally in the opposite direction to the growth
effects seen in nasally obstructed monkeys. Linder-Aronson, however,
Suggests that adaptation of the lips at rest, rather than the tongue, is more
likely to be the cause of dental repositioning after the reduction of na-
sopharyngeal obstruction by adenoidectomy. Although his views appear
to contradict those of Harvold, it is possible to reconcile them. What the
precise role of respiratory behavior is in morphogenesis is not clear.
However, it possibly lies in an appreciation of individual variations in
adaptive behavior which humans employ for the maintenance of nasal
respiration. It now seems that complete nasal obstruction is rare and total
oral respiration, while possible in man, is the exception rather than the
rule because it is both uncomfortable and difficult to sustain.
The primary physical factor determining the pattern of airflow seems to
be airway resistance. Even allowing for a strong inherent urge for nasal
respiration, there will be a tendency toward oronasal respiration in some
individuals due to a high measure of nasal resistance. Airway resistance is
a function of relative aperture size in the oral and nasal air passages and,
to some extent, a function of nasal cavity contents which impede the
laminar flow of air and induce turbulence.
If we can make the assumption that the strong physiologic tendency in
normal relaxed respiration is to maximize the nasal airflow component,
it is evident that mechanisms must exist for the control of Oronasal
aerodynamics.
For 100% nasal respiration, an oral seal would be required. Similarly,
for 100% oral respiration a seal of the nasal passages somewhere between
the nares and the oropharynx would be necessary. For oronasal respira-
tion the existence of a combination of partial seals or valves that regulate
the direction and volume of air flow can be postulated.
Such mechanisms are not only possible, but have been observed clini-
cally. Figure 5 is a composite diagram illustrating the main features of
adaptive behavior which are capable of this regulatory function. The
existence of variations in the mode of producing an oral seal has been
previously postulated by Ballard ('62).
244
Vig
Figure 5. (A) Adaptation for anterior oral seal or valve production involving both
lip activity and mandibular posture. (B) A summary of orofacial adaptive possi-
bilities for the control of airflow. Additional adaptations such as craniocervical
posture are also possible.
The diagram in Figure 5 depicts the following variations in mechanism
by which the volume and direction of airflow are possibly regulated:
1. elevation of soft palate to form a seal with the posterior pharyngeal
wall;
2. contact between the dorsum of the tongue and the soft palate to
form a posterior oral seal or valve;
3. protrusion of the tongue (dotted outline) to contact dentoalveolar
structures in the anterior region of the mouth;
4. approximation of the lips with or without increased circumoral
muscle activity beyond the postural tone of the lips as determined by the
presence or absence of lip competence (the definition of which is that
when the mandible is in the rest position and the circumoral muscles are
at rest, the lips are parted);
5. the posturing of the mandible in the direction of the arrows which is
sometimes seen in conjunction with the the mechanisms described in 3
and 4.
In addition to these variations in regulatory mechanisms of airflow
direction and volume, other postural elements may also contribute signifi-
cantly to the preservation of the post-lingual airway. The variations in

245
Respiratory Mode and Morphological Types
craniocervical (natural head) posture described by Solow and Tallgren
('77) in adults and Thompson and Vig (79) in growing children may also
arise for respiratory reasons. Correlations between cranial extension-
flexion and the vertical development of the facial skeleton and dentoal-
veolar structure has been noted in both these studies.
Of all the physiologic activities in which the orofacial complex partici-
pates, respiration is the most essential, being vital for survival. To remain
viable one must accommodate successfully both to the constantly chang-
ing morphology which occurs at a relatively slow rate during growth and
development years and to immediate and temporary environmental
changes. Both call for reflex responses to altered respiratory require-
ments, which, unless incompatible with survival, will produce abnormal
compensatory morphogenesis (such as that seen in the nasally obstructed
monkeys of Harvold, '73). *
It is, therefore, considered a biologic necessity, which incidentally
confers evolutionary advantages for man, to have at his disposal such
alternative methods of regulating the direction and volume of airflow as
have been described. Considering the extent of variability in the pattern
of orofacial form in human populations, it is not at all surprising to find
such concomitant diversity in the variations of muscle behavior which
control the position of the mandible, lips, tongue and cranium. Such
variations in muscle activity may be seen as morphogenetic influences in
growing bone. The suggestion of such biophysical stimuli as morphoge-
netic influences is in agreement with the experiments of McNamara and
colleagues (75), who demonstrated altered growth patterns in response
to induced changes in muscle activity.
From the preceding discussion, it is feasible to formulate a general
hypothesis regarding respiration. In normal or relaxed respiration, pos-
tural adaptations in each individual act to maintain both the maximal
nasal component of respiration and the patency of the post-lingual airway
by facilitating maintenance of optimum aerodynamic efficiency through
operation of valving mechanisms. The maintenance of such adaptive be-
havior patterns is reflexly reinforced through continuous feedback mech-
anisms which are sensitive to the rate and volume of airflow, as well as
the organism’s total respiratory requirements.
A result of such an organizational scheme would be that the muscula-
ture of the orofacial, pharyngeal and craniocervical complex would be, at
all times, in a state of muscle activity over and above that which is simply
required to resist the force of gravity. Such a heightened state-of-tone
beyond the minimum electrical activity of a true resting posture, would
provide a long-acting, low-level biophysical stimulus for a morphogenetic
effect to occur. This influence on the growing bones of the face, as well as
the developing dentition, is analogous in principle with that produced by
246
Vig
functional appliances such as activators or the “function regulator” of
Fränkel.
For example, a relatively common mode of adaptive behavior employs
a down and forward mandibular posture with the tongue resting over the
lower teeth producing a seal or valve either by circumoral contraction or
anterior tongue contact. Such a combination of sustained and constantly
repeated postural adaptations could explain a number of morphologic
trends that occur during growth. The excessive posterior dentoalveolar
development in the maxilla while mandibular eruption is opposed would
lead to a relatively greater down and mesial movement of maxillary buc-
cal teeth. This in turn would create a Class II molar relationship and
coincidentally produce a higher palatal vault as measured from the occlu-
sal surfaces of the teeth. Excessive posterior eruption in the maxilla
would also contribute to a clockwise rotation of the mandible, tending to
create skeletal post-normality and increased gonial and mandibular plane
angles.
In a patient with such morphologic characteristics, the appropriate
appliance indicated would be an activator or Fränkel appliance. The
purpose of these appliances is to reverse such growth patterns. Hence, a
correctly designed appliance would prevent further eruption of the max-
illary posterior teeth and allow the mandibular posterior teeth to erupt
unimpeded. A forward postured activator bite would also diminish the
anterior growth of the maxilla while holding the mandible in a forced
forward position. Differential control of vertical eruption of the poste-
rior teeth would effect an auto-rotation of the mandible and result in
mandibular growth being expressed more in the horizontal than vertical
VeCtOr.
The retroclination of lower incisors which is seen when the mandible
rotates downward and backward, is corrected by altering the resting
lower lip's relation to these teeth. This results from a combination of
forward mandibular auto-rotation diminishing the anterior lower face
height and from muscle stretching if the lip pads of a Fränkel appliance
are used.
These hypothetical considerations seem compatible with a body of ob-
served fact and may be useful in explaining certain aspects of etiology and
treatment effects. But how does such a postulate explain stability of treat-
ment results after the removal of appliances when normal respiration is
resumed? For this, it is necessary to assume that the following two factors
come into play. First, growth would have to favor respiratory modes
compatible with the morphology produced by treatment. The growth of
the lips, which seems to occur both later than and to a greater amount
than the lower facial height (Vig and Cohen, '79), tends to reduce lip
incompetence. Facilitation of anterior oral seal production would thus
247
Respiratory Mode and Morphological Types
tend to minimize the need for other adaptive strategies for the production
of nasal respiration. This and other accommodations in adaptive postural
requirements for maximal nasal respiration to a new skeletodental envi-
ronment would promote orthodontic stability. Failure of this to occur
would result in long-term orthodontic relapse which would be the individ-
ual’s price for continued respiratory efficiency and, hence, survival.
Although much of the preceding argument is speculative, it hopefully
provides a basis for the formulation of testable hypotheses. Even though
respiratory mode may act as an invisible activator, it is no longer an
intangible. The orthodontic tradition of diagnosis based on static analysis
is epitomized by the endeavors of the Rocky Mountain Data Systems,
Inc. Indeed, Schulhof (78) maintains that a mere seven measurements
from a cephalometric radiograph can..determine which is the appropriate
choice of treatment, complete or partial adenoidectomy, palate separa-
tion or allergy treatment. Modern instrumental techniques are available
for quantitative studies of airflow dynamics. The recognition of postural
adaptations as a significant morphogenetic influence suggests the need for
a more dynamic approach to the diagnosis of craniofacial anomalies.
Considerably more convincing evidence for the need or the benefits of
surgical intervention to improve nasal respiration is necessary before
these procedures should be endorsed.
REFERENCES
Ballard, C. F. The clinical significance of innate and adaptive postures and motor
behavior. Dent. Pract. 219–227, 1962.
Bloch, E. Der hohe Gaumen. Ztschr. f. Ohrenh. v. f. Krankh d. Luftwege. 44:1,
1903.
Brash, J. C. The aetiology of irregularity and malocclusion of the teeth. The
Dental Board of U. K., London, pp. 207-217, 1956.
Harvold, E. P., K. Vargervik and G. Chierici. Primate experiments on oral
sensation and dental malocclusion. Am. J. Orthodont. 63:494-508, 1973.
Harvold, E. P. Experiments in mandibular morphogenesis. In: Determinants of
Mandibular Form and Growth, J. A. McNamara, Jr. (ed.), Center for Human
Growth and Development, Monograph No. 4, Craniofacial Growth Series,
University of Michigan, Ann Arbor, 1975.
Hastings, S. and W. James. Discussion on mouthbreathing and nasal obstruction.
Proc. Roy. Soc. Med. 25:1943-1947, 1932.
Humphrey, H. F. and B. C. Leighton. A survey of anteroposterior abnormalities
of the jaws of children between the ages of two and five and a half years of
age. Brit. Dent. J. 88:3, 1950.
Leech, H. L. A clinical analysis of orofacial morphology and behavior of 500
patients attending an upper respiratory research clinic. Dent. Practit. 9:57-68,
1958.
248
Vig
Linder-Aronson, S. Adenoids: Their effect on mode of breathing and nasal air-
flow and their relationship to characteristics of the facial skeleton. Acta Oto-
Laryngol. Suppl. 265, pp. 118-127, 1970.
Linder-Aronson, S. Naso-respiratory function and craniofacial growth. In: Naso-
respiratory Function and Craniofacial Growth, J. A. McNamara, Jr. (ed.),
Monograph No. 9, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, 1979.
Linder-Aronson, S. and D. G. Woodside. The growth in the sagittal depth of the
bony nasopharynx in relation to some other facial variables. In: Naso-respira-
tory Function and Craniofacial Growth, J. A. McNamara, Jr. (ed.), Mono-
graph No. 9, Craniofacial Growth Series, Center for Human Growth and
Development, The University of Michigan, Ann Arbor, 1979. •
McKenzie, D. Adenoids, deformities of the palate and artificial infant feeding.
An analysis of 222 cases. Brit. Dent. J. 30:159-165, 1909.
McNamara, J. A., T. G. Connelly and M. C. McBride. Histologic studies of
temporomandibular joint adaptations. In: Determinants of Mandibular Form
and Growth, J. A. McNamara, Jr. (ed.), Monograph No. 4, Craniofacial
Growth Series, Center for Human Growth and Development, The University
of Michigan, Ann Arbor, 1975.
Meyer, W. On adenoid vegetations in the naso-pharyngeal cavity, their pathol-
ogy, diagnosis and treatment. Med. Chir. Trans. (London), 53:191, 1870.
Montgomery, W., P. S. Vig, P. Jaques and S. R. Matteson. Rapid maxillary
expansion effects on nasal cavity computed tomography study. IADR;
58:1248, 1979.
Montgomery, W., P. S. Vig, E. V. Staab and S. R. Matteson. Computed tomog-
raphy: A three-dimensional study of the nasal airway. Am. J. Orthodont.
76:363-375, 1979.
Morrison, W. W. The interrelationship between nasal obstruction and oral defor-
mities. Int. J. Orthodont. 453-458, 1931.
Quinn, G. Deformity of the face, jaws and dentition: A preventable disease nasal
obstruction. N. C. Dent. J. 61:14, 1978.
Rasmus, R. L. and R. M. Jacobs. Mouth breathing and malocclusion: Quantita-
tive technique for measurement of oral and nasal airflow velocities. Angle
Orthodont. 39:296-300, 1969.
Ricketts, R. M. On early treatment (Part 1). J.C.O. Interviews. J. Clin. Ortho-
dont. 13:23–38, 1979.
Solow, B. and A. Tallgren. Dentoalveolar morphology in relation to craniocervi-
cal posture. Angle Orthodont. 47:157-163, 1977.
Subtelny, J. D. The significance of adenoid tissue in orthodontia. Angle Ortho-
dont. 24:59–69, 1954.
Schuloff, R. J. Consideration of airway in orthodontics. J. Clin. Orthodont.
12:440-444, 1978.
Thompson, B. and P. Vig. Associations between craniofacial morphology, inter-
maxillary space variables and head posture. IADR, 57:1253, 1979.
Vig, P. and A. M. Cohen. Vertical growth of the lips: A serial cephalometric
study. Am. J. Orthodont. 75:405-415, 1979.
249
Respiratory Mode and Morphological Types
Warren, D. W. Aerodynamic studies of the upper airway: implications for
growth, breathing and speech. In: Naso-respiratory Function and Craniofacial
Growth, J. A. McNamara, Jr. (ed.), Monograph No. 9, Craniofacial Growth
Series, Center for Human Growth and Development, The University of Michi-
gan, Ann Arbor, 1979.
Watson, R. M., D. W. Warren and N. D. Fischer. Nasal resistance, skeletal
classification and mouth breathing in orthodontic patients. Am. J. Orthodont.
58:367-379, 1968.
Wertz, R. A. Changes in nasal airflow incident for rapid maxillary expansion.
Angle Orthodont. 38:1-11, 1968.
250
THE ROLE OF TONSILS AND ADENOIDS IN THE
OBSTRUCTION OF RESPIRATION
Charles D. Bluestone M. D.
Department of Otolaryngology
University of Pittsburgh
It is estimated that approximately 700,000 Americans underwent surgery
to remove their tonsils, adenoids or both during 1977 (Professional Activ-
ity Study, 1979). More than half of these patients had both their tonsils
and adenoids removed, about one third had only their tonsils removed,
and 10 percent had only their adenoids removed. Despite a steady decline
in the frequency of tonsillectomies, adenoidectomies and the two com-
bined procedures during the past 10 years (Fig. 1), they are still the most
common major surgical operations performed in this country. This de-
cline is reflected primarily by the lower number of combined procedures
(tonsillectomies with adenoidectomies) which decreased more than 50
percent. During the same period, the number of tonsillectomies alone
changed little, and although the number of adenoidectomies performed
without tonsillectomies remained relatively small in comparison to the
number of the combined procedures, there was a significant increase in
their number. It is estimated that about one-fourth of all children have
had one or both procedures performed, and these operations represent
approximately half of all major surgical operations in the pediatric age
group. Over 75 percent of tonsil/adenoid operations are performed on
children of less than 15 years of age, and 60 percent on children under six
years of age; the modal age of children undergoing this type of Surgery is
five years (National Center for Health Statistics, 1974). Tonsillectomy in
combination with adenoidectomy is more common in boys, but twice as
many females as males undergo tonsillectomies alone, perhaps because
this procedure is primarily performed on adolescents and adults.
INDICATIONS FOR SURGERY
Despite the frequency with which tonsillectomies and adenoidectomies
are performed, it has never been established through controlled scientific
studies that the health benefits of tonsillectomy/adenoidectomy exceed
their cost in any age group. The Ad Hoc Committee on Tonsillectomy
and Adenoidectomy agreed (on the basis of clinical reasoning, not on the
251
Tonsils and Adenoids

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TONSILLECTOMY
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Figure 1. Frequency of tonsillectomies and adenoidectomies in all United States
non-federal short-term hospitals (Professional Activity Study, 1979).
basis of data from controlled studies) that tonsil and adenoid surgery was
“certainly indicated” only for alveolar hypoventilation due to airway ob-
struction caused by tonsils/adenoids, or for dysphagia and weight loss for
six months or more due to tonsillar obstruction of the digestive tract (Blu-
estone et al., '75). These “certain” criteria for tonsillectomy and adenoi-
dectomy are met by only a tiny fraction of the children undergoing these
procedures. Other conditions were considered “possible” indications for
surgery, but there was insufficient evidence to reach a final conclusion.
Thus, the vast majority of children who have undergone tonsil/adenoid
surgery have problems or symptoms, the favorable response of which to
surgery is, at best, uncertain and controversial. While the procedures in
question can probably be justified for use in an appreciably larger number
of children than can be categorized as having “certain” indications for
surgery, there are no data from which conscientious physicians could de-
velop guidelines for performing, or not performing, surgery.
Tonsillectomy and adenoidectomy, either in combination or separately,
are most frequently performed to correct the following conditions: 1)
recurrent or chronic throat infection or, more specifically, pharyngoton-
sillitis; 2) hypertrophy and; 3) recurrent attacks of acute otitis media or
chronic otitis media with effusion.
Accurate incidence and prevalence rates for these conditions have not
been reported; however, some information is available. Upper respiratory
tract infections are the most common of all acute medical conditions. Chil-
dren under six years of age suffer twice as many attacks per child per year
as does the population as a whole, the number being somewhat higher in
252
Bluestone
girls than in boys (National Center for Health Statistics, 1973). McCam-
mon ('71), in a study of the natural history of respiratory infections and
their variations by age, reported that the occurrence of upper respiratory
infection peaked between the ages of one and six years and significantly
declined thereafter in both sexes. However, no data are available on the
prevalence, incidence and natural history of pharyngotonsillitis.
The precise prevalence of hypertrophy of the tonsils and adenoids also
is not known. One survey reported that although the condition is more
common among younger age groups, 15 percent of persons aged 20 to 25
years have enlarged tonsils. Hypertrophy of the tonsils and adenoids is
more common in boys under six years of age than in girls, but hypertro-
phy of the tonsils is twice as common in adult females as in adult males
(National Center for Health Statistics, 1973).
Otitis media is the most commonly diagnosed disease of childhood next
to upper respiratory infection. It is almost certainly the most prevalent
due to its propensity to become chronic (McEldowney and Kessner, '72).
Children under 10 years of age are at particular risk of suffering from
otitis media; the highest prevalences is seen in children six to 18 months
and four to six years of age (Solomon and Harris, '76). It would appear
from these data that the incidence and prevalence of the most common
conditions - hypertrophy of the tonsils and adenoids, upper respiratory
infections and otitis media - for which the tonsil and adenoid operations
are performed, decrease as a function of age after the age of six years.
There have been five prospective clinical trials of tonsillectomy and
adenoidectomy: one conducted in Rochester, New York, in the 1920's
(Kaiser, '30); three in England in the 1960's (McKee, '63a, '63b; Mawson
et al., '67, '68; and one reported from New Zealand in 1970 (Roydhouse,
'70).
All of these studies, unfortunately, suffered from one or more short-
comings in design or method. Among these were: failure to classify pa-
tients according to severity of disorder; nonrandom selection of subjects
to be operated upon; failure to distinguish between the effects of tonsil-
lectomy, adenoidectomy, and tonsillectomy with adenoidectomy, respec-
tively; limited follow-up; and lack of sophistication in the detection of
middle ear disease. More limiting than any of these shortcomings, how-
ever, was the fact that, as a group the studies explicitly excluded from
consideration children most severely affected by tonsil and adenoid re-
lated conditions, and instead, tested the efficacy of tonsillectomy and
adenoidectomy in children whose indications of need for these procedures
were questionable or at best unimpressive. In these mildly affected chil-
dren, the following results of tonsillectomy and adenoidectomy were re-
ported: (1) a measurable, but not striking, reduction in the incidence
and/or severity of throat infections (Kaiser, '30; McKee, '63a, ’63b;
253
Tonsils and Adenoids
Mawson et al., '67, '68; Roydhouse, '70); (2) some reduction in mouth-
breathing (Mawson, '68); (3) a modest reduction in the incidence of otitis
media reported in some studies (McKee, '63a, '63b) but no reduction in
others (Kaiser, 30; Mawson et al., '67; Roydhouse, '70).
No prospective, controlled clinical trial of tonsillectomy or adenoidec-
tomy in severely affected children has been reported to date. Nor are data
available on such children who have been treated only medically, or not
treated at all. It may be fairly concluded, therefore, that in most of the
conditions for which tonsillectomy/adenoidectomy may be performed, the
decision must be based either on unwarranted interpretations of the re-
Sults of existing studies, or on personal opinion or experience. Similarly,
it seems apparent that some of the decisions against operating also lack
Scientific support or stem from prejudice against tonsillectomy/adenoidec-
tomy engendered by the seemingly excessive performance in the past of
Such procedures.
THE PITTSBURGH STUDY
In order to determine the indications for performing tonsillectomy/
adenoidectomy, a prospective clinical study of these two surgical proce-
dures, initiated in 1971 (Jack L. Paradise, Principal Investigator), is cur-
rently in progress at the Children's Hospital of Pittsburgh. The investiga-
tors are attempting to answer the following major questions related to the
indications for performing tonsillectomy and adenoidectomy: (1) Does
tonsillectomy reduce the incidence of recurrent throat infections; (2) does
adenoidectomy relieve nasal obstruction; (3) does adenoidectomy prevent
recurrent or persistent otitis media with effusion and; (4) what is the
effect of obstructing adenoids on, and their subsequent surgical removal
on, cranio- and dentofacial morphology? Severely affected children are
the focus of this study. Patients are operated upon promptly if they have
urgent indications for surgery. The first of these indications is severe
upper airway obstruction associated with alveolar hypoventilation (abnor-
mal levels of arterial blood pC), and pCO2, sometimes found only during
sleep), with or without cor pulmonale leading to hypersomnolent obstruc-
tive sleep apnea. Depending upon the respective size and anatomic rela-
tionships of the tonsils and/or adenoids, this condition may call for either
tonsillectomy or adenoidectomy, or both.
The second condition indicating an urgent need for surgery is tonsillar
enlargement sufficient to cause significant difficulty in Swallowing; in
these instances tonsillectomy is the only treatment indicated, although
only a few children are so categorized. In the majority of children these
conditions are not present, and there is no urgent need for their tonsils
and/or adenoids to be removed. Stringent surgical criteria must be met, .
254
Bluestone
For Recurrent For Persistent For Otitis Media
Throat Infection Nasal Obstruction with Effusion
Tonsillectomy Minimum frequency:
3/yr for 3 yrs
Or
5/yr for 2 yrs
Or
7 in one yr
Clinical features Jº
(at least one):
Fever > 38.3°C
(101°F)
Tonsillar exudate
Enlarged (> 2cm)
and/or tender
cervical nodes
Positive Group A
beta hemolytic
streptococcus
Documented
Adenoidectomy Clinical & radio- Recurrent or per-
graphic evidence sistent otitis
of adenoid enlarge- media with
ment, and effusion, and
Manifested by mouth- Myringotomy and
breathing, hypo- insertion of
nasal speech, or tympanostomy
obstructive sleep tube must have
apnea, and been performed
Apparently not due at least once
to allergy previously
Table 1. Criteria for entry into the Children's Hospital of Pittsburgh clinical trial.
therefore, before either or both of these procedures is performed on
these children. Children who satisfy the criteria are, subject to parental
consent, assigned randomly to surgical or control groups.
Table 1 summarizes the major criteria employed in the Pittsburgh study
for tonsillectomy and adenoidectomy. Tonsillectomy is considered to be
of possible benefit when either of the following conditions is present.
1. Recurrent tonsillitis. This is defined by a history of at least seven
episodes in the preceding year, or five episodes in each of the last two
~,
255
Tonsils and Adenoids
years, or three episodes in each of the last three years. These illnesses
must have been confirmed by clinical observation and must have been
characterized by either a fever of 101°F or more, or a positive culture for
Group A beta-hemolytic Streptococcus, or enlarged, tender cervical
lymph nodes. All or most of the episodes must also have been treated
with antibiotics.
2. Chronic tonsillitis. This is defined as tonsillitis persisting for at least
six months despite intensive antibiotic therapy.
The patients are examined by the pediatricians and otolaryngologists
involved in the study. Patient evaluation upon entry into the study in-
cludes a history and physical examination, pedodontic examination, basic
allergy screening (nasal smears for eosinophils and a battery of skin tests
employing the common inhalants), nose and throat cultures, complete
blood count, lateral cephalometric roentgenogram of the head, speech
evaluation, audiometry, tympanometry, rhinometry and Eustachian tube
function test.
Each patient is examined by a nurse practitioner every six weeks and
every time there is an ear, nose or throat illness. The pediatrician and
otolaryngologist may also examine the child at these times, but every
child involved in the study is examined by a pediatrician at least every six
months. A trained interviewer telephones the parents of each patient
every two weeks to determine the child’s health status. In the projected
protocol, the total collection of data through 1982 (when the last entrants
will have been followed for three years) is expected to include 25,000
patient visits and 90,000 phone interviews.
The variation in the reliability of histories given by parents is well
known to clinicians, but unreliability of history is especially to be guarded
against when the patient is a tonsillectomy prospect. If the described
illnesses are not completely documented as meeting study criteria (and
they often are not), parents are told that the child will be followed and
further episodes observed before a decision is made as to whether surgery
is indicated. In some children the history of illness is confirmed, but in
many cases it is not, and an appreciable number of children have no
attacks of illness which would be treated by this type of surgery during
the long period of subsequent observation. During the course of the
study, 65 children with histories of recurrent throat infections that seemed
impressive and met all the criteria but lacked documentation were fol-
lowed (Paradise et al., '78). During the first year of observation, only 11
of the 65 children (17 percent) had episodes of throat infections with
clinical features and patterns of frequency conforming to those described
in their presenting histories. Of the remaining 54 children, 43 (80 percent)
experienced no, one or two observed episodes, and most of the episodes
were mild. Only 22 were followed for a second year. Of these, one
256
Bluestone
became eligible because of recurrent throat infections, two because of
Symptoms of upper airway obstruction, seven experienced no episodes of
throat infection, seven had one episode each, and five had two episodes
each. Undocumented histories of recurrent throat infection do not validly
forecast the clinician's subsequent observations and should not constitute
the basis for subjecting children to tonsillectomy.
It is too early in the study to draw even tentative conclusions concern-
ing the efficacy of tonsillectomy in those children who have been ran-
domly assigned to undergo this procedure. This is because the number of
patients in the various clinical categories is small, and the follow-up pe-
riod is still relatively short. However, the preliminary data appear to
show that a substantial proportion of those children who met the rather
strict criteria for but who did not have tonsillectomies, had few throat
infections, and virtually all of the children who had tonsillectomies expe-
rienced very little morbidity from throat infections. However, there is no
way at present to predict whether a particular child who meets the criteria
for tonsillectomy will do well if the operation is performed or poorly, if it
is withheld.
Adenoidectomy is considered of possible benefit to, and was performed
on a randomized basis on, children who had one or more of the following
conditions present.
1. Persistent nasal obstruction due to enlarged adenoids. Clinical and
radiographic evidence must show that the adenoids are the cause of the
obstruction and not allergy. The nasal obstruction must result in mouth-
breathing most or all of the time and in hyponasal speech (characterized
by little air passing through the nose).
2. Recurrent otitis media with effusion. This must have been treated at
least once previously by myringotomy and insertion of a tympanostomy
tube; allergic rhinitis must be absent.
A preliminary analysis of the effect of adenoidectomy on nasal obstruc-
tion in children who had no apparent allergies indicates that during a
two-year postoperative observation period, there was significant improve-
ment in functioning of the nasal airway and in speech, compared with
control group subjects (Paradise et al., '78).
It is not clear whether adenoidectomy has any positive effects on chil-
dren with middle ear disease. Following adenoidectomy, middle ear dis-
ease is not eliminated but continues to be a significant problem in many
children. The effects of adenoidectomy in treating otitis media with effu-
sion must be evaluated by observation of a larger population over an
appreciable period of time. The following variables are being examined to
determine whether or not they effect the outcome of the adenoidectomy
that is performed to relieve middle ear disease: age, sex, race, allergy,
adenoid size and Eustachian tube function.
257
Tonsils and Adenoids
Degree of Obstruction
Intermittent Known Cardiorespiratory Possible or Potential
or Persistent - Complications Complications and Sequelae
Effect on Pulmonary Venti-
lation
Mild Hypersomnia Obstructive Effect on Cranio- and Dento-
Sleep Apnea facial Morphology
Abnormal Speech
Moderate Alveolar Hypoventila- Decreased or Absent Olfac-
tion tion
Retardation of Growth and
Development
Cor Pulmonale Nasal and Paranasal Sinus
Disease
Severe Middle Ear Disease
Other, e.g., Cognition, Lan-
guage, School Performance,
and Psychosocial Abnormalities
Table 2. Classification of respiratory obstruction by the tonsils and/or adenoids.
CLASSIFICATION OF RESPIRATORY OBSTRUCTION DUE TO
- TONSILS AND ADENOIDS
It is apparent from the foregoing review of the indications for the
surgical removal of the tonsils and adenoids that a great many of the
operations are being performed to relieve hypertrophy of the adenoids
and/or tonsils and, therefore, presumably to relieve obstruction of the
respiratory tract. However, the benefit of these operations for the vast
majority of such patients remains moot (Paradise, '72).
In order to evaluate a patient properly for clinical or investigative
purposes, it is valuable to establish a system for classifying the degree to
which the tonsils and/or adenoids obstruct the airway. Table 2 presents a
classification system which is derived from experience gained in Pitts-
burgh and from a review of the literature. Respiratory obstruction can
occur in the nasopharynx as a result of adenoids that are too large for the
space they must occupy, or in the oropharynx as a result of tonsils that
258
Bluestone
are too large, or in both at the same time The obstruction can be inter-
mittent, which is usually the case when it is caused by an acute inflamma-
tion, (infection, allergy, or both), or it can be persistent (possibly, but not
necessarily, due to chronic inflammation).
Obstruction which is not associated with a known severe complication
or sequela is arbitrarily classified as mild, moderate or severe. Mild ob-
struction is characterized by mouthbreathing, stertor (snoring) and distor-
tion of speech. Hyponasal speech is the result of obstructing adenoids,
whereas muffled or “hot potato” speech is associated with tonsil obstruc-
tion. In addition to a greater degree of severity of the signs and symptoms
which characterize the mild form, moderate respiratory obstruction in-
cludes disturbance of sleep. Parents usually describe the child’s sleep as
being restless and possibly including short periods of cessation of breath-
ing. Severe obstruction is not only marked by more pronounced degrees
of the signs and symptoms noted in moderate obstruction, but also by
periods of obstructive sleep apnea.
There are three known serious complications attributed to obstruction
of the upper airway by the tonsils/adenoids, and all three affect the car-
diorespiratory tract. They are: (1) hypersomnolent obstructive sleep ap-
nea syndrome; (2) alveolar hypoventilation and; (3) cor pulmonale.
In addition to the above cardiorespiratory complications, varying de-
grees of intermittent or persistent obstruction may cause other potential
complications or sequelae, including inadequate pulmonary ventilation;
malformations of dento- and craniofacial structures; difficulties or abnor-
malities in speech, olfaction, and growth and development of the nose,
paranasal sinus and middle ear. Impaired cognition, language develop-
ment, school performance, and psychosocial development may be secon-
dary effects of upper airway obstruction.
FACTORS INFLUENCING THE DEGREE OF OBSTRUCTION
In the foregoing discussion, the terms “hypertrophy”, “hyperplasia” or
“enlarged tonsils or adenoids” have not been used purposely to describe
the pathophysiology of the obstruction problem, but rather to identify the
frequent diagnosis made by physicians as an indication for the need of
their removal. The actual size of these structures may be important, but
the degree of obstruction is primarily related to the size of the tonsils and
adenoids relative to their surrounding compartment (bone and soft tis-
Sue). In addition, this relationship is not static but dynamic, since patho-
logic as well as physiologic conditions can alter the degree of obstruction.
Recurrent or chronic inflammation of the tonsils, adenoids or surround-
ing tissue can cause or increase the degree of obstruction. An acute
rhinitis in association with only moderately obstructing adenoids can re-
259
Tonsils and Adenoids
Sult in a marked decrease in nasal airflow. Body position may also affect
the degree of obstruction. Recumbency in general, and the supine posi-
tion in specific appear to increase upper airway obstruction. This has
been attributed to the collapse of the oropharyngeal soft tissue, e.g., soft
palate, constrictor muscles, and tongue, as well as to the collapse of the
tonsils against the posterior pharyngeal wall. Sleep appears to compound
the problem further as relaxation of the soft tissues occurs. Some indi-
viduals appear to have more collapse than others, the reasons for which
remain obscure.
Anatomic factors can affect the degree of obstruction. A given adenoid
mass may not affect nasal airflow in the nasopharyngeal cavity of one
child, but in another child, even of the same age, height and weight, it
could cause significant obstruction if the nasopharynx were smaller. Cer-
tain types of craniofacial malformations, such as Down's syndrome, re-
present the extreme forms of this respiratory compromise because of the
relationship in these cases between the tonsil/adenoid mass and the space
it occupies. Children who have Down's syndrome can have a severe ob-
struction present in the nasopharynx and/or oropharynx, even though
their tonsils and/or adenoids are small, simply because the space that
these structures must occupy is not large enough due to its unusual ge-
ometry. Many children who do not have a recognized craniofacial malfor-
mation may still have varying degrees of micrognathia which can cause
severe oropharyngeal obstruction even when the tonsils are small.
Anatomic variation of the position of the tonsils can also create an
obstruction; for instance, severe oropharyngeal obstruction may occur
when the tonsils are pedunculated (i.e., most or all of the tonsil lies
within the oropharynx). Another child may have tonsils of an identical
size to those described above, but these tonsils, if deeply imbedded in the
tonsillar fossa and, thus, barely visible behind the anterior pillar, make
respiratory obstruction unlikely. An anatomic deformity of the nasal cav-
ity (e.g., septal deviation, choanal stenosis), when associated with an
adenoid mass, could result in respiratory obstruction, when either one
alone would not.
METHODS OF ASSESSING DEGREE OF RESPIRATORY
OBSTRUCTION
A thorough history and physical examination is the best way of evaluat-
ing the degree of respiratory obstruction caused by the tonsils and/or
adenoids. The history should establish not only the presence or absence
of the important signs and symptoms of obstruction, but also the severity,
duration and frequency of the obstruction. It should also include as com-
plete a description as possible of the child’s sleep habits. The signs and
260
Bluestone
symptoms that are associated with upper airway obstruction and compli-
cations are stertor (snoring), mouthbreathing, distortion of speech, hy-
persomnia, headaches, fatigue, lethargy, mood and behavior changes,
hyperactivity, respiratory tract infection, recent extreme weight gain,
restlessness, and apneic episodes during sleep, periods of cyanosis, dysp-
nea, Somnambulance, Orthopnea, insomnia, nightmares, diaphoresis, and
difficulty in awakening.
The physical examination should not only include an assessment of the
head and neck, but also of the entire body, with special emphasis placed
on the chest, abdomen and extremities, since a cardiorespiratory compli-
cation may be present. The appearance of the face and the presence of
mouth-breathing are of particular importance. Observation of the child in
both the sitting and supine position is an important part of the examina-
tion, since signs and symptoms of respiratory obstruction may only be
manifested when the child is lying flat on his back. Examination of the
adenoids is somewhat difficult but can usually be accomplished by direct
inspection through the nasal cavities. This procedure may require a topi-
cal decongestant if significant nasal Swelling is present. A nasal speculum
and a headlight or head mirror should ideally be used in such an examina-
tion, but the nasal speculum attachment to the otoscope is acceptable. If
the posterior nasal choanae can be seen and if the adenoids are causing
an obstruction, they can frequently be seen to protrude into the posterior
nasal cavity during swallowing. The nasal cavities should be examined to
determine the presence or absence of significant pathology, such as nasal
allergy or polyps. If the adenoids cannot be seen by routine direct inspec-
tion, then a right-angle nasopharyngeal mirror should be used through
the mouth. Recently developed instruments such as the right-angle tele-
Scope and the flexible fiberoptic nasopharyngoscope, which are used to
examine the posterior nasal space, are particularly helpful when the con-
ventional techniques are not successful.
When examining tonsils, their size in relation to the size of the oropha-
rynx can be classified conveniently in the following way: 1+ the tonsils
are not visible behind the anterior pillar, 2+ the tonsils are visible just
beyond the pillar, 3+ the tonsils are almost touching, and 4+ the tonsils
meet in the midline.
Speech also should be assessed to determine if it is either hyponasal or
muffled, or both. Markedly hyponasal speech lacks resonance and sounds
the same whether the nares are open or pinched closed by the examiner.
Less severe hyponasality is harder to judge but can be graded as no, mild,
or moderate hyponasality. Speech recordings are usually needed to clas-
Sify the degree of hyponasality.
Roentgenographic films used to detect adenoid obstruction are best
when obtained in three dimensions: lateral, posteroanterior and submen-
261
Tonsils and Adenoids
Figure 2. Submental vertex roentgenogram of child who had nasal obstruction
Secondary to adenoids (arrow) completely obstructing the patient’s nasal choanae.
tal vertex (Fig. 2). A small amount of radiopaque contrast material in-
stilled into the nose will further enhance the results obtained on film (Fig.
3). However, the combination of the clinical examination and a lateral
Soft tissue radiograph of the nasopharynx usually enables the clinician to
adequately evaluate the size of the adenoids and the degree of posterior
nasal obstruction. Pre- and postoperative roentgenograms are necessary
to determine whether or not sufficient adenoid tissue was removed (Fig.
4). Dynamic roentgenographic studies employing tele- or cineradiography
in three dimensions, with the addition of contrast material, have also
been advocated and are more precise than a single lateral view. In addi-
tion, speech recordings made at the same time that the clinical exams are
conducted and films taken should be used in this type of study. This is
currently the best method available for evaluating the relation between
Speech, adenoids and the velopharyngeal closing mechanism.
To determine the effect of adenoidectomy on craniofacial growth and
development, standardized cephalometric lateral roentgenograms should
be obtained and the patient followed for several years (Fig. 5). The tonsil
size in relation to the posterior pharyngeal wall can be evaluated on
lateral soft-tissue radiographs.
262

Bluestone
Figure 3. Lateral soft tissue roentgenogram of a child with nasal obstruction in
whom radiopaque contrast material was instilled through the nose to enhance the
assessment of the degree of adenoid obstruction.
263

Tonsils and Adenoids
Figure 4. Pre- and postoperative lateral soft tissue roentgenograms of a child who
received an adenoidectomy.
A chest roentgenogram should be obtained on any child in whom sig-
nificant upper airway obstruction is present to determine if the heart is
enlarged.
If a child is suspected of having hypersomnolent sleep apnea, the na-
ture, duration and degree of the respiratory irregularity during sleep can
usually be determined by clinical observation. However, monitoring the
child when asleep provides more accurate data and can include the use of
electroencephalograms, measurements of eye movements and muscular
activity, blood gas determinations and an electrocardiogram. Fiberoptic
nasopharyngoscopy and cinefluoroscopy also are helpful in determining
the site of the obstruction during sleep in patients with the obstructive
sleep apnea syndrome (Borowiecki et al., '78). For children who are
Suspected of having a cardiac complication, cardiac catheterization may
be required.
Nasal obstruction can be assessed more precisely by either passive or
active rhinometry, or both. These techniques document the degree of the
obstruction.
264

Bluestone
Figure 5. Example of a cephalometric lateral roentgenogram of a child who is
enrolled in the Pittsburgh study.
KNOWN CARDIORESPIRATORY COMPLICATIONS OF UPPER
RESPIRATORY OBSTRUCTION DUE TO TONSILS AND/OR
ADENOIDS
Only three complications of obstructing tonsils, or adenoids, or both
are known to cause serious cardiorespiratory problems. These are hyper-
Somnolent obstructive sleep apnea syndrome, alveolar hypoventilation
and cor pulmonale. In 1956, Burwell and co-workers first described fully
the Pickwickian syndrome in which the classic features are obesity, hyper-
Somnolence, alveolar hypoventilation and cor pulmonale. In 1959, Cole
and Alexander established the relationship between obesity, alveolar hy-
poventilation and pulmonary hypertension; and in 1965, Menasche and
co-workers first described cor pulmonale in two children who had ob-
Structing tonsils and adenoids; their symptoms included lethargy, adenoid
facies, dull appearance, mouth-breathing, hyponasal speech, excessive
265

Tonsils and Adenoids
sleep during the daytime, stertorous breathing, cyanosis, diaphoresis,
weight gain and elevated hematocrit. The alveolar hypoventilation, cor
pulmonale and heart failure were relieved by tonsillectomy and adenoi-
dectomy. Following these initial case reports, many similar cases reported
in the literature supported the existence of this clinical entity (Noonan,
'65; Luke et al., '66; Levy et al., '67; Gerald and Dungan, '68; Massumi et
al., '69; Gresham, '71). Ainger ('68) reported two deaths that occurred
among six children, all of whom had cor pulmonale and an obstruction
that was due to the tonsils and adenoids. The obstruction was not diag-
nosed in the two children who died. He also reported that the remaining
four children did not respond to conventional medical management of the
heart disease until either an artificial airway was created or the obstruct-
ing tonsils and/or adenoids were removed. McCartney and co-workers
(69) also described children with this complication and suggested that
they suffer from abnormal reactivity of the pulmonary vasculature to
hypoxia. They cautioned against the administration of oxygen to these
children or preoperative sedation prior to the surgical removal of the
tonsils or adenoids. Table 3 shows the sequence of events in the patho-
genesis of cor pulmonale starting with upper airway obstruction by tonsils
and adenoids, which has been modified after Cayler et al. ('59). Freeman
('73) described two children who had concurrent congestive heart failure
and obstructing adenoids resulting in cor pulmonale. Cardiac operations
to relieve the cyanosis, hypoxia and right ventricle failure were unsuccess-
ful until an adenoidectomy was performed. Edison and Kerth ('73) de-
scribed two children with cor pulmonale secondary to obstructing tonsils
and adenoids, one of whom had Down's syndrome. These authors
stressed the need for both a tonsillectomy and adenoidectomy in certain
patients, since one procedure alone may not relieve the obstruction. Stool
and co-workers ('77) described three children who were extremely obese
and who had upper airway obstruction due to tonsils and adenoids result-
ing in cor pulmonale. They have termed the condition the “chubby puf-
fer” syndrome and explained the pathophysiology as being a combination
of the Pickwickian syndrome and upper airway obstruction.
Some children do not have cor pulmonale but have the hypersomnolent
obstructive sleep apnea syndrome. Respiratory irregularities during sleep
have been defined by Guilleminault and colleagues ('76) as: (1) respira-
tory pause which is a cessation of airflow of less than 10 seconds; (2)
apneic episode or cessation of airflow for more than 10 seconds and; (3)
sleep apnea syndrome, defined as at least 30 episodes of apnea during a
seven hour period. However, other investigators use different criteria,
and this definition must be considered only preliminary at present. Apnea
has been divided into three types: (1) central apnea is purported to be
related to a failure of the respiratory center to initiate a respiratory effort;
266
BluestOne
Obstruction of the nasopharynx due to
adenoids and/or oropharynx due to tonsils
Increased upper airway resistance
Increased O2 cost of breathing
Decreased ventilatory capacity
Alveolar hypoventilation
Pulmonary vasoconstriction
(susceptible pulmonary vasculature)
Pulmonary hypertension
Right sided heart decompensation
Pulmonary edema
!
Congestive heart failure
Table 3. Pathophysiology of cor pulmonale due to tonsils and/or adenoids.
(2) obstructive (peripheral) apnea is related to upper airway obstruction
to airflow and; (3) mixed apnea is a combination of the central and
obstructive types. However, this classification is not definitive since the
etiology and pathophysiology of the sleep apnea problem in general re-
main poorly understood.
The severe form of the sleep apnea condition is seen in children with
obstructing tonsils/adenoids and is called the obstructive sleep apnea syn-
drome. It has the following signs and symptoms: hypersomnolence, ob-
structive sleep apnea, snoring, restlessness, Somnambulance, nocturnal
enuresis, insomnia, night terrors, morning headaches, easy fatigability,
mood and behavior disturbances, and hyperactivity. Some children with
obstructing tonsils/ adenoids can have alveolar hypoventilation, which can
only be determined by assessing the blood gases at night. Unfortunately,
just as we have no data on the sleep patterns of normal children during
Sleep, we have no data on the blood gas values of normal children during
sleep. Until these data become available, a pCO2 of more than 45 mg Hg
and a pCO2 of less than 87 mg Hg while a child is awake or asleep
267
Tonsils and Adenoids
be considered abnormal. The interrelationships between obstructive hy-
persomnolent sleep apnea, alveolar hypoventilation, and cor pulmonale,
require a great deal more investigation before we can speculate about the
pathophysiology involved.
In any event, it would appear that certain factors increase the risk of a
child developing one or a combination of these severe problems when
obstructing tonsils and adenoids are present. These would include the
factors, described previously, that influence the degree of obstruction, as
well as other factors such as pre-existing congenital heart disease (Fig. 6)
and Susceptible pulmonary vasculature. It has also been suggested that
obesity may contribute to the occurrence of cor pulmonale caused by
obstructing tonsils and adenoids, but the obesity may be related to the
hypoxia or lack of exercise or both. It has also been suggested that blacks
are more susceptible to these complications than whites, since many of
the cases reported in the past have been black children. However, it may
be that these children were not afforded adequate medical care when they
were less severely affected, rather than that they are more susceptible.
POTENTIAL COMPLICATIONS AND SEQUELAE
The serious cardiorespiratory complications described above represent
the only known complications of upper respiratory obstruction due to
tonsils and adenoids. There is no conclusive scientific evidence that respi-
ratory obstruction not associated with any of these complications is dele-
terious to the child. A serious concern is the effect of episodes of obstruc-
tive sleep apnea which are not of sufficient degree to result in the classic
stigmata of the hypersomnolent obstructive sleep apnea syndrome. In the
Pittsburgh study it is estimated that between 20 and 30 percent of parents
of children who have obstructing tonsils or adenoids describe their chil-
dren as having sleep irregularities including histories of sleep apnea of
varying duration and frequency. Just how many of these children actually
have sleep apnea and to what degree is not known. It would be interest-
ing, and perhaps enlightening, to know the blood gas compositions of
these patients. Until the problem is further investigated, a history of sleep
apnea in a child with obstructing tonsils and adenoids should be regarded
as a potentially serious problem and the child’s parents questioned re-
garding this possibility. An adequate physical examination, including an
examination of the child in the supine position, should also be included in
the evaluation, as should, if possible, observation of the child during
sleep.
A relationship between obstructing tonsils and adenoids and cranio-
and dentofacial anomalies has been suggested (Ricketts, '68) but remains
-- unproven. While both hyponasality and mouthbreathing may gradually
268
Bluestone
Figure 6. Child with Down's syndrome with obstructing tonsils and adenoids and
concurrent congenital heart disease who had hypersomnolent obstructive sleep
apnea Syndrome.
diminish with age as the adenoids atrophy, some orthodontists hypothe-
Size that mouthbreathing during childhood exerts a lasting influence on
the dentition and facial configuration and causes so-called “adenoid
facies.” Using cephalometric radiography, Linder-Aronson ('74) found
that children with large adenoids tended to have longer and narrower
faces, lower tongue placement, narrower upper jaws, steeper mandibles
and more open anterior bites than those with small adenoids. One year
after these children had undergone adenoidectomies, he observed a “nor-
malization” of their dentofacial measurements. However, a cause-and-ef-
fect relationship has not been established between large adenoids and the
presumably abnormal dentofacial findings, nor is it known whether con-
trol subjects not undergoing adenoidectomy would experience the same
“normalization” spontaneously. The Pittsburgh study may supply addi-
tional information on this question, since children with adenoid enlarge-
269


Tonsils and Adenoids
ment sufficient to cause hyponasality and mouthbreathing are being ran-
domly assigned to adenoidectomy or control groups and will then be
followed with periodic dental evaluations and cephalometric roentgeno-
grams for three years postoperatively.
The question of whether or not obstructing tonsils cause “tongue
thrust” which subsequently adversely affects dentofacial structures has
also not been answered. Like the adenoid-nasal obstruction problem,
there are no studies available to prove a cause-and-effect relationship
Unfortunately, the Pittsburgh study will not answer this question.
There is no question that obstructing tonsils and adenoids cause distor-
tion of speech (i.e., hyponasality or muffled speech), but whether there
are lasting effects from the distortion of speech is unknown. It appears
that speech normalizes after either surgical removal or spontaneous re-
gression of the tonsils and adenoids, but again this has not been deter-
mined scientifically. Hopefully, the Pittsburgh study will shed some light
on this question.
It has frequently been observed by parents that there is an apparent,
sudden and rapid growth spurt after the removal of the tonsils/adenoids.
This common observation has not been substantiated, but if it is true, it
could be related not only to relief of nasal obstruction, but to impaired
olfaction, chronic inflammation, or other as yet unknown factors as well.
Ghorbanian and colleagues (78) reported that children with nasal ob-
struction due to the adenoids had impaired olfaction, compared to chil-
dren who had relatively unimpaired nasal breathing. The effect of nasal
obstruction on the occurrence of nasal, paranasal sinus and ear disease
has not been determined, but there remains a possibility that there is a
relationship. The adverse affect that obstruction has on cognition, lan-
guage, school performance and psychosocial behavior may be related to
hypoxia and hypercarbia, but again there is no evidence to confirm such a
relationship.
CONCLUSION
Upper airway obstruction can be caused by the tonsils, adenoids, or
both, and can result in serious cardiorespiratory complications. However,
in the absence of such complications, the effect of respiratory obstruction
in cranio- and dentofacial growth and development remains to be shown.
Until this question is resolved, children with persistent nasal obstruction
due to adenoids, and not due to infection or allergy, would seem to
benefit from their removal, although this is based on quality-of-life rea-
sons at present since we have too little scientific evidence to support any
other reasons. The efficacy of removal of “hypertrophied” tonsils in the
hope of preventing or improving a dentofacial abnormality has not been
270
Bluestone
proven, which makes this condition an uncertain indication for tonsillec-
tomy. Further research into the relationship between obstructing tonsils
and adenoids and craniofacial morphology is needed and should be an
interdisciplinary effort.
REFERENCES
Ainger, L. E. Large tonsils and adenoids in small children with cor pulmonale.
Brit. Heart J. 30:356, 1968.
Bluestone, C. D. et al. Workshop on tonsillectomy and adenoidectomy. Ann.
Oto., Rhino. Laryngol. 84(Suppl. 19):1-79, 1975.
Borowiecki, B., C. P. Pollak, E. D. Weitzman et al. Fiberoptic study of pharyn-
geal airway during sleep in patients with hypersomnia obstructive sleep apnea
syndrome. Laryngoscope 88:1310-1313, 1978.
Burwell, C. S., E. D. Robin, R. D. Whaley and A. G. Bickelkiann. Extreme
obesity associated with alveolar hypoventilation: A Pickwickian syndrome.
Am. J. Med. 21:811–818, 1956.
Cayler, G., J. Mays and H. Riley. The Pickwickian syndrome in children. Am. J.
Dis. Child. 98:663, 1959.
Cole, V. N. and J. K. Alexander. Clinical effect of extreme obesity on cardiopul-
monary function. South. Med. J. 52:435, 1959.
Edison, B. D. and J. D. Kerth. Tonsilloadenoid hypertrophy resulting in cor
pulmonale. Arch. Otolaryngol. 98:205-207, 1973.
Freeman, W. J. Adenoid hypertrophy, cyanosis and cor pulmonale in children
with congenital heart disease. Laryngoscope 83:238–248, 1973.
Gerald, B. and W. T. Dungan. Cor pulmonale and pulmonary edema in children
secondary to chronic upper airway obstruction. Radiology 90:679-682, 1968.
Ghorbanian, S. N., J. L. Paradise and R. L. Doty. Odor perception in children in
relation to nasal obstruction. Ped. Res. 12:371, 1978.
Gresham, E. L. and J. G. Armstrong. Cardiac failure from tonsillar enlargement
- A reminder. Clin. Ped. 10:236-238, 1971.
Guilleminault, C., A. Tilkian and W. C. Dement. The sleep apnea syndromes.
Ann. Rev. Med. 27:465-484, 1976.
Kaiser, A. D. Results on tonsillectomy: A comparative study of 2,200 tonsillecto-
mized children with an equal number of controls three and ten years after
operation. JAMA 95:837-842, 1930.
Levy, A. M., B. S. Tabakin, J. S. Hanson and R. M. Narkewicz. Hypertrophied
adenoids causing pulmonary hypertension and severe congestive heart failure.
New Eng. J. Med. 277:506, 1967.
Linder-Aronson, S. Effects of adenoidectomy on dentition and nasopharynx. Am.
J. Orthodont. 65:1, 1974.
Luke, M. J., A. Mearizi, G. M. Folger and N. D. Rowe. Chronic nasopharyngeal
obstruction as a cause of cardiomegaly, cor pulmonale and pulmonary edema.
Ped. 37:762, 1966.
Massumi, R. A., R. K. Sarin, M. Pooya et al. Tonsillar hypertrophy, airway
271
Tonsils and Adenoids
obstruction, alveolar hypoventilation, cor pulmonale in twin brothers. Dis. Chest,
10:114, 1969.
Mawson, S. R., P. Adlington and M. Evans. A controlled study evaluation of
adenotonsillectomy in children. J. Laryngol. and Otol. 81:777-790, 1967.
Mawson, S. R., P. Adlington and M. Evans. A controlled study evaluation of
adenotonsillectomy in children. Part II. J. Laryngol. and Otol. 82:963-979,
1968.
McCartney, F. J., J. Panday and O. Scott. Cor pulmonale as a result of chronic
nasopharyngeal obstruction due to hypertrophied adenoids and tonsils. Arch.
Dis. Child. 44:585, 1969.
McCammon, R. W. Natural history of respiratory tract infection patterns in basi-
cally healthy individuals. Am. J. Dis. Child. 122:232-236, 1971.
McEldowney, D. and D. M. Kessner. Review of the Literature: Epidemiology of
the National Conference. Callier Hearing and Speech Center. A. Glorig and
K. S. Gerwin (eds.), Charles C. Thomas, Springfield, Ill., pp. 11-25, 1972.
McKee, W. J. E. A controlled study of the effects of tonsillectomy and adenoi-
dectomy in children. Br. J. Prev. Soc. Med. 17:49-69, 1963a.
McKee, W. J. E. The part played by adenoidectomy in the combined operation of
tonsillectomy with adenoidectomy: Second part of a controlled study in chil-
dren. Br. J. Prev. Soc. Med. 17:133-140, 1963b.
Menasche, V., C. Farrehi and M. Miller. Hypoventilation and cor pulmonale due
to chronic upper airway obstruction. J. Pediat. 67:198-263, 1965.
National Center for Health Statistics. Prevalence of Selected Chronic Respiratory
Conditions, United States, 1970; (DHEW Publication No. HRA-74-1151),
United States Department of Health, Eduction and Welfare, Rockwille, Md.,
1973.
National Center for Health Statistics. Surgical Operations in Short-Stay Hospitals,
United States, 1971 (DHEW Publication No. HRA-74-1769), United States
Department of Health, Education and Welfare, Rockwille, Md., 1974.
National Center for Health Statistics. Current Estimates from the Health Inter-
view Survey, United States, 1974 (DHEW Publication No. HRA-76-1527),
United States Department of Health, Education and Welfare, Rockwille, Md.,
1975.
Noonan, J. A. Reversible cor pulmonale due to hypertrophied tonsils and ade-
noids: studies in two cases. Circ. 32(Suppl. 2):164, 1965.
Paradise, J. L. Why T&A remains moot. Ped. 49:648-651, 1972.
Paradise, J. L., C. D. Bluestone, R. Z. Bachman et al. History of recurrent sore
throat as an indication for tonsillectomy: Predictive limitations of histories that
are undocumented. New Eng. J. Med. 298:409–413, 1978.
Professional Activity Study, Ann Arbor, Michigan (Personal Communication),
1979.
Ricketts, R. M. Respiratory obstruction syndrome. Am. J. Orthodont.
54:495-507, 1968.
Roydhouse, N. A controlled study of adenotonsillectomy. Arch. Otolaryngol.
92:611-616, 1970.
Solomon, N. E. and L. J. Harris. Otitis Media in Children: Assessing the Quality
272
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of Medical Care Using Short-Term Outcome Measures. Eight Disease-Specific
Applications. (Rand Report R-2021/2-HEW). Rand Corp., Santa Monica,
Calif., pp. 565-576, 1976.
Stool, S. E., R. D. Eavey, N. L. Stein and W. G. Sharrar. Upper airway obstruc-
tion and obesity, with intermittent somnolence, cardiorespiratory embarras-
ment and learning disabilities - a chubby puffer syndrome. Clin. Pediatr.
16:43-57, 1977.
*-**xr.
273
ALLERGIC RESPONSES IN THE UPPER
RESPIRATORY SYSTEM
William R. Solomon, M. D.
Department of Internal Medicine (Allergy)
The University of Michigan
Allergists suggested many decades ago that there might be an association
between prolonged nasal obstruction and maxillofacial abnormalities, in-
cluding open bite (Duke, '30; Balyeat and Bowen, 34; Todd et al., "39;
Marks, '65). However, their clinical successors only rarely pursued these
observations, and as a result, they have been mostly witnesses of, rather
than participants in, the recent progress that has occurred in this field.
Considering this role, I will focus the present discussion strictly on the
nature and the evaluation of allergic nasal problems. If the result is a
digression, it is still a relevant one, since allergic rhinitis remains a major
Source of prolonged nasal blockage during formative years.
ALLERGIC RHINITIS
The occurrence and impact of nasal allergy was recognized first in
persons with dramatic seasonal symptoms or “hay fever.” This term is
used when observation reveals typical nasal pruritus (itching) and ob-
struction, repetitive sneezing and rhinorrhea, and ocular itching and in-
flammation, occurring as a result of exposure to hay fields flowering in
early summer. Grass pollen soon was implicated as the specific offender,
and the production of typical symptoms during experimental pollen expo-
sures in winter confirmed its role. (The term “hay fever” today is used
generically to denote seasonal allergic rhinitis.) Further observations dis-
closed that there were many people suffering from hay fever symptoms in
early summer who had no direct hay field exposure, which supported the
idea of widespread aerial transport of grass pollen. Additional pollens
prevalent during other seasons were identified later, and a group of aller-
gic offenders or “allergens” gradually were identified (Table 1).
These allergens include agents such as house dust, animal epidermal
materials (danders) and foods which, clearly, are present during all sea-
Sons. Not surprisingly, affected persons were found to have continual
nasal symptoms of greater or lesser severity. In these “perennial” rhinit-
ics, pruritus, sneezing and rhinorrhea often are relatively minor, seldom
275
Allergic Responses
OFFENDERS IN RESPIRATORY ALLERGY
WINDBORNE POLLENS
FUNGUS SPORES
ARTHROPOD EMANATIONS
HOUSE DUST (& HD MITES)
ANIMAL DANDERS
ADDITIONAL ORGANIC DUSTs
INGESTANTS
Table 1
approaching the dramatic intensity of florid hay fever. Their problems,
instead, relate to persistent nasal obstruction, often accompanied by copi-
ous postnasal discharge. Besides being prone to mouthbreathing, these
persons also are predisposed to recurrent nasal and paranasal sinus infec-
tion with prolonged morbidity. In turn, infection promotes mucosal
edema which leads to further nasal obstruction; in some, discrete edema-
tous outgrowths of the nasal membrane (viz., nasal polyps) also develop.
Adenoid and tonsillar hypertrophy often add to upper airway obstruction
and its consequences, especially when persistent nasal blockage and infec-
tion supervene in childhood. In addition, impaired eustachian tube func-
tion and chronic serous otitis with hearing loss often occur as a result of
chronic infection and airway obstruction. Affected youngsters also may
show swelling and hyperpigmentation of infraorbital tissues, adding to an
appearance of ill health.
The prevalence of nasal allergy is difficult to estimate and may vary
geographically with the distribution of major inhalant allergens. In those
sections of North America where ragweeds are abundant, rates from
8-12% in unselected populations (Broder et al., '62) to almost 20% in
university student groups (Hagy and Settipane, '69) have been reported;
a majority of these people had only mildly severe hay fever, however.
Severe perennial symptoms seem to occur in less than a quarter of the
total allergic rhinitis population.
276
Solomon
IMMUNOLOGIC MECHANISM OF NASAL ALLERGY
Nasal allergy differs from other forms of rhinitis in its basic immunologic
mechanism. In turn, the presence of specific immunoreactants defines the
population at risk for this condition. Like other immune processes, that
underlying allergic rhinitis has characteristics of specificity (i.e., triggering
by specific agents or allergens) and amplification or the capacity to induce
tissue changes by recruiting one or more basic effector mechanisms.
Specificity is conferred by antibodies, especially of the immunoglobulin
E (IgE) class, which are present in the serum and tissues of allergic per-
sons. A pair of sites on each antibody molecule have atomic and spatial
arrangements which permit stable binding of a particular allergen. Such
allergen-reactive patches are common to antibodies in general and also
determine reaction specificity of IgG, IgM, IgA, etc. However, unlike
these other immunoglobulins, IgE molecules have additional unique recep-
tors which permit them to attach to defined membrane sites on tissue mast
cells, and, there, to direct powerful mechanisms of inflammation. Mast
cells usually are deployed close to blood vessels, contain prominent gran-
ules and have the ability to secrete a variety of tissue active substances into
their environment. Some of these agents mediate tissue effects directly
while others recruit or activate secondary humoral substances or cellular
elements at the site of reaction. As shown in Figure 1, the secretory process
is initiated when a specific allergen bridges appropriate reactive patches on
two adjacent, mast cell-bound IgE molecules. A series of intracellular
reactions follows and activities, including those promoting vasodilatation,
increased vascular permeability and visceral muscle spasm, are generated.
Although the relative importance of individual secreted mediators is un-
clear, many of the tissue changes of allergic rhinitis could be explained
plausibly as histamine effects. This simple amine (molecular weight 111) is
a potent vasodilator and permeability promoter and is almost unique in
eliciting a sensation of pruritus in skin and certain mucous membranes.
Histamine is also a modest eosinophil attractant — a property which may
reinforce the effects of ECF–A (the eosinophil chemotactic factor of
anaphylaxis), which is now identified with a pair of tetrapeptides also
derived from mast cells. The allergen- induced, IgE-dependent release of
mediator substances takes place in several steps. Abnormalities in one or
more of these could, by facilitating mediator release, determine or
strengthen a predisposition to allergic rhinitis.
THE ATOPIC INDIVIDUAL
At present, the most evident trait shared by affected persons is a
heightened capacity to produce IgE antibodies in response to allergens
encountered at mucous surfaces; viz., the respiratory and gastrointestinal
277
Allergic Responses
_--> TISSUE
Eosinophils EFFECTS
2.
Eosinophil Platelets
Chemotactic 2.
Factor
Platelet
Activating
Factor
Histamine
Eº SRS – A
é Pºſ == _^
Figure 1. Release of inflammatory mediator substances by a sensitized mast cell in
response to specific antigen (Ag). The process is begun when antigen bridges two
IgE molecules (the Y-shaped structures) deployed at surface receptors (R). A
Series of reactions terminates with release of mediators from granules (G) follow-
ing their fusion with cell membrane. These substances may have direct tissue
effects (e.g., histamine and SRS-A) or act to release or recruit additional reac-
tants (e.g., platelet activating factor).
tracts. This feature, and a related tendency to clinical conditions including
allergic rhinitis and asthma, gastrointestinal allergies and atopic dermati-
tis, is often characterized as “atopy” while involved persons are termed
“atopic.” Such persons often experience two or more atopic diseases in
their cumulative health histories and many (ca. 50%) have parents, si-
blings or children who are affected similarly. The familial tendency to
manifest atopic conditions is a distinctive and long-recognized feature.
Although specific syndromes (e.g., allergic rhinitis) are not clearly trans-
mitted, both IgE responses to specific allergens and total IgE production
reflect some genetic control. Why certain atopic persons develop allergic
rhinitis alone, others solely allergic asthma and a third group remains
Symptom-free, despite roughly comparable IgE responses, remains to be
explained. However, the presence of a tissue- fixed, allergen-specific anti-
body is demonstrable in all as wheal and erythema reactions (frequently
there are multiple reactions) to skin testing with common inhalant and
ingestant allergens (Fig. 2). That such reactivity signifies a potential for
clinical disease, rather than proof of its occurrence and etiology, is an
essential tenet in evaluating atopic individuals.


278
Solomon
-
Figure 2. Multiple positive wheal and flare reactions on the arm of an atopic
Subject. These responses develop in 10–20 minutes and validly reflect tissue-fixed
IgE molecules of numerous specificities. However, such reactivity does not ensure
that natural exposure to the corresponding allergens will elicit clinical symptoms.
279

Allergic Responses
Remarkably few reports (Rappaport et al., 53; Strömme, ’55; Bryan
and Bryan, '69) have described tissue changes in allergic rhinitis, although
the affected mucosa is accessible to biopsy. Brief challenges of sensitive
subjects with pollen in threshold doses reproduces acute allergic rhinitis
with copious, thin nasal Secretions containing many eosinophils. Addi-
tional tissue changes at this time, however, have been confined to edema
of connective tissue and some vascular engorgement. The eosinophils
present may show a characteristic vacuolation but neither mucosal cell
swelling nor defects in microvilli or cilia have been evident. More exten-
sive changes have been described in chronic (perennial) allergic rhinitis
with frank loss of ciliated epithelial cells, as well as deformation and
separation by edema of those remaining. Deeper tissues also have re-
flected prolonged fluid excess with swelling and fragmentation of connec-
tive tissue elements and changes in the staining properties of ground
Substance.
Vascular plethora, with swelling, vacuolation and fenestration of endo-
thelial cells, has impressed several authors (Ritter, '78). Once estab-
lished, these results of the disease may contribute to its perpetuation and
to abnormal functional responses typical of allergic rhinitis. The “water-
logged” mucous membrane, for example, could be abnormally permeable
to allergens eluted at the surface and, thereby, might facilitate challenge
of sensitized mast cells within the mucosa. A measure of hyperpermeabil-
ity has been suggested in asymptomatic atopic persons by at least one
recent study (Kontou-Karakitsos et al., '75) (though not by others;
Buckle and Cohen, '75). Whether atopics deviate from normals in this
way remains unclear, especially since lingering chronic changes could
have accounted for the group differences reported.
Related changes produced by rhinitis may underlie the phenomenon
described as “priming” (Connell, '69), in which the allergen exposure
threshold needed to elicit a response falls with repeated challenges. Inti-
mations of such an effect derive from observations that, among hay fever
patients, group symptom means often remain high late in a pollen season,
at exposure levels which caused little or no distress early in that season.
Daily pollen exposures of single subjects also have shown sequential de-
creases in the doses needed to elicit symptoms or to raise nasal airway
resistance (NAR; Solomon et al., '65). Heightened reactivity apparently
is not allergen-specific, however, and seems to diminish over one to three
weeks.
During periods of hay fever, the nasal airway also is abnormally re-
sponsive to physical stimuli acting directly or through reflex mechanisms.
Affected persons experience greater nasal blockage from non-painful
chilling and with recumbency than do their normal peers with equivalent
baseline NAR. Depending on the measurement criteria used, responses
280
Solomon
to local irritants or inflammatory mediators have been reported as normal
or heightened in allergic rhinitis.
EVALUATION OF NASAL ALLERGY
Although florid (seasonal) hay fever is virtually unmistakable, the iden-
tification of perennial nasal allergy often requires detailed and prolonged
evaluation. Since a chronic stuffy nose and recurrent infection dominate
the picture, affected children resemble those with inordinately frequent
colds and perennial nonallergic (or “vasomotor”) rhinitis. Additional
considerations include overuse of nose drops and sprays, cystic fibrosis
(especially with polyps present) and antibody deficiency syndromes. In
children with or without other primary illness, adenoid hypertrophy also
can mimic chronic rhinitides convincingly.
Since there is no single diagnostic test for nasal allergy, it is recognized
usually by the “weight of evidence” derived from several sources. In this
effort, details of the clinical history assume a dominant importance. The
primary goal of the fact-finding process is recognition that symptoms com-
patible with allergy occur in response to exposures known to involve spe-
cific allergens.
HEALTH HISTORY
Symptom-exposure associations may be approached in several ways. In
many instances, answers to the question, “What factors precipitate your
symptoms?”, permit implication of factors such as animal epidermals
(danders), house dust, feathers and even certain foods as allergens. These
associations are not always evident to patients, but when clear-cut, pro-
vide the most easily elicited evidence of allergy.
Data describing when and where symptoms occur also have value if
temporal and spatial patterns of allergen prevalence are known. For ex-
ample, in the Midwest annual bouts of typical hay fever occurring from
early June to mid- July can be ascribed to airborne grass pollen with
considerable assurance. Similarly, symptom flares on exposure to com-
posting or dense standing vegetation most often reflect sensitivity to asso-
ciated saprophytic fungi. Discrete seasons of tree, grass and ragweed
pollen prevalence are well-defined in North America while high airborne
fungus levels provide a background throughout the growing season.
Although seasonal sensitivities serve as markers in evaluating many
atopic persons, their impact is characteristically recurrent and transient.
Longstanding nasal obstruction far more commonly reflects perennial ex-
posure to allergens, in domestic or work settings, which are more subtle
and unvarying in their effects. Consequently, affected persons seldom
281
Allergic Responses
suspect these sensitivities, and, initially, only the fact (and intensity) of
exposure may be established. However, estimates of total contact with
factors including house dust, kapok, feathers, animal danders, environ-
mental fungi and various foods can have substantial correlative value.
Variations in symptoms with manifest or inferred changes in specific ex-
posure often may be recalled; effects of travel, a new home and acquisi-
tion or loss of pets and furnishings hold particular interest.
Additional features of atopy, serving essentially as “risk factors”, can
add weight to an impression of nasal allergy. Conditions, including child-
hood asthma, infantile eczema and gastrointestinal allergy, have strong
statistical associations with allergic rhinitis, and their occurrence in health
histories is carefully sought. Similarly, the presence of atopic conditions
in close (especially, first degree) family members enhances the personal
risk of related illness. A family history of atopy can be elicited from
approximately half of atopic patients while among entirely normal per-
sons, only about 10% have relatives with atopic conditions.
PHYSICAL EVALUATION
Physical evaluation can offer few findings that specifically indicate aller-
gic rhinitis but has major value in excluding similar or associated condi-
tions. The pale violaceous, moist, edematous nasal mucosa typical of
uncomplicated hay fever seldom is encountered in chronic nasal allergy.
More commonly, effects of infection with or without topical medication
are manifest with a pink or frankly infected membrane that may be dry
and exudate-covered. Examination can reveal instances of septal buck-
ling, polyps, lymphoid tissue enlargement of Waldeyer’s ring, pus in mea-
tal recesses or, occasionally, stigmata of a foreign body. Acute pruritic
conjunctivitis may be striking in uncontrolled hay fever but seldom mani-
fests as a perennial problem. Instead, stigmata associated with nasal ob-
struction often are encountered, including darkened, swollen infraorbital
tissues (“shiners”), malar flattening and oral respiration with accompany-
ing open-mouth posture. These symptoms commonly are described as
“allergic” but more correctly seem to arise from any long-term nasal
blockage regardless of its cause; in childhood, their linkage with allergy is
real but basically statistical in nature, since allergy so commonly deter-
mines chronic nasal obstruction in young persons.
The presence of numerous eosinophils in nasal and/or conjunctival se-
cretions suggests atopy, although the association is far from perfect.
These distinctive cells typically show bilobed nuclei and numerous, dis-
crete granules staining red with eosin. Since eosinophil attractants are
generated in IgE-mediated reactions, migration of the cells from blood to
affected tissues is not surprising. However, where infection is prominent,
282
Solomon
eosinophils may be lost in a “rising tide” of pus cells, and, in mild peren-
nial rhinitis, their numbers may be low at best. In hay fever, nasal secre-
tions may show few inflammatory cells but many mature eosinophils.
Moreover, where the diagnosis of rhinitis is doubtful, there is no level of
these cells that categorically assures (or excludes) nasal allergy. The eval-
uation of secretion cytology, like other points of evidence, must be
guided by associated clinical facts.
Skin Testing
Skin testing has established value in studying rhinitis patients since it
can identify tissue-fixed immunoreactants capable of generating atopic
responses (Norman, '78). With a highly suggestive history of symptoms
on specific exposure, a strongly positive skin test provides sufficient con-
firmation to form a basis for clinical strategy. However, considered alone,
even intense skin test reactions indicate only a capacity for specific reac-
tivity and give no proof that clinical illness will occur at naturally occur-
ring levels of exposure. One or more positive skin reactions to extracts of
inhalant allergens may be elicited in approximately one-fourth of the
general population; yet a portion of these have lifelong freedom from
atopic diseases. Furthermore, many persons with isolated clinical sensi-
tivities (e.g., pure ragweed hay fever) may show a wide spectrum of
intense skin test positivity. Reactive sites develop diffuse redness, often
with a raised central wheal or hive. Relevant reactions develop maximally
in 10-20 minutes corresponding to the time course of inflammatory me-
diator release by allergen-challenged mast cells. We favor initial epider-
mal testing, in which shallow pricks are made through surface droplets of
allergen extract solutions. Since relatively little material is introduced
(and that which is introduced is deposited superficially), this method is
relatively safe and detects only higher grades of skin sensitivity. Less
intense reactivity may be assayed using intradermal (intracutaneous) tests
in which 0.02 ml portions of extract are injected into the upper dermis
using a sterile technique. The validity of epidermal and intradermal test
reactions is enhanced by demonstrating responses to the diluent used in
extract preparation. This control serves to identify responses (present in
< 5% of persons) merely to penetration of the skin. In addition, it is wise
to confirm that a pharmacological histamine liberator (e.g., codeine phos-
phate) will produce the expected hive and redness response when intro-
duced into the epidermis. Such a positive control serves to exclude rare
individuals with impaired release of, or vascular response to, mast cell-
derived mediators.
Recognition of IgE as the immunoglobulin class containing tissue-fixing
antibodies held out hope that total IgE levels might separate atopic from
283
Allergic Responses
nonatopic persons. Unfortunately, it now appears that only a limited
distinction is possible. While Immunoglobulin E group means for atopic
persons are significantly above those for normal persons, distributions of
values for the two populations overlap. A total IgE level exceeding 500
International units (I.U.)/ml does strongly suggest atopy, but it can also
suggest other unrelated conditions. However, many children with chronic
rhinitis present intermediate values (200-400 I.U./ml) which neither sup-
port nor impugn an impression of atopic allergy. Somewhat greater speci-
ficity has fostered increasing use of assays of serum IgE reactive with
individual allergens. In the radioallergosorbent (RAST) test (Wide et al.,
'67), specific immunosorbents are prepared by conjugating allergens with
cyanogen bromide-activated carbohydrate carriers such as filter paper or
Sephadex. During incubation of test serum with the conjugate, specific
IgE binds firmly to allergen groups on the carrier. After washing the
mixture, an anti-human IgE (which is usually derived from the goat and is
tagged with a radionuclide) is added. This anti-IgE binds to the IgE
present on the allergosorbent and the radioactivity incorporated becomes
a measure of allergen-specific IgE present in the original serum sample.
The RAST test has particular value where competent skin testing is un-
feasible or changes, specifically in serum antibody, must be related to
therapeutic interventions or patterns of exposure. RAST results generally
correlate well with skin test data, and the procedure offers sensitivity of
measurement intermediate between that of epidermal and that of intra-
dermal testing.
Where patterns of clinical symptoms and of skin reaction conflict, clari-
fication may come through periodic reevaluation and reexamination of
the patient. Direct testing of the nasal mucosa with aerosolized allergen
extracts may be considered, but it is often confounded by the nonspecific
reactivity of the upper airway and lack of widely available means (e.g.,
direct measurement of nasal flow resistance) to document changes objec-
tively. Even where well-controlled nasal mucosal testing is possible, posi-
tive responses are not infallible indicators of symptoms anticipated from
prolonged, low-level, natural exposures. However, a lack of response to
the necessarily brief and massive challenges (aerosolized allergen doses)
used suggests a low potential for clinical reactivity if the test allergen is
appropriate and active.
Altering the Environment
Related information can be obtained by varying natural exposure to
any of several environmental agents. Symptom trends after application of
dust avoidance procedures or with extended removal and reintroduction
of a household pet may be extremely persuasive to both patients and
284
Solomon
physician. Food allergens also may be evaluated by observing clinical
changes that follow substantial controlled feedings. To facilitate this, a
group of foods to be tested are first withdrawn from the diet during an
initial period, generally 5 to 14 days. Thereafter, large quantities of indi-
vidual foods are added singly, to the diet at two or three day intervals.
Even while offending foods are being withheld, chronic rhinitis symptoms
may persist due to residual inflammation, infection or additional inhalant
allergens. Therefore, attention centers on possible worsening (or reap-
pearance) of nasal problems when specific foods are reintroduced. Each
new addition, of course, must be made in amounts well above the normal
daily intake to provide an adequate test challenge. A systematic diary-like
recording of both foods eaten and symptom severity levels, facilitates the
retrospective analysis of diet manipulation.
CONCLUSIONS
It should be clear by now that the identification of perennial (chronic)
nasal allergy can pose a resistant and, at times, frustrating problem. Diffi-
culties in allergen recognition are compounded by the non-specific hyper-
reactivity and proneness to infection of the involved upper airways. Results
of drug treatment with antihistaminic and sympathomimetic agents (or
even steroids) offer minimal differential help since they may be equally
favorable in allergic and non-allergic rhinitis. Similarly, subjective regres-
Sion of nasal symptoms with allergen-specific immunotherapy provides
only limited (retrospective) support for the allergic nature of the original
complaint. Controlled trials of immunotherapy often have improvement
with such injection treatment in one-third or more of subjects receiving a
placebo (Norman, '74). Allergen-induced worsening of symptoms remains
the hallmark of allergic rhinitis, but this association may require lengthy
observation and demanding environmental measures to establish. How-
ever, proper assessment of the child with chronic rhinitis has fundamental
importance. Erroneous overdiagnosis of nasal allergy leads to unjustified
expense and inconvenience, while drawing attention from other, poten-
tially remediable diseases. Conversely, failure to recognize nasal allergy
may deprive a patient of specific treatment measures (viz., allergen avoid-
ance and immunotherapy), with established and often dramatic efficacy.
The results of this error are not confined to prolonged misery and parental
concern, but, as described elsewhere in this volume, also may seriously
impact respiratory function and craniofacial development.
ACKNOWLEDGEMENTS
This research was supported in part by research grant AI 10181 from NIAID,
the National Institutes of Health.
285
Allergic Responses
REFERENCES
Balyeat, R. M. and R. Bowen. Facial and dental deformities due to perennial
nasal allergy in childhood. Internat. J. Orthodont. 20:445-460, 1934.
Broder, I., P. P. Barlow and R. J. M. Horton. The epidemiology of asthma and
hay fever in a total community: Tecumseh, Michigan. J. Allergy, 33:513-523,
524–531, 1962.
Bryan, M. P. and W. T. K. Bryan. Cytologic and cytochemical aspects of ciliated
spithelium in the differentiation of nasal inflammatory disease. Acta Cytol.
13:515-522, 1969.
Buckle, F. G. and A. B. Cohen. Nasal mucosal hyperpermeability to macromole-
cules in atopic rhinitis and extrinsic asthma. J. Allergy Clin. Immunol.
55:213-221, 1975.
Connell, J. T. Quantitative intranasal pollen challenges. III. The priming effect in
allergic rhinitis. J. Allergy, 43:33-44, 1969.
Duke, W. W. Deformity of the face caused by nasal allergy in childhood. Arch.
Otolaryng. 12:493-498, 1930.
Hagy, G. W. and G. A. Settipane. Bronchial asthma, allergic rhinitis and allergy
skin tests among college students. J. Allergy, 44:323-332, 1969.
Kontou-Karakitsos, K., J. E. Salvaggio and K. P. Mathews. Comparative nasal
absorption of allergens in atopic and nonatopic subjects. J. Allergy,
55:241-248, 1975.
Marks, M. B. Allergy in relation to orofacial dental abnormalities: a review. J.
Allergy, 36:293-302, 1965.
Norman, P. S. In vivo methods of study of allergy. In: Allergy: Principles and
Practice. E. Middleton, Jr., C. E. Reed and E. F. Ellis (eds.), C. V. Mosby
Co., St. Louis, 1978.
Norman, P. S. Specific therapy in allergy: pro (with reservations). Med. Clin. N.
Am. 58:111-126, 1974.
Rappaport, B. Z., M. Samter, H. R. Catchpole and F. Schiller. The mucopro-
teins of the nasal mucosa of allergic patients before and after treatment with
corticotropin. J. Allergy, 24:35-51, 1953. s
Ritter, F. N. Physiology of the nose, paranasal sinuses and middle ear. In: Al-
lergy: Principles and Practice. E. Middleton, C. E. Reed and E. F. Ellis (eds.),
C. V. Mosby, St. Louis, 1978.
Solomon, W. R., J. A. McLean, C. Cookingham, G. Ahronheim and G. R.
DeMuth. Measurement of nasal airway resistance. J. Allergy, 36:62-69, 1965.
Strömme, O. On histological reactions in allergic nasal mucosa caused by pollen.
Acta Allergol. 8:251-255, 1955.
Todd, T. W., M. B. Cohen and B. Broadbent. The role of allergy in the etiology
of orthodontic deformity. J. Allergy, 10:246-248, 1939.
Wide, L., H. Bennich and S. G. O. Johansson. Diagnosis of allergy by an in vitro
test for allergen antibodies. Lancet, 2:1105-1107, 1967.
286
AN APPROACH TO THE MEDICAL
MANAGEMENT OF CHRONIC
MOUTHEREATHING
Bob Lanier, M.D. and Normand Tremblay, M.D.
Fort Worth, Texas
There is considerable evidence suggesting that certain dental problems
may be related, at least partially, to prolonged mouth breathing (Paul and
Nanda, ’73). The practicing dentist may be the only link to health care for
an otherwise healthy, mouthbreathing individual. Mouthbreathing, unfor-
tunately, is considered by many busy, primary care physicians to be a
minor, non-medical problem. It therefore becomes incumbent upon any
interested health care provider to be knowledgeable about the differential
diagnosis of mouthbreathing and nasal congestion and to be familiar with
simple and commonly available medications and avoidance procedures
designed to promote better nasal breathing as part of a comprehensive
medicine program.
AN ANATOMICAL APPROACH TO MOUTHEREATHING
There are many complex reasons for mouthbreathing, but the majority
of cases are probably due to some anatomical obstruction. Simplistically,
there are two high-yield areas for the practitioner to examine: the ade-
noid pad and the anterior portion of the interior nasal cavity. The ade-
noid pad can be examined radiologically and the interior nasal cavity by
direct inspection. Since both areas may be involved simultaneously, a
complete evaluation is required to make logical, therapeutic decisions.
The Adenoid Pad
Both the tonsils and the adenoids are part of a collection of lymphoid
tissues known as Waldeyer’s ring. This tissue encircles the posterior phar-
ynx and consists of lymphoid tissue at the base of the tongue (lingual
tonsil), the two familiar faucial (palatine) tonsils and the pharyngeal ton-
sils or adenoids (Fig. 1). The adenoids, in particular, are in a critical
anatomic site for immune protection since their location results in signifi-
cant physical contact with viruses and bacteria because of nasal airway
flow.
287
Chronic Mouthbreathing
Figure 1. Waldeyer’s Ring is composed of tonsils (T), adenoids (A), and lingual
tonsil (L).
The principal problems of the adenoids are infection and hypertrophy,
although hypertrophy is often thought to be transient and related either
to allergy or repeated infection. The very soft and spongy adenoid tissue,
which is usually abundant in the posterior nasopharynx, can Swell to
various degrees. Occasionally, a swelling of two to three centimeters of
tissue thickness is observed. This swelling can interfere with the passage
of air through the nasal cavity and obstruct both the eustachian tubes and
openings to the maxillary sinuses.
Clinically, the presence of adenoid hypertrophy should be suspected if
Such common symptoms as mouthbreathing, nocturnal snoring or re-
peated episodes of either otitis media or sinusitis are present. The diagno-
sis can be confirmed by direct digital palpation, examination of the vault
with an indirect mirror or, preferably, by radiologic examination such
that not only is anatomic size quantified, but physiologic dysfunction
demonstrated. The optimal radiologic technique is lateral exposure of the
neck and adenoid area when the mouth is open and the soft palate is
depressed against the tongue. In this manner, the adenoids usually are
sharply defined against an air column in the posterior pharynx, and the
presence of an obstruction can easily be determined. It would seem pref-

288
Lanier and Tremblay
Figure 2. Illustration of the “allergic salute.”
erable to take the films during expiration, since the turbulence produced
by expiration is so much greater than that of inspiration that films taken
then would demonstrate an obstruction's maximum interference with phy-
Siologic function.
Anterior Nasal Inspection
Examination of the exterior of the nose will often provide information
On the etiology of mouthbreathing. A nasal crease or linea nasalis often
results from the “allergic salute” performed most often by smaller chil-
dren who repeatedly rub their nose in an upward motion because of
chronic nasal itching (Fig. 2). Since it usually takes from one to two years

289
Chronic Mouthbreathing
of consistent rubbing to produce this crease, it is a valuable tool in diag-
nosing the presence of allergies because allergies are one of the few
processes that will cause a nose to itch over an extended period of time.
Often this nasal crease will not be a thin line, but rather a broad band of
reddened or traumatized tissue which both the patient and his parents
may consider to be the result of some unrelated phenomenon such as
Sunburn.
The general size of the nose, especially the width, relative to the size of
other craniofacial structures may give the practitioner some idea of the
functioning of this Organ. An externally large nose, especially a broad
one, does not guarantee that the interior space will match the outward
appearance, but certainly these individuals have less of a problem with
complete nasal obstruction than those individuals with very thin or nar-
row nasal structure. The narrow nose is often present as part of congeni-
tal premaxillary, dental or palatal malformations since embryologically
the upper incisor teeth and part of the palate, as well as a portion of the
nasal septum, arise from the premaxilla area (Smith and Ware, '72).
The interior of the anterior portion of the nasal cavity can be examined
easily without unusual or expensive equipment (Fig. 3). In children, a
nasal speculum or an otoscope with a large speculum works quite well.
Lacking this equipment, a penlight, together with a cotton Swab to ma-
nipulate the fleshy portion of the nose, can be used to directly examine
the immediate surface anatomy.
The nasal septum divides the nasal cavity into two compartments, with
entrance gained by passing the vestibules on either side. The septum
should equally divide the area, but when it is not in the midline (deviated
Septum), it can cause a significant amount of obstruction. The vestibules
are lined with skin containing hairlike structures known as vibrissae.
Upon entering the vestibule and passing the vibrissae, one can see on the
lateral walls several sets of structures stacked on top of one another
known as turbinates (Fig. 4). There are four sets of turbinates, but usu-
ally only the inferior and middle turbinates can be seen. The apparent
function of turbinates is to increase the amount of surface area of the
nasal tissue that is covered with ciliated epithelium and its mucus blanket,
and to induce turbulence into the inspired air to facilitate warming, hu-
midifying and filtrating actions. The inferior turbinate is encountered first
since it is in the most anterior position, and the middle turbinate is more
posterior and superior.
Usually the turbinates are pink and glistening, but they can be a variety
of hues. It is sometimes said that allergy creates a pale or bluish appear-
ance and infection, a fiery red one. There are, however, no absolute
guidelines, since a number of processes of an immunologic, infectious or
vascular nature may coexist simultaneously.
290
Lanier and Tremblay
Figure 3. The inferior turbinate is plainly evident with exposure gained from a
Speculum.
Exactly what percentage of the total volume of the nasal cavity the
turbinates should occupy is a topic of debate. Even in normal subjects the
turbinate size varies considerably during the day according to the time
and the position of the subject (Ritter, '78). They are extremely vascular
Structures which engorge and retract on a four-to- six hour cycle. When
chronic mouthbreathing is caused by nasal obstruction due to turbinate
Swelling, the turbinates exhibit persistent engorgement which rarely
cycles. If the swelling remains for an appreciable period of time, it is
termed hypertrophy. Surgery or only the most aggressive medical therapy
Seems to improve this condition.
The color of the mucus blanket is sometimes indicative of the cause of
the nasal obstruction. Most of the time, drainage will be bilateral. If there
is unilateral drainage (especially if it is purulent in nature), one must

291
Chronic Mouthbreathing
/ )
/
/
/
A
2^ /
º *7, Yº
f 'ſ s %
s Ş
ſ” ~ *
( | »ºrsºgº //
\ º X
uM& //
Figure 4. Cutaway showing stacked turbinates.
strongly consider the presence of a foreign body or infection. Generally,
green or yellow mucus indicates the presence of white blood cells asso-
ciated with infection. Thin, watery mucus is associated with an allergic or
vasomotor process. There are many exceptions to the above rules, and a
definitive diagnosis usually can be made only with microscopic examina-
tion of stained mucus.
No matter what the appearance of either the interior of the nose or the
radiologic examination of the adenoid pad, the crucial parameter in de-
termining the degree of obstruction and its possible role in the creation of
dental malocclusion is nasal airway resistance. The measurement of air-
way resistance takes into account not only the observed obstruction, but

















292
Lanier and Tremblay
Non-allergic Rhinitis
Allergic Vasomotor and Eosinophilia
Itching + + + - + + +
Sneezing + + + *E* + + +
Rhinorrhea + + + +/– + + +
Obstruction + + + + +
Aggravating
Factors Obvious + +/– *
Response to Meds + + E--> +/–
Family Hx. Allergy + + +/– +/–
Nasal Mucosa Pale, Blue Hyperemic, Pale, Blue
Wet, Swollen Swollen Wet, Swollen
Salute + sº- +
Shiners + + +
Dennie's Lines + + +
Nasal Crease + gº +
Total Eos. Count High WNL WNL
Nasal Smear EOS Polys EOS
Skin Test POS. Neg. Neg.
Table 1. Forms of rhinitis
also the obstruction created by turbulence. It should be noted that turbu-
lence and air flow patterns are considerably different during inspiration
than during expiration. Many attempts have been made to simplify the
measurement of nasal airway resistance, and while there has been some
success with rhinomanometry (Cottle, '68), the only method that with-
stands statistical analysis is that done with a rather sophisticated instru-
ment known as a pneumotachygraph (Hershey et al., '76). Unfortunately,
this instrument is available in only a few research centers since it is rather
Sophisticated and expensive.
DIFFERENTIAL APPROACH TO THE MEDICAL CAUSES OF NASAL
OBSTRUCTION
If a patient is a mouth breather and the adenoid pad does not seem to
be impinging on the nasal airway (or even if it is, but there is also obvious
nasal swelling), rhinitis in its various forms should be considered as a
possible cause of the mouthbreathing. Table 1 lists some of the major
features of the three major forms of rhinitis: allergic,
293
Chronic Mouthbreathing
non-allergic rhinitis with eosinophilia, which may lead to nasal stuffiness.
Vasomotor Rhinitis
This is possibly the most difficult condition to deal with since the exact
etiology for tissue swelling has not yet been determined.
The key to the diagnosis of this particular condition is careful question-
ing of the patient. Individuals afflicted with this particular disorder ordi-
narily are affected most by physical agents, including heat, cold and non-
specific irritants such as perfumes, powders and cigarette Smoke. Ob-
struction of the nasal airway is the primary complaint rather than sneez-
ing or itching. The blood vessels seem to contract and expand in an
exaggerated manner producing obstruction during the expansion stage.
Most patients eventually try and receive significant relief from topically
applied pressor agents such as Neo-Synephrine. Unfortunately, when
these agents are used for an extended period of time, a “rebound” syn-
drome known as rhinitis medicamentosum (Blue, '69) predictably is pro-
duced. The longer-acting nasal sprays seem to have less rebound effect,
but still are generally not recommended by physicians because of the
possibility of damaging the nasal mucosa, causing irritation, decreasing
ciliary activity and producing atrophic changes.
With chronic use the likelihood of bacterial overgrowth in the spray or
dropper bottle is great. It therefore follows that an increased number of
nasal infections, including sinusitis, might be expected to occur in habit-
ual users. Patients are generally advised that if they must use nasal sprays,
they should use the very smallest quantity possible. The duration of time
between usages must be considered as well as the amount used at any
given time. The patient should be discouraged from buying the “large
economy size” containers of nasal spray since the larger volume bottles
will last for an appreciably longer time than the smaller volume bottles
and, therefore, will be much more likely to become contaminated. A
Small, 2.5 cc bottle used, washed and refilled from a stock bottle will
lessen the chances of reinfection. Orally administered drugs for this con-
dition include alpha-adrenergic stimulators or decongestants. Either
ephedrine or pseudo-ephedrine containing medications used in conjunc-
tion with adrenergic stimulators (phenylpropanolamine, phenylephrine)
may be used at bedtime and are usually effective as long as they don’t
cause the individual to have excessive difficulty sleeping. Caution must be
exercised in prescribing these drugs for individuals with hypertension.
Decongestant-antihistamine combinations are not nearly as effective in
the treatment of vasomotor rhinitis as they are in the treatment of allergic
rhinitis, but they do offer some relief, especially if used in a rotating
fashion so that tolerance is not built up.
294
Lanier and Tremblay
Allergic Rhinitis
The public thinks that allergies are a much more commonly occurring
problem than is actually the case. Informal surveys reveal that a majority
of the public believe they have “allergies” and consider almost everyone
to have an allergy to one thing or another. The actual gene frequency for
this inherited trait in children under seventeen years of age is reported to
be no more than 10.8% (Barkin and McGovern, '66). The reason for the
confusion is that the lay public equates all histamine release, regardless of
the etiology, with “allergy.” The symptoms produced by histamine re-
lease in pepper inhalation, for example, are identical to those produced
by ragweed pollen inhalation in a sensitive person. The mechanism, how-
ever, is entirely different. Truly allergic persons suffer because the air-
borne proteins to which they are sensitive are practically impossible to
avoid, whereas other individuals experiencing histamine release on an
irritant basis quickly learn what to stay away from and how to do it
efficiently.
True allergic nasal disease involves individuals with the peculiar talent
to nasally recognize and respond to proteins such as pollen, mold or
animal dander. Response involves the formation of a sizeable amount of
antibody E which diffuses through the blood and tissue to fix specifically
to mast cells containing pharmalogically active materials. Once the anti-
bodies are attached, the cell membrane becomes rather fragile. If anti-
body-combining sites are bridged with the allergic protein initially stimu-
lating antibody production (reexposure), the cell membrane ruptures.
The ensuing reaction releases a variety of chemical mediators, the most
common of which in humans is histamine.
There are three basic methods of treatment of allergic rhinitis: avoid-
ance, medication and immunotherapy.
Avoidance. It is difficult to know how to implement an avoidance pro-
gram without knowing exactly to what the individual is sensitive (or what
the sensitivity pattern contains). Allergy testing is, therefore, indicated,
at least in the screening manner, if an individual has a compatible history
and appropriate laboratory parameters such as nasal eosinophilia.
If animal dander sensitivity is identified, for example, the solution is
obvious but rarely invoked, especially when long-term family members
are animals. A less acceptable compromise is to keep the animal(s) in-
volved strictly out of the bedroom at all times and, preferably, out of the
home altogether.
If airborne pollen is involved, the addition of a special filter to the
air-conditioning system often works very well. The usual filters do not
trap very small pollen or mold spore particles (5 to 20 microns in diame-
295
Chronic Mouthbreathing
ter). By inducing a charge on either a plastic or metal matrix, most of the
particulate matter can be removed from the air by electrostatic precipita-
tion (Kranz, '63). Newer, plastic air cleaners are relatively inexpensive
but are probably not quite as efficient as the older, electrostatic air
cleaners.
Other avoidance procedures include simple endeavors such as nightly
hair washing during the seasons of most exposure. Individuals with long
hair who cannot wash nightly, should cover it during sleep so as not to be
exposed to the allergic protein gathered during a normal day.
Mold sensitive individuals find that frequent maintenance (washing and
warm-air drying) of pillows is very helpful. Excessive use of vaporizers
and humidifiers in the bedrooms of mold sensitive individuals is ineffec-
tual and potentially harmful.
The production of a “dust-free bedroom” is a laudable, but practically
impossible, endeavor in the authors’ experience. The nebulous allergic
entity in “dust” is usually a microscopic mite which lives in “house dust”
(Berren, '70). Excessively ritualistic suggestions such as “no carpets, no
drapes, and no toys” in a child’s bedroom accomplish little except to
create frustration in the involved family and should be tempered with
reason and taste.
The role of food in producing nasal congestion remains controversial
despite years of debate and research (May, '75; Crook, '75). Feelings
seem to be polarized, with most academic workers believing that true
IgE-mediated allergy is rarely involved in nasal congestion unless the
material makes physical contact with the involved organ system (i.e., milk
refluxing into the nasal cavity in a baby or flour inhaled by bakers).
Foods most likely to be involved include corn, milk, wheat, eggs, choco-
late, tomatoes and peanuts. It must be stressed that skin testing for foods
is difficult at best. Various techniques have been designed to study the
role of foods in allergy, but so far only the radio allergosorbent test
(RAST) seems to have statistical validity. This test suffers because it
often misses low level allergy and has a relatively high cost. The time-
honored approach of elimination and provocation still seems to be the
least expensive and most rewarding effort, albeit inconvenient to the
patient.
Medication. Since the primary cause of allergic symptoms is histamine,
antihistamines seem to be the pharmacologic agents of choice for initial
therapy of allergic rhinitis. Antihistamines work by competitive inhibition
(they compete with histamine for binding sites) and, therefore, generally
do not work as effectively on an elective basis and so must be used
chronically. The most common side effect of antihistamines is drowsiness
which can adversely affect the school performance of children. In an
296
|
Classification Properties Brand Names
Class I Highly efficient Benadryl (Diphenhydramine)
Ethanolamines Possess atopine-like activity Rondec (Carbinoxamine)
Side effects are drowsiness
and drying action which
limit their usefulness
Class II
Ethelendiamines Mildly sedative Pyribenzanime (PBZ-
They have local anesthetic properties Tripelennamine)
although weak Copyronil (Methapyrilene)
May cause gastro intestinal side Triaminic (Pyrilamine)
effects
Class III Drowsiness less marked than in Dimetane (Brompheneramine)
Alkylamines other groups Actidil (Tripolidine)
Causes CNS stimulation Polaramine (Dexchlorphen-
iramine)
Chlortrimeton (Chlorphenara-
mine)
Class IV Marked sedation effects Phenerzan (Promethazine)
Phenothiazive Marked drying effects Temaril (Trimeperazine)
Class V Also produces sedation but some have Bonine (meclizine)
Cyclizines the advantage of extended half-lives Atarax (Hydroxyzine)
Class VI Periactin (cyproheptadine)
Miscellaneous Optimine (azatadine)
Table 2. Properties and classification of Antihistamines
§
Chronic Mouthbreathing
effort to offset these effects, a pressor agent which generally acts as a
stimulant, is sometimes given in combination with an antihistamine. Since
it is not likely that a given dosage combination will be completely appro-
priate for all individuals, parents sometimes complain that the antihista-
mines produce drowsiness or hyperactivity. Some experimentation, there-
fore, must be anticipated before a satisfactory dosage can be determined
(Karlin, '75).
Continuous antihistamine use produces tolerance to the drug. To com-
bat this phenomenon, the antihistamines should be rotated every two to
three weeks. This should involve not only a brand name change, but a
change of generic chemical class as well. A listing of the five classes and
the commonly used brand names are given Table 2.
A very potent manner of managing nasal allergy includes the use of
corticosteroids. In particular, the Decadron Turbinaire gives excellent
results with only minimal absorption (used according to package instruc-
tions). Shortly, a beclomethosone spray (Vanceril, Beclovent) which has
an extremely small systemic effect will be available for nasal use (Nor-
man, '65). This inhaled medication has been extremely effective in the
control of asthma and is expected to be significant in the control of
chronic nasal allergy also. There are other, less common methods of
controlling nasal allergy. One such method is topical nasal irrigation with
sodium cromolyn (Handelman et al., '77). A medication ordinarily used
by asthmatics, cromolyn seems effective in preventing mediator release of
histamines by interfering with calcium ion reflux in the mast cell mem-
brane. At present, this medication is used experimentally in the United
States. The dosage being used is one 20 mg capsule mixed fresh daily in
four ounces of water. This solution is then used as a nasal irrigant two to
three times daily. The advantage of this modality seems to be a low
incident of any side effects. In the near future this medication will be
available in a pre-mixed, stabilized form.
IMMUNIZATION
Hyposensitation, “allergy shots” or allergy immunotherapy is an at-
tempt to teach the patient’s immune system to react less vigorously to
inhaled allergens by a series of protein injections or immunizations. In-
itially used in 1911, this procedure provided almost the only allergy treat-
ment until the early 1940’s, when antihistamines became commercially
available.
Immunotherapy is an extremely complicated procedure which is poorly
understood theoretically. Best results are obtained when the therapy is
prescribed by a knowledgeable physician who follows his patients closely
298
Lanier and Tremblay
MOUTH BREATHER Adenoids impunging Seek Ped/ENT,
on our way support, especiolly if
there is a history of
4% recurrent infection
HISTORY especially eqrs— sinuses
ls potient other wise
BOTH AREAS ARE -
T INVOLVED ||| 2
Lot of neck
Nosol inspect.
3->
ETHICAL DILEMMA
Estoblish ropport with primory
core physician and watch
for previously over looked
Nosol turbino tes R/O unusuol - -
ore lorge 8 cquses for nosol infections/symptoms
obstructed obstruction
WO Consider
|s no so eos. Voso no for
o Rhinitis
|S there: O present &
itching, sneezing W º
• F. H
little reactivity to
physical exposures
* good post response
to onfihistomines
Consider
|s nosol eds. . - - - -
S ſho S Non-allergic Rhinitis
present 2
g
- inophili
or steroids Q *Jº Eosinophilio
Repeot lob -
Positive skin tests
YES
Consider
Nasol Allergy
Figure 5. Approach to the patient with chronic mouthbreathing.
and who bases it on a very accurate data base collected from skin or
RAST testing, or both.
Non-Allergic Rhinitis with Nasal Eosinophilia (Nares Syndrome)
This condition is poorly understood and only recently recognized. It
appears to be a common cause of mouth breathing. The affected patient
typically complains of perennial episodes of sneezing spells, itching of the
nose and profuse, watery rhinorrhea (Jacobs et al., '79). As opposed to
the patient with allergic rhinitis, the patient with nares syndrome cannot
pinpoint an obvious aggravating factor, such as mowing grass or being
near Cats.
Examination of a nasal smear during an attack reveals the definite
presence of eosinophils, but skin tests taken at the same time are nega-
tive. Total serum IgE antibody levels are within normal limits.
Although the exact cause of this condition is unknown, it appears that
histamine is being released from mast cells lining the nasal mucosa with-
out the attachment of an allergen to IgE antibody on these mast cells.
Perhaps one of the normal control mechanism in these mast cells is dys-
functioning, but this is purely speculative.
Treatment resembles that of allergic rhinitis with the exception that
avoidance measures and allergy injections play no role. Antihistamines,
decongestants, topical cromolyn and topical steroids appear to offer
symptomatic relief.




299
Chronic Mouthbreathing
SUMMARY AND CONCLUSION
Mouthbreathing can usually be attributed to hypertrophied lymphoid
tissue or swollen nasal turbinates. An approach to the differential diagno-
sis is summarized in Figure 5. Teamwork between the dental and medical
disciplines is essential to the resolution of mouthbreathing and its effects
on facial orthopedics.
REFERENCES
Barkin, G. D. and J. P. McGovern. Allergy statistics. Ann. Allergy, 24:602-609,
1966.
Berren, L. The allergens in house dust. Prog. Allergy, 14:259-264, 1970.
Blue, J. A. Over-medication of nasal mucosa. Mod. Med. 37:90-94, 1969.
Cottle, M. H. Rhino-sphygmo-manometry, an aid in physical diagnosis. Int.
Rhin. 6:7-26, 1968.
Crook, W. Food allergy -- The great masquerader. Ped. Clin. N. Am.
22(1):227-238, 1975.
Handelman, N. I. Cromolyn sodium nasal solution in the prophylactic treatment
of pollen induced seasonal allergic rhinitis. J. Allergy Clin., Immuno.
59(3):237-242, 1977.
Hershey, H. G., B. L. Steward and D. W. Warren. Changes in nasal airway
resistance associated with rapid maxillary expansion. Am. J. Orthodont.
3(6a):274-284, 1976.
Jacobs, R. L., P. M. Freedman and N. A. Boswell. Non-allergic rhinitis with
nasal eosinophilia - clinical characteristics of fifty-two patients. Presented at
the Thirty-Fifth American Academy of Allergy, New Orleans, Louisiana,
March 20-24, 1979.
Karlin, J. M. The use of antihistamines in allergic disease. Ped. Clin. N. Am.
22(1):157-162, 1975.
Kranz, P. Indoor air cleaning for allergy purposes. J. Allergy, 34:155-164, 1963.
May, C. Food allergy: A commentary. Ped. Clin. N. Am. 22(1):217-220, 1975.
Norman, P. Suppresion of hay fever symptoms with intranasal dexamethisone
aerosol. J. Allergy, 36:284-287, 1965.
Paul, J. L. and R. S. Nanda. Effect of mouthbreathing on dental occlusion, Angle
Orthodont. 43:201-206, April, 1973.
Prahl, P., K. Wilken-Jensen and N. Mygind. Beclomethasone dipropionate aero-
sol in treatment of hay fever in children. Arch. Dis. Child. 50:875-878, 1975.
Ritter, F. Physiology of the nose, paranasal sinuses and middle ear. In: Allergy:
Principles and Practice, Vol. I, C. V. Mosby, St. Louis, 1978.
Smith, L. and L. Ware. Embryology, Applied Anatomy and Physiology in Pediat-
ric Otolaryngology, Vol. II, pp. 1015-1023, W. B. Saunders, 1972.
300
DIAGNOSIS AND TREATMENT PLANNING OF
NASOPHARYNGEAL OBSTRUCTIONS
Robert S. Bushey, D.D.S., M.S.
Department of Orthodontics
University of Colorado
For years Orthodontists have sought various means of assessing respira-
tion and deglutition as basic vegetative functions associated with the cor-
rection of malocclusions. The present state-of-the-art allows for use of a
wider range of factors from clinical and radiographic examinations. The
collation and correlation of these factors may then result in a truly differ-
ential diagnosis. The orthodontic diagnosis can then be reviewed with the
patient’s pediatrician and possibly with an otolaryngologist and a pediat-
ric allergist to provide a comprehensive treatment plan.
The purpose of this paper is to present the “state of the art” in the
analysis of nasopharyngeal airway obstruction relative to orthodontic
treatment considerations; i.e., the criteria for assessment of patients with
enlarged adenoids and tonsils by clinical examination and cephalometric
analysis; classification of airway obstruction; tongue-tonsil problem cases;
and mode of treatment as an interdisciplinary approach.
CRITERIA FOR CLINICAL AND ROENTGENCEPHALOMETRIC
EXAMINATIONS
The Clinical Examination
The six-point clinical examination routine presented below is designed
to alert the orthodontist to the significant morphologic and functional
characteristics of the mouth-breathing patient. -
The most commonly seen feature and the first to look for in the clinical
examination is “mouthgaping” or lip incompetency when the patient is in
a relaxed posture. Typical of the “adenoid facies” is the short and flaccid,
atrophic upper lip. This lip separation may be a result of an indepen-
dently short upper lip or a reflection of an increased lower face height
dimension. Posen ('72) indicated that a measured weakness in the perio-
ral musculature will indicate a poor prognosis for response to both the
removal of adenoidal obstruction of the airway and correction of maloc-
clusion. Linder-Aronson ('70, '74) underscored the importance of lip
301
Nasopharyngeal Obstructions
muscle strength in the “normalization” of the interincisal relationship of
the anterior teeth following adenoidectomy.
The second step of the clinical examination is evaluating the nares and
nasofacial angle. Viewed above the lips are the widths of the nares and the
nasofacial angle. Narrow-faced, obstructed individuals tend to have nar-
row, pinched-together type nares. Furthermore, the entire base of the nose
is often tipped up, with the nares directly visible, as described by Bimler
('65) and Bench and co-workers (78) in the microrhino dysplasia syn-
drome, indicating an upward cant of the anterior portion of the maxilla.
The mode of respiration is evaluated next to determine if there is
complete or partial mouthbreathing or complete nose breathing. In addi-
tion to the highly sophisticated airflow and nasal airway resistance mea-
surement techniques described previously (Bushey, '79), there are several
simple, clinical tests of nasal patency. First, by having the patient seal his
lips for a period of 1-2 minutes, the examiner can readily assess ability
and ease of nasal breathing. A second approach is to seal the lips and
alternately collapse each nostril to evaluate nasal and/or pharyngeal ob-
struction. The potential obstruction is amplified by having the patient
“hum” through one nostril while the other is held closed. Other tech-
niques involve the use of a cold mirror to observe the relative amount of
condensation of the humidified air on each side or the movement of a tuft
of cotton held under each nasal portal. While examining the mode of
respiration, it is appropriate to take a history of the onset, frequency and
duration of upper respiratory infections, tonsillitis, strep throat, middle
ear infections, conductive hearing loss, mouthbreathing during waking
and sleeping time, and respiratory allergies. The medical history may
require confirmation by the patient’s pediatrician, supplemented by ante-
rior and posterior rhinoscopic evaluations by an otolaryngologist. It is
imperative that potential nasal obstruction be assessed separately from
potential adenoidal obstruction of the upper airway.
The fourth step in the clinical examination requires a determination of
whether there is a tooth-together or tooth-apart type swallow. The pre-
sence of a simple or complex tongue thrust can alert the clinician to
potential complications caused by an adaptive or active tongue habit,
especially when reviewed in the context of relative lip competence and
amount of incisor overbite.
The fifth step is the clinical assessment of frontal facial morphology. In
the literature, the long and narrow or dolicofacial form has been more
often associated with mouthbreathing when discussing the hypothesis that
enlarged adenoids lead to mouthbreathing in certain types of faces and
dentitions, than the broad, short or brachyfacial form which is associated
with skeletal deepbite. The more severe the dolicofacial form, the greater
the tendency for skeletal open bite, facial asymmetry and unilateral pos-
302
Bushey
terior crossbite to be present (Bushey, 77). Particularly significant is a
functional shift of the lower facial midline laterally when the patient is
asked to bring the teeth into maximum intercuspation from the resting
posture of the mandible.
The sixth step is assessment of the most significant clinical characteris-
tics which are found within the oral cavity. The first five of these are
dental and the second five are palatal and pharyngeal features.
Dental midlines are an extension of the facial symmetry evaluation.
Significant deviations in the mandibular midlines which correspond to the
functional shift of the mandible from “rest” to “occluded” positions,
indicate the presence of a bilateral construction of maxillary posterior
segments. The functional shift to a “convenience” bite to one side, if not
corrected in early development, may result in facial asymmetry.
Incisor overbite or open bite and axial inclination should be noted next.
Linder-Aronson ('70) found a characteristic increase in interincisal angu-
lation in mouth-breathing subjects. A dental open bite tendency may then
be correlated to skeletal open bite and lip incompetence tendencies as-
sessed earlier.
Anterior crossbite or overjet should be noted as an additional indication
of a potential skeletal open bite, with the attendant unilateral crossbite
tendency (Bushey, 77).
Posterior crossbite, as evidenced by a unilateral or bilateral narrowing
of the maxillary segments, is a key diagnostic feature of adenoidal ob-
struction of the nasopharynx.
The interpretation of posterior arch width initiates questions of relative
and absolute size dimensions of maxillary and mandibular arches. Treat-
ment potential should be based on palatal expansion or mandibular con-
striction if basic tongue posture can be altered by changes in the mode of
breathing.
The first non-dental feature to be assessed is the height and contour of
the palatal vault. Skeletal expansion of the palate has proved to be espe-
cially stable if the nasal capsule breadth is significantly increased (Turby-
fill, '76). This is in contrast to the relapse tendency of posterior dental
(non-skeletal) crossbites corrected by rapid palatal expansion (Bushey,
'77).
Faucial (palatine) tonsils should be evaluated next for degree of en-
largement. By depressing the tongue, the fauces will tend to close, bring-
ing the tonsils more clearly into view. Large and infected tonsils will often
303
Nasopharyngeal Obstructions
meet at the midline, indicating a significant potential for tongue displace-
ment, as described earlier (Bushey, '65; ’79).
The next factor analyzed should be the gag reflex which is elicited by
tongue depression. Individuals extremely sensitive to tongue depression
are often found to have inflamed tonsils which may not necessarily be
significantly enlarged, but may still be causing a lower and forward
tongue posture, thus eliminating the support for normal maxillary arch
width development.
The fourth non-dental characteristic which should be assessed is the
adenoid tissue. This requires either use of a dental mirror or lateral roent-
gencephalograms. When using the mirror, the uvula must be moved to
one side. While the dental light is focused, the dental mirror is tilted
above the posterior level of the hard palate. However, when compared to
the clearly superior view of the posterior pharyngeal wall afforded by the
lateral roentgencephalogram, the mirror technique is of questionable
value.
The tenth and final oral examination procedure concerns the evaluation
of the soft palate. If the palate is observed to have a bifid uvula and/or a
noticeably deep oropharynx, the posterior palate should be palpated. The
presence of a notch is an indicator for palatopharyngeal insufficiency.
Adenoidectomy for this type of patient is contraindicated because of the
potential for creating hypernasality or cleft palate speech.
Cephalometric Evaluation
The measurement of certain relationships on the lateral and posterior-
anterior cephalometric films provides an objective technique to compare
a given individual’s dimensions to the group means developed from the
research findings described in the previous paper in this volume (Bushey,
’79). The mouth breather cephalometric analysis is designed to evaluate
factors of adenoidal enlargement relative to the nasopharyngeal airway
and the nasopharyngeal sagittal dimensions, followed by assessments of
lower face height, maxillary-mandibular morphology, and growth direc-
tion and amount. Finally, functional alterations in the posturing of the
tongue, velum and mandible are evaluated in relation to the size, position
and density of the tonsillar image, and to the inclination of the incisors.
Lateral Aspect. 1. Adenoidal Enlargement Relative to Nasopharyngeal
Airway. Two sets of airway measurements have been developed by
Linder-Aronson and Henrickson ('73) and by Schulhof (78). The Linder-
Aronson-Henrickson approach qualifies adenoidal obstruction of the na-
sopharyngeal airway if the patient is free of clinical signs of upper respira-
tory infection. Linear measurements of airway space were derived
304
Bushey
NO
ANS
P NS
Figure 1. Statistically significant measurements in determining which patients are
experiencing adenoid blockage of nasopharynx: (1) Airway percentage: percent-
age of nasopharynx occupied by adenoid tissue (ratio of striped area to trapezoid
area). (2) D-AD1:PNS: distance from PNS to nearest adenoid tissue measured
along the line PNS-BA. (3) D-AD2:PNS: distance from PNS to nearest adenoid
tissue measured along a line through PNS perpendicular to S-Ba. (4) D-PTV:AD:
distance to nearest adenoid tissue from a point on PTV 5 mm above PNS. (5)
Posterior height: the length of the line S-AA. (6) O: the angle formed by the
intersection of the lines PNS-ANS and BA-NA. (7) Depth 1: the angle AA-S-
PNS. (8) Depth 2: the angle BA-S-PNS (Schulhof, '78).
from a comparison of nose breathers and mouth breathers ranging from 6
to 12 years of age (Fig. 1).
Ages 6-8 Ages 9-12
AD - PM(PNS) < 12 mm × 15 mm
AD, - PM(PNS) < 10 mm × 12 mm
The Schulhof analysis employed by Rocky Mountain Data Systems
(Fig. 1) is composed of three linear measurements and the airway per-
centage in an epipharyngeal trapezoidal area as described by Handelman
and Osborne ('76). Table 1 lists the norms for males and females from 6
to 16 years of age. An adenoidal obstruction is deemed to be present if
three or more measurements are more than one standard deviation from
the norm. The 1965 University of Illinois sample of mouth breathers was
Subjected to the Rocky Mountain Data Systems airway analysis using the
pre-adenoidectomy lateral cephalometric films. The computer predicted
Success in post-adenoidectomy airway changes with an 80% accuracy,
failure with a 47% accuracy, and possible success (borderline airway ob-

305
Nasopharyngeal Obstructions
Measurement
Percent
Airway D-AD1:PNS D-AD2:PNS D-PTV:AD
Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Male
6 Years of Age 50.55 15.85 20.66 5.50 15.89 3.53 7.07 3.84
16 Years of Age 63.96 12.80 26.48 5.45 22.44 4.26 14.59 6.10
Female
6 Years of Age 50.99 13.49 14.74 5.69 14.93 3.52 7.02 3.87
16 Years of Age 62.68 16.09 26.32 4.28 21.78 4.67 14.56 4.70
Table 1. Norms for airway measurements. If three or more measurements are
more than one standard deviation below the norm, an adenoid problem probably
exists. (Schulhof, '78)
structed cases) with an 80% possibility of failure. The above findings
suggest that the computer analysis errs on the conservative side in not
predicting success for all successful results and in predicting failure in a
significantly high percentage of borderline and relatively less obstructed
subjects who, in spite of less presurgical adenoidal obstruction, do im-
prove their nasal breathing significantly following adenoidectomy.
2. Nasopharyngeal Dimensions. As an additional verification of small
sagittal dimensions of the nasopharynx, the angular and linear depths and
angular height means of Table 2 may be used. It should be underscored
that the relative amount of adenoid tissue had a greater bearing on the
potential for obstruction than the absolute dimensions of the nasopha-
rynx. By the same token, the degree of completeness of surgical excision
in the adenoidectomy is a significant factor in determining the success of
the prediction procedure. -
3. Lower Face Height. The angular measurement of palatal plane-
mandibular plane divergence beyond one standard deviation of 30° or the
ANS-Xi-Po angle of 50° are excellent indicators of an excessive, lower
face height. Individual linear lower face heights can be assessed by mean
age data described earlier (Bushey, '79). However, Linder-Aronson and
Woodside ('79) caution that increases in lower face height induced by
airway obstruction cannot be determined by a single measurement, but
are indicated by the individual's serial increments crossing two channels
of percentile plottings of growth curves over a period of years.
306
#
Depth Height Cranial Base
AA-PNS (mm) Ba-S-PNS (°) S-Ba-PNS (°) Ba-S-N (°)
Study Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Ricketts
1954 (N=20) 42.0 33.0–55.0" 61.0 52.0–69.0" 63.0 54.0–71.0" 130.0 121.0–141.0"
Subjects 8.5 years old 34.5 3.5 62.0 4.0 61.9 4.0 129.0 3.0
Subjects 13.5 years old 36.3 3.5 60.2 5.2 63.4 4.5 129.4 4.4
1969 (N=40) 0.395 /yr —0.39 0.7/yr 0.3 0.68/yr 0.025 0.43/yr
Bushey—1965
Group I (N=6) 35.5 1.9 6.3.3 4.0 56.3 4.5 137.2 5.1
Group IIA (N=17) 34.2 3.9 62.0 5.6 59.6 3.7 133.1 4.9
Group IIB (N=12) 34.4 4.2 63.0 5.2 59.8 4.7 131.1 5.1
Group III (N=6) 34.3 4.0 62.5 5.7 60.2 3.6 134.5 5.0
1969 (N=40)
1969 (N=40)
* , indicates range.
Table 2. Nasopharyngeal Sagittal Dimensions.
§
Nasopharyngeal Obstructions
4. Maxillary-Mandibular Morphology. The position of the maxilla is
assessed to determine if an increased lower face height is the result of the
upward tilt of the palate or the downward (clockwise) rotation of the
mandible. The palatal plane is normally found to be parallel to the Frank-
fort horizontal plane, with a 7°-8° divergence to the sella-nasion line.
Bimler ('65) has described the microrhino dysplasia individual as having
an upward tilt of the palatal plane 3°-4° relative to the Frankfort horizon-
tal line and a 3°-4° divergence to the sella-nasion line.
The position and morphology of the mandible is assessed by the man-
dibular plane to Frankfort horizontal and sella-nasion planes. The normal
variation is 21° E 3° to the the Frankfort horizontal plane and 28° = 3° to
the Sella-nasion line. Increases of more than one standard deviation to
either plane can be assessed for concomitant increase in lower face
height. The mandibular contribution to lower face height can be assessed
for its morphologic influence in contrast to a positional or rotational
influence. The characteristic increase in the gonial angle of the mandible
is described earlier in this book (Bushey, '79; Table 3). Koski and col-
leagues (75), in measurements of the mandible in children with adenoids,
supported earlier findings of the author (Bushey, '72, '74) of an increased
gonial angle as a postural adaptation. The authors surmised that such a
basic morphologic alteration was induced by a ventral flexure of the head
to the cervical column. Their explanation has subsequently been docu-
mented independently by Linder-Aronson and Woodside ('79) and Solow
and Greve ('79).
The relative size of the maxilla and mandible is significant as a further
explanation of the increase in lower face height (Harvold, '71). By sub-
tracting the maxillary unit length (ANS to condylion) from the mandibu-
lar unit length (gnathion to condylion), an effective length difference is
obtained. Differences equal to, or greater than 28–30 mm, are said to
indicate a skeletal Class III tendency. If, however, the dental relationship
is Class I, then the Class III effective length difference is found to be
expressed as a downward and backward rotation of the mandible into a
skeletal open bite. The skeletal open bite tendency (or long face syn-
drome) can be verified by the linear measure of lower face height. Tables
of craniofacial standards have been provided by Harvold ('71) for males
and females ages 6, 9, 12, 14 and 16 years.
The analysis of severe skeletal Class III subjects (Bushey, '77) indi-
cated that 66% of those with a vertical facial growth pattern had posterior
crossbites, regardless of their mode of respiration. Thus, the presence of
a disproportionately large mandible carrying the tongue mass down and
forward will greatly enhance the effect of an already low tongue posture
in the mouth-breathing individual by not supporting upper arch width
development.
308
#
Group I Group IIA Group IIB Group III Total
Variable Mean S.D. Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Angular
ANS-Xi-PO 50.75 6.92 50.58 3.58 53.31 2.81 51.87 2.59 51.59 3.94
Palatal plane
Mandibular plane 31.16 5.27 31.07 3.44 34.13 4.61 32.25 8.09 32.15 4.90
Linear
ANS”-Gn
(Harvold) 58.31 3.87 61.19 6.19 62.02 6.43 58.13 5.39 60.56 5.89
Sp’-Gn
(Linder-Aronson) 58.80 3.28 62.50 5.98 63.58 6.47 59.37 5.27 61.82 5.83
% Total face
height 56.48 1.75 56.88 2.22 57.76 2.89 56.58 2.44 57.03 2.37
Gonial Angle 127.66 6.14 129.58 5.07 135.5 6.77 127.67 2.34 130.76 6.21
Table 3. University of Illinois study (Bushey 1965). Comparison of skeletal variables in lower face height.
§
Nasopharyngeal Obstructions
5. Craniofacial Growth. Facial growth direction in mouth breathers has
been found to be in a more vertical direction than in nose breathers
(Linder-Aronson, '70; Bushey, '72). Interpretation of growth direction is
readily accomplished by determining the orientation of the facial axis to
the basion-nasion line measurements of the Rocky Mountain Data Systems
analysis according to Ricketts ('69). Table 4 illustrates that mouth
breathers who improved (Groups I and IIA) were within one standard
deviation of the mean for the normative data (90° E 3.5°). The unimproved
mouth breathers (Group IIB) were more retrognathic or a minus 6° from
normative mean for the facial axis or within two standard deviations.
The amount of facial growth remaining is of particular significance in
the mouth-breathing individual. Linder-Aronson ('74) illustrated that a
“normalization” occurred in post-adenoidectomy subjects over a five year
period from approximately 8 to 13 years of age. The clinical implication is
that for the mouth breather to respond to a reduction in lower face height
by becoming a nose breather, the adenoidectomy must be performed at
an early age (6-8 years) to provide a postsurgical growth period of suffi-
cient duration.
Lower face height growth increments, according to the craniofacial
standards derived from the Burlington longitudinal growth sample by
Harvold ('71), are approximately 1.0 mm per year from 6 years (mean of
57 mm) to 16 years of age (mean of 65 mm) for females. Males have
approximately the same growth rate, but show a mean growth of 3 mm
from 14 to 16 years, contrasted to the mean of 1 mm during the same
period for females.
In summary, growth factors for facial growth direction, Class III skele-
tal tendency, lower face height and amount of growth are of paramount
importance in assessing the potential response of a mouth-breathing pa-
tient to adenoidectomy, orthodontic treatment and orthopedic force ap-
plication (Turbyfill, '76).
6. Functional Relationships of the Tonsils, Tongue, Velum and Mandi-
ble. The greatest controversy in the relief of airway obstruction by aden-
oidectomy/tonsillectomy debate concerns the influence of the faucial ton-
sil masses on respiration and tongue posture. The role of enlarged tonsils
in holding the tongue in a down and forward posture has been docu-
mented by Ricketts ('58, '68) and Bushey ('65) and described by Subtelny
and Subtelny ('73). The resting posturing of the tongue as viewed in serial
lateral roentgencephalograms has been studied by Thompson (38) and
McKee (’56). They found that the tongue had a stable, reproducible
position which descended from near contact with the palatal vault in the
deciduous dentition phase to a position above the maxillary molar crowns
in the early adult dentition phase. Significant to normal nasal respiratory
310
#
Rocky Mt. Data
Group I Group IIA Group IIB Group III System Norms Total
Mean S.D. Mean S.D. Mean S.D. Mean S.D. Mean S.D. Mean S.D.
Dental
Lower anterior
facial height 50.6 7.0 50.6 3.6 53.3% 2.8 51.9 2.6 47.0 3.0 51.59 3.94
Skeletodental
Occlusal Plane-
Ramus 2.6* 0.5 2.1 2.9 0.9 4.9 0.6 4.1 1.0 - 1.31 3.2
SNA 80.0 6.3 81.1 3.5 81.9 4.6 80.8 4.7 81.0 3.0 81. 12 4.32
SNB 76.2 4.7 76.1 3.8 76.6 4.4 75.6 4.9 79.0 3.0 76.22 4.09
Craniofacial
Facial Axis
(Ba-N to
Facial Axis) 87.72 4.2 87.3 4.3 85.6* 3.1 85.2 2.3 90.0 3.5 86.63 3.77
Facial Taper
(Go-Gn to N-Po) 65.7 6.5 64.8% 3.1 62.8% 3.5 63.5 3.7 68.0 3.5 64. 18 3.94
Maxillary Depth
(F.H. to NA) 92.5 5.5 92.0 3.5 92.7 3.3 93.0 2.7 90.0 3.0 92.47 3.57
Palatal Plane
(to SN) —6.9% 3.0 –7.1% 3.4 –6.8% 3.5 –6.5* 4.5 4.0–0.5/yr 3.5 —6.95 3.45
Deep Structure
Cranial
Deflection 28.83 2.1 29.4° 1.8 29.8% 2.4 30.6 1.4 27.0 3.0 29.64 2.01
Mandibular
Arc 28.89 6.9 25.0 4.9 21.5% 5.3 25.1 2.2 26-0.5/yr 4.0 24.58 5.43
Table 4. University of Illinois study, 1972.
:
Nasopharyngeal Obstructions
posture of the tongue is the contact of the dorsum of the tongue with the
velum or soft palate. This contact is not present in mouth breathers with
large tonsils. Table 5 illustrates that the tongue is found to be elevated
3.4-4.1 mm in the mouth breathers who became nose breathers after
surgery (Groups I and IIB) and 3.5 mm in the nose breathers (Group III)
following the removal of enlarged tonsils. Tongue size can be assessed by
comparing the level of its dorsal surface to the cervical margin of the
maxillary first molars by using the hyoid bone as a “postural marker.” In
cases of macroglossia and skeletal open bite, the hyoid was found to be
positioned significantly lower than at its normal level between the third
and fourth cervical vertebrae (Bench, '63).
When reviewing the tongue-velum posture relative to large adenoids, it
is essential to consider the potential for velopharyngeal insufficiency or
cleft palate, hypernasal speech as a side effect of adenoidectomy. Dimen-
Sions for hard and soft palates and pharyngeal depth in normal and insuf-
ficient airway function subjects have been described by Lawson and col-
leagues (72) and Hoopes and co-workers ('70).
Yet another factor relative to tonsil mass and tongue velum contact is
that of the resting and centric occlusion postures of the mandible. In
complete mouth breathers the author found that it often was impossible
to obtain a reliable lateral roentgencephalogram in centric occlusion (or
maximum intercuspation) presurgically (Bushey, '65). Furthermore, the
resting position of the mandible was found to assume a more upward and
posterior posture postoperatively.
Incisor inclination can serve as an indication of the degree of lip com-
petence mentioned earlier in the description of the clinical examination.
A high interincisal angulation preoperatively indicates lip approximation
with significant tonicity, in spite of mouthbreathing, with a good progno-
sis for lip closure postoperatively. Conversely, the presence of a smaller
than average interincisal inclination and increased incisor overjet preop-
eratively, in spite of a high lower face height dimension, indicates an
inherent weakness in the perioral musculature with poor potential for
adaptation to a closed lip posture and for nasal breathing postoperatively.
Posterior-Anterior Aspect. 1. Facial Proportion and Symmetry. The
frontal cephalometric analysis for potential mouth breathers provides
valuable means of assessing the relative dimensions of nasal, maxillary
and bigonial widths. Facial proportioning can be interpreted to determine
if a long, narrow, dolicofacial form is present. By comparing maxillary,
dental, mandibular and facial midlines, a judgement can be reached as to
the amount and location of asymmetry. Functional deviation in midlines
should be evaluated for the influence of skeletal and/or dental arch width
disharmonies. As was discussed earlier (Bushey, '77), the more extreme
312
#
- Significant
I IIA IIB III Differences
- - - - - Between
Range X SD Range X SD Range X SD Range X SD Group Means
AA-S-PMF (°) 45.0–54.0 48.8 +3.3 33.5–52.0 44.4 +5.0 29.0–58.5 43.8 + 8.3 42.5–55.5 48.0 +5.4 I: IIA*
Ba-S-PMF (°) 56.0–68.0 63.3 + 4.0 52.0–70.5 62.0 +5.6 55.5–71.5 63.0 +5.2 57.0–70.5 62.5 +5.7
AA-PMF (mm) 31.9–37.0 35.5 + 1.9 29.3–41.5 34.2 +3.9 28.0–40.7 34.4 + 4.2 31.5–40.4 34.3 + 4.0
Anterior Height
S-AA-PMF (°) 50.0–70.0 60.3 +6.9 55.0–77.0 65.5 +6.1 60.0–75.0 66.5 +4.8 58.5–71.0 64.0 +4.8 I:IIB”
S-BA-PMF (°) 51.0–63.5 56.3 + 4.5 55.0–68.0 59.6 +3.7 52.0–68.0 59.8 +4.7 55.0–65.5 60.2 + 3.6
PMF-S (mm) 36.3—46.5 40.9 +3.6 36.1–52.4 44.0 +4.1 39.7–48.4 44.5 +3.6 35.4–44.5 41.4 +3.5 I:IIB”
Posterior Height
BA-S (mm) 38.1–46.6 42.5 +3.5 34.6–47.9 43.1 +3.1 37.9–50.0 43.1 +4.2 33.0–44.2 40.0 +4.7
AA-S (mm) 40.5–47.4 44.2 +2.5 35.4–50.7 45.1 +4.1 38.7–53.2 45.0 + 4.4 35.6–48.4 42.6 + 4.5
Cranial Base Angulation
BA-S-N (*) 133–147 137.2 —5.1 125–142 133.1 +4.9 125–142 131.1 +5.1 127–139 134.5 +5.0 I:IIB”
Measured Along Line S-H
Sphenoid body III:IIA***
thickness (mm) 16.4—20.0 18.0 — 1.5 15.5–24.8 19.7 -E2.4 16.6–23.5 19.1 + 1.9 13.5–18.6 16.3 + 1.7 III:IIB” *
tongue eleva-
tion (mm) –2.5–7.2 3.4” –3.3 0–9.3 4.1 ** +2.6 – 5.5–5.5 1.3 +3.3 0–7.7 3.5* +3.2 IIA: IIB."
Hyoid eleva-
tion (mm) –2.0–8.1 4.8° —3.6 –2.5–9.6 3.0** +3.7 – 7.0-9.9 0.7 -t- 4.7 – 5.0–8.0 1.0° -- 4.2
Respiratory Groups
Depth
*Significant at 0.05
**Significant at 0.01
***Significant at 0.001
Table 5. Respiratory group comparison based on linear and angular dimensions of the epipharynx
#.
Nasopharyngeal Obstructions
the skeletal openbite tendency, the greater the tendency for asymmetric
functional disharmonies.
2. Posterior Crossbite Evaluation. The narrowing of the maxillary pos-
terior dental segments has been a consistent characteristic of mouth
breathers (Ricketts, '68; Linder-Aronson, '70, 74). The frontal cephalo-
metric analysis provides an objective measurement of the maxillary inter-
molar dimension compared to that of the mandibular molar width. Thus,
a determination can be made as to whether the posterior crossbite is the
result of a narrow maxillary arch, a wide mandibular arch, or both. It also
provides for an interpretation as to whether the posterior crossbite is of a
dental or skeletal nature. The potential stability of crossbite correction by
palatal expansion is determined by its degree of skeletal contribution;
skeletal expansions of dental crossbites were not found to be stable
(Bushey, '77). •
In summary, the radiographic analysis in the lateral and posterior-ante-
rior aspects provides a systematic means of evaluating airway space, the
morphogenetic pattern factors of lower face height, maxillomandibular
morphology and facial growth in mouth breathers. As stated earlier,
mouthbreathing has its most significant impact on individuals with inhe-
rent vertical facial growth characteristics of lower facial axis values,
higher gonial angle and nasal to mandibular plane angle values with in-
creased lower face height. Finally, functional response of the velum,
tongue, mandible and teeth are assessed for genetic versus environmental
influences to establish a differential diagnosis and prognosis.
CLASSIFICATION OF AIRWAY OBSTRUCTION AND
TONSIL-TONGUE DISPLACEMENT CASES
The preceding clinical and radiographic assessment techniques have
been used clinically to differentiate typical combinations of facial types
and adenoidſtonsils enlargement (Bushey, '74) to provide more specific
treatment rationales. Table 6 summarizes the clinical and radiographic
characteristics of six types of problem cases confronting the orthodontist.
Type 1 – Enlarged Adenoids in a Good Facial Pattern
There are a significant number of orthodontic patients first observed
during the deciduous or mixed dentition phase who have enlarged ade-
noids and posterior crossbites but otherwise normal dental and facial
features. Although these patients are partial mouth breathers, the
strength of the inherent facial pattern prevails over the aberrant respira-
tory pattern. The orthodontist will often find that the early correction of
314
Bushey
the posterior crossbite is difficult to maintain and will require re-
correction in the permanent dentition until the involution of the nasopha-
ryngeal lymphoid obstruction has occurred. These cases resemble Group
III of the control sample described by Linder-Aronson ('70).
Type 2 – Large Tonsils but Adequate Airway in a Good Facial Pattern
A more perplexing type of orthodontic problem is found in the patient
who has enlarged tonsils which are producing significant tongue displace-
ment. These cases evidence uncommonly wide lower dental arches with
severe posterior crossbites, but have an apparently normal upper arch
width and an adequate epipharyngeal airway. Often there is a large
tongue present which will result in an open bite and in significant loss of
lip competence. If a Class III tendency is present, there may be a minor
anterior crossbite. If a tonsillectomy is performed early, this type of case
may respond with a spontaneous correction of the anterior crossbite and/
or open bite and a significant increase in the upper arch width, thus
improving the crossbite relationship. The most perplexing feature of these
cases is the difficulty encountered in convincing the pediatrician and some
otolaryngologists that a critical obstruction is present. If a tonsillectomy is
not performed, the crossbite correction must be retained for an extremely
long time. If an extremely large tongue is present, there will be a compro-
mise in the profile esthetics requiring either the acceptance of a double
protrusion or the extraction of four bicuspids.
Type 3 – Adenoidal Obstruction with Increased Lower Face Height
The clinical evaluation of this type of orthodontic patient is character-
ized by the separation of lips of adequate length, narrow nares, partial
mouthbreathing and a moderately dolicofacial form. The dental examina-
tion reveals upright incisors with minimum overbite and overjet, with a
possible midline deviation from mandibular rest position to centric occlu-
Sion. The maxillary arch is typically narrow with a moderate palatal vault
height. The faucial tonsil enlargement is variable. The lateral cephalomet-
ric analysis indicates a moderate to large adenoid mass confined in a
nasopharynx of average to small dimensions. In contrast to Type 1 above,
the lower face height dimensions are greater by one standard deviation in
the angular measurement and are advanced approximately 3 years in the
linear measurement of Harvold. The maxillomandibular relationship is
characterized by an increased value for the gonial angle or an upward tilt
of the mandible to account for the 3° increase in mandibular plane/nasal
plane divergence. The hyoid is often positioned at or below the level of
the fourth cervical vertebra signifying a low tongue posture. Even moder-
ate enlargements of the faucial tonsils may contribute to the tongue dis-
placement from mouthbreathing.
315
Adequate Facial form—wide to Small above average prolonged retention
airway Openbite—severe Max/mand—brachyfacial Asymmetry not significant if no tonsillectomy
posterior mandible . unless dental
Tongue dis- Tongue normal to large Growth normal to Class III
placement Tonsils large to very Tonsils—large, signifi
large cant tongue displacement
Type III Lip—mouthgape to lip Adenoids average to small Intermolar width, maxilla Adenoidectomy (& possible
competence Nasopharynx average to decreased tonsillectomy) indicated
Adenoidal Nares narrow Small Nasal, max, mand, facial Maxillary expansion
obstruction Breathing—partial Lower face height—1 SD mod reduced Slow lymphoid involution
mouthbreathing Max/mand—increased Asymmetries—dental and if no tonsillectomy and
Lower face Lower face height gonial angle skeletal possible adenoidectomy
height increased Growth vertical tendency
~ 1 SD Maxillary arch narrow Tonsils—possible tongue
Classification*
Clinical Examination
Cephalometric Factors
Lateral
Fontal (P.A.)
Treatment Indications
Type I
Large adenoids
Normal facial
Lip competence
Nares normal
Breathing—nose/partial
mouth breathing
Adenoids borderline obstr.
Nasopharynx average to
large
Lower face height normal
Intermolar width, normal
range
Nasal, max, mand facial
widths normal
Adenoidectomy not
indicated
Orthodontic treatment
Airway patency with
pattern Facial symmetry Max/mand size, position Facial or dental asymmetry adenoid involution
Openbite—moderate normal not significant
posterior Growth—direction, amount
Tonsils small normal
Tongue/velum near contact
Tonsils—small
Type II Lip separation but Adenoids average to large Intermolar width, maxilla Tonsillectomy indicated
Large Tonsils
competent
Nares wide
Breathing—nose
Nasopharynx average to
large
Lower face height normal
normal and mandible
large
Facial width normal to
Orthodontic treatment—
arch expansion,
bicuspid extractions,
Tonsils possible
enlarged
displacement even if
Small
#
;
Type V
Large adenoids
Velopharyngeal
incompetence
Type VI
Abnormal tongue
posture
Abnormal neuro-
muscular co-
ordination
Lip competence
Breathing—nose to
partial mouthbreathing
Hard palate short, submu-
cous cleft
Bifid uvula
Hypernasal speech, poor
coordination possible
Normal clinical features
ranging from macroglo-
ssia with dental open-
bite to low tongue
posture with deep bite-
poor coordination
Type IV
Adenoidal
obstruction
Lower face
height
> 2 SD
Lip incompetence, severe
short upper lip
Nares small, tilted up
Breathing—severe mouth-
breathing
Dolichofacial with
asymmetry
Max/mand arches narrow
Tonsils possible enlarged
Adenoids large
Nasopharynx small
Lower face height—- 2 SD
Max/mand—skeletal open-
bite tendency, Class III
mandible
Growth strongly vertical
Tonsils variable
Adenoids large
Nasopharynx large and deep
Lower face height variable
Maxilla—short, hard
palate
Growth variable
Velum incomplete eleva-
tion/pharyngeal contact
Adenoids—may have early
Nasopharynx variable
Lower face height increased
Max/mand variable
Growth often vertical
tendency
Tongue/hyoid—low posi-
tioning, poor coordina-
tion
Intermolar widths, maxilla
and mandible small
Molar openbite unilateral
Nasal, max widths small
Asymmetries—definite
dental and skeletal
Factors are variable
Adenoidectomy and tonsil-
lectomy indicated
Orthopedic forces—
palatal expansion, vert.
growth control
Allergy work-up if
continued mouthbreathing
Adenoidectomy—possible
lateral adenoidectomy
OI. In One
Pharyngeal flap
Speech training
Orthodontics—conventional
Intermolar widths,
mandible increased
Nasal, max widths small
or variable
Asymmetry—dental and
skeletal frequently
Clear airway
Maximum orthodontic control
through entire growth
period
Speech training
Table 6. Classification of airway obstruction and tongue/tonsil problems in orthodontics
É
Nasopharyngeal Obstructions
The frontal cephalometric analysis shows a composite picture of a nar-
row maxilla and a maxillary arch with a tendency for dental and skeletal
asymmetry. Special care should be taken to determine if a unilateral
centric occlusion crossbite is the result of a functional shift caused by a
moderately narrow maxillary arch.
Treatment response may be excellent if an adenoidectomy is performed
at an early age and conventional orthodontic treatment is instituted. Type
3 individuals are represented by Group 5 of Linder-Aronson ('70) and
Groups I and IIA described by the author (Bushey, '65).
Type 4 – Severe Adenoidal Obstruction with a Pronounced Vertical Facial
Pattern
These cases represent the greatest challenge to the orthodontist as the
airway should be cleared at an early age, and this requires a coordinated,
indisciplinary approach to treatment. Performing an adenoidectomy (and
tonsillectomy) often is not all that is needed to complete the transition to
nasal breathing. Sometimes extensive pediatric allergy therapeutic sup-
port is also needed because of the inherently small nasal passages. There-
fore, the orthopedic expansion of the maxilla by the orthodontist can
greatly enhance nasal respiration if not done at the expense of maxillary
molar extrusion and rotation of the mandible. The greater the mandibular
growth contribution combined with delayed treatment, the greater the
potential for insufficient orthodontic control. The skeletal open bite
which may result can elicit a sequence of balancing and protrusive func-
tional occlusal interferences because of the lack of anterior guidance.
These unsuccessfully treated cases exhibit the most extreme relapse ten-
dencies and often lead to myofascial pain dysfunction which can only be
successfully treated with surgical orthodontics.
Type 5 – Large Adenoids with Velopharyngeal Incompetence
A special note of caution is warranted in diagnosing young individuals
with large adenoids when potential velopharyngeal incompetence may
exist. The large adenoid mass may mask hypernasal speech by compen-
Sating for a significantly deep pharyngeal airway as measured from PNS-
AA (normal mean of 34.5 mm) or PNS-Ba (normal mean of 43 mm).
Ricketts reported a PNS-AA mean of 42 mm in individuals with hyperna-
sal speech and submucous clefts. Although the more typical anatomical
deficit may be revealed by a bifid uvula and a palpable notch in the
posterior hard palate, Lawson and colleagues (72) reported that 13 of 40
patients with velopharyngeal dysfunction had normal cephalometric mea-
surements. These individuals could only be diagnosed by a combination
of speech, rapid frame cinefluorographic, and coordination pattern re-
318
Bushey
cordings. Treatment must be carefully coordinated through speech spe-
cialists, plastic Surgeons and otolaryngologists.
Type 6 — Abnormal Tongue Posture and Neuromuscular Coordination
Encountered in as low a frequency as Type 5, are those individuals with
bizarre tongue posture and coordination patterns. The low tongue pos-
ture thought to be the result of enlarged tonsils or a mouth-breathing
pattern may simply not respond by postural elevation to tonsillectomy
and/or adenoidectomy. Tongue size may be a factor, and an extensive
neurological evaluation may be required before treatment can be coordi-
nated. Treatment may be compromised in spite of prolonged speech
training and orthodontic correction.
MODES OF TREATMENT: AN INTERDISCIPLINARY APPROACH
In consideration of the amount of diagnostic criteria available for a
comprehensive differential diagnosis of nasopharyngeal airway obstruc-
tion and the potential for classifying patients into significantly different
therapeutic categories, a more effective interdisciplinary approach to
treatment is warranted. If, as reported by Bluestone ('77), more than
60% of tonsillectomies and adenoidectomies are performed on children
under 6 years of age, then new and earlier referral patterns between the
pediatrician, pedodontist, orthodontist, otolaryngologist and pediatric al-
lergist are required.
The orthodontist often finds himself in the middle of the referral pat-
tern. To improve medico-dental cooperation, the orthodontist should (1)
perform the clinical and radiographic examination, (2) classify the treat-
ment problem and prognosis and (3) report his findings to the patient’s
pediatrician and otolaryngologist. The orthodontist’s report should in-
clude an assessment of (1) adenoidal obstruction relative to nasopharyn-
geal dimensions, (2) lower face height and the maxillomandibular rela-
tionships and (3) growth direction and the potential for functional and
transverse dental relationships. The lateral and frontal roentgenograms
should accompany the cephalometric analysis to enable the direct visual-
ization of the areas of obstruction. The pediatrician, in turn, should re-
spond with a comprehensive report of the patient’s history and physical
examination. Additional consultations with the allergist and otolaryngolo-
gist will complete the circle of interdisciplinary collaboration.
It should be stressed that any classification system is only as useful as
the degree of individual interpretation given to each patient. For ex-
ample, care must be exercised in separating individuals with moderate to
large adenoids into types 1, 3, 4 and 5 by means of assessing their cranio-
319
Nasopharyngeal Obstructions
facial variations (Table 6). Types 3 and 4 are sometimes only clearly
distinguishable after mouthbreathing and unfavorable growth have per-
sisted for more than half of the patient’s growth period.
A truly interdisciplinary cooperation in diagnosing and treating indi-
viduals with naso-respiratory obstruction will occur when all concerned
health professionals (1) agree on current diagnostic criteria, (2) have a
group awareness of new criteria, (3) have group agreement to evaluate
the new criteria for a specific time and, finally, (4) assess the new criteria.
The long-term study of tonsillectomy and adenoidectomy individuals be-
ing conducted at Children’s Hospital in Pittsburgh should provide a broad
data base upon which new criteria for diagnosis and treatment can be
established (Paradise and Bluestone, '76).
SUMMARY AND CONCLUSIONS
The purpose of this paper is to offer a more comprehensive diagnostic
and treatment approach for different types of obstructed and functionally
altered orthodontic patients. We may conclude that:
1. A systematic sequence for clinical and radiographic examinations of
potentially obstructed individuals has been established to provide a more
critical assessment of their functional and anatomical variations.
2. A patient classification which integrates the degree and type of ade-
noidal obstruction with different nasopharyngeal facial patterns may be of
use in diagnosing and treating these complex cases.
3. A patient referral system which combines the diagnostic and treat-
ment skills of orthodontists, pediatricians, pediatric allergists and otolar-
yngologists will provide the optimum opportunity for these patients to
enjoy normal growth and development while receiving effective ortho-
dontic treatment which is functionally stable.
REFERENCES
Bench, R. W. Growth of the cervical vertebrae as related to tongue, face and
denture behavior. Am J. Orthodont. 49:183–214, 1963.
Bench, R. W., C. F. Gugino and J. J. Hilger. Bioprogressive therapy. J. Clin.
Orthodont. 12(1):48-69, 1978.
Bimler, H. P. Uber die Microrhine Dysplasie. Fort. Kieferorthopadie, 26:4, 1965.
Bluestone, C. D. Status of tonsillectomy and adenoidectomy. Laryngoscope,
87:1233-1243, 1977.
Bushey, R. S. Alterations in certain anatomical relations accompanying the
change from oral to nasal breathing. Master's Thesis, University of Illinois,
1965.
Bushey, R. S. Recent research findings relating nasopharyngeal function to oral
320
Bushey
physiology and craniofacial development. Proc. Found. Orthodont. Res.
April, 1972.
Bushey, R. S. The relationship of nasopharyngeal airway obstruction to dentofa-
cial development and its implications for orthodontic treatment. Angle Soc.
Pap. 1974.
Bushey, R. S. Posterior crossbite: A four-dimensional assessment. Angle Soc.
Pap. 1977.
Bushey, R. S. Adenoid obstruction of the nasopharynx. In: Naso-respiratory
Function and Craniofacial Growth. J.A. McNamara, Jr. (ed.), Monograph 9,
Craniofacial Growth Series, Center for Human Growth and Development,
The University of Michigan, Ann Arbor, 1979.
Handelman, C. S. and G. Osborne. Growth of the nasopharynx and adenoid
development from one to eighteen years. Angle Orthodont. 46(3):243-259,
1976.
Harvold, E. P. Personal communication. 1971.
Hoopes, J. E., A. L. Dellon, J. I. Fabrikant, M. T. Edgerton, Jr., and A. H.
Soliman. Cineradiographic definition of the functional anatomy and patho-
physiology of the velopharynx. Cleft Pal. J. 7:443-454, 1970.
Koski, K. and P. Lahdemaki. Adaptation of the mandible in children with ade-
noids. Am. J. Orthodont. 68:660-665, 1975.
Lawson, L. I., A. C. Chierici, E. P. Harvold, E. R. Miller and J. Q. Owsley, Jr.
Effects of adenoidectomy on the speech of children with potential velopharyn-
geal dysfunction. J. Speech Hear. Dis. 37:390-402, 1972.
Linder-Aronson, S. Adenoids: Their effect on mode of breathing and nasal air-
flow and their relationship to characteristics of the facial skeleton and the
dentition. Acta Oto-Laryngologica Supplementum 265:3-132, 1970.
Linder-Aronson, S. and C. O. Henrickson. Radiocephalometric analysis of ante-
roposterior nasopharyngeal dimensions in 6 to 12 year old mouth breathers
compared with nose breathers. Practica-Otorhinolaryngologica, 212, Swiss,
1973. .
Linder-Aronson, S. Effects of adenoidectomy on dentition and nasopharynx. Am.
J. Orthodont. 65:1-15, 1974.
Linder-Aronson, S. and D. Woodside. The channelization of upper and lower
anterior face heights compared to population standard in males between ages 6
to 20 years. Europ. J. Orthodont. 1:25-40, 1979.
McKee, T. L. A cephalometric radiographic study of tongue position in individu-
als with cleft palate deformity. Angle Orthodont. 26:99-109, 1956.
Paradise, J. L. and C. D. Bluestone. Toward rational indications for tonsil and
adenoid surgery. Hosp. Pract. 11(2):79-87, 1976.
Posen, A. L. The influence of maximum perioral and tongue force on the incisor
teeth. Angle Orthodont. 42:285-309, 1972.
Ricketts, R. M. Respiratory obstructions and their relation to tongue posture.
Cleft Pal. Bull. 8(3):4, 1958.
Ricketts, R. M., C. H. Steele and R. C. Fairchild. Forum on the tonsil and
adenoid problem in orthodontics. Am. J. Orthodont. 54:485-514, 1968.
Ricketts, R. M. Personal Communication, 1969.
321
Nasopharyngeal Obstructions
Robert, A. Memoire sur le Gonflement Chronique des Anygdales cez les En-
fants. Bull. Gen. De Therap. 24:343-351, 1843.
Schulhof, R. J. Consideration of airway in orthodontics. J. Clin. Orthodont.
12:440-444, 1978.
Siebenmann. Uber adenoide Habitus und Leptoprosopie, sowie uber das kurze
Septum der Chamaeprospoen. Much. Med. Wschr. (cit. Nordlund, H.), 1897.
Solow, B. and E. Greve. The effect of adenoidectomy on head posture and nasal
respiratory resistance. In: Nasorespiratory Function and Craniofacial Growth,
J. A. McNamara, Jr. (ed.), Monograph No. 9, Craniofacial Growth Series,
Center for Human Growth and Development, The University of Michigan,
1979.
Subtelny, J. D. The significance of adenoid tissue in orthodontia. Angle Ortho-
dont. 24:59–69, 1954.
Subtelny, J. D. and J. D. Subtelny. Oral habits -- studies in form, function and
therapy. Angle Orthodont. 43:347-383, 1973.
Thompson, J. R. A cephalometric study of movements of the mandible. J. Am.
Dent. Assoc. 29:925-941, 1938.
Tomes, C. S. On the developmental origin of the v-shaped contracted maxilla.
Month. Rev. Dent. Surg. 1:2, 1872.
Turbyfill, W. J., Jr. The longterm effect of rapid maxillary expansion on nasal
airway resistance. Master's Thesis, Fairleigh Dickinson University, 1976.
Wallis, H. R. E. Medical aspects of malocclusion. Dent. Rec. 73:519, 1953.
Watson, R. M., Jr., E. W. Warren and N. D. Fischer. Nasal resistance, Skeletal
classification and mouthbreathing in orthodontic patients. Am. J. Orthodont.
54:367-379, 1968.
Woodside, D. G. The present role of the general practitioner in orthodontic.
Dent. Clin. N. Am. 3:483-508, 1968.
Yip, A. S. G. and J. F. Cleall. Cinefluorographic study of velopharyngeal func-
tion before and after removal of tonsils and adenoids. Angle Orthodont.
24:59-69, 1971.
322
THE ORTHODONTIST'S RESPONSIBILITY IN
PREVENTING FACIAL DEFORMITY
Robert M. Rubin, D. M. D., M.S.
Norfolk, Virginia
The recognition that crisis care in medicine is the least effective and most
expensive therapy has focused the attention of health providers on pre-
vention. Similarly, in dentistry, the understanding of the pathology of
dental caries and periodontal disease has led to a preventive orientation:
control of plaque. Yet, in orthodontics it is common practice to allow the
course of detrimental growth to proceed until its virtual completion be-
fore commencing treatment. This observation does not ignore those ap-
proaches that include serial extraction, the correction of crossbites in the
mixed dentition and early extraoral traction. It suggests that these ap-
proaches are often too little - too late.
The largest increments of growth occur during the earliest years of life.
In the first five months of life, the child’s weight doubles. This never
occurs again in a similar span of time. In the first three years, the child’s
height doubles (Nelson et al., '69) which never occurs again. Each day in
a child’s life witnesses a smaller increment of growth than the previous
day, except for those well-documented spurts of growth around puberty.
By age four the craniofacial skeleton has reached 60% of its adult size.
By age twelve, the age when many orthodontists initiate treatment, 90%
of facial growth has already occurred (Meredith, '53). To wait until 90%
of a deformity is established before instituting treatment is not consistent
with a preventive philosophy. Since successful treatment of anteroposte-
rior and vertical discrepancies is linked to growth changes, it suggests that
we should initiate interceptive measures far earlier than is conventionally
done.
Even more important than interception is the possibility of prevention
by removing adverse influences that interfere with normal facial growth.
The development of the face is one of the key occurrences during the 5th
to 12th weeks in utero. It has been shown that there are many environ-
mental influences on the developing fetus at this time.
One influence is the nutritional intake of the mother. The orthodontic
waiting room is an excellent place to disseminate literature on nutrition
during pregnancy, since frequently, adult female patients and the mothers
of young patients are of child-bearing age.
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Facial Deformity
The influence of drugs and medication on the developing fetus is be-
coming more apparent. Fetal alcohol syndrome (Jones et al., '73) has
been described recently. Diazepam (Valium, Roche), the most prescribed
drug in the U.S. pharmacopea, is suspected of causing cleft lip/palate
when ingested during the 5th to 12th weeks (Safra and Oakley, 75).
Meclizine hydrochloride, an antihistamine (Bonine) has been shown to
cause cleft lip/cleft palate in rats, even in low doses (Kendrick and King,
'64). It is sold without prescription and commonly was recommended for
the morning nausea associated with pregnancy. Now it carries a warning
to women of child-bearing age. Caffeine, nicotine and aspirin should be
regarded as potential teratogens when consumed by pregnant women
during the critical period of orofacial development. The orthodontist can
influence the expectant mother to practice excellent prenatal habits for
the welfare of her baby. He can communicate his concern to his col-
leagues in obstetrics to promote better orofacial health in children.
Postnatally, there are many possible causes of altered facial growth
leading to varying degrees of facial deformity. One hundred years ago,
the first articles appeared describing the “adenoid face” (Tomes, 1872).
The concept remained current for many years until the attention of our
profession turned to mechanotherapy. “Etiology is unimportant, the ma-
locclusion must be treated” was a common refrain.
Only in the past twenty years has the notion that the patient's mode of
respiration can profoundly influence facial growth received new currency.
Linder-Aronson (75), Subtelny (74), Ricketts ('68a), Quinn ('78),
Bushey ('65) and others have addressed the issue. The term “respiratory
obstruction syndrome” (Ricketts, '68) was used to describe the constella-
tion of characteristics associated with obstruction of the nasal airway
during the years of facial growth. Other common terms are the “long face
syndrome” (Schendel et al., '76) and “vertical maxillary excess.” These
characteristics include excessive anterior face height, incompetent lip pos-
ture, excessive appearance of maxillary anteriors, narrow external nares,
steep mandibular plane and posterior crossbite (Figs. 1 and 2).
Thompson ('61), in his classic text “On Growth and Form”, notes that
the “. . . form of an object is (its) diagram of forces.” Applied to cranio-
facial morphology, one can say that the form and spatial position of the
craniomaxillary complex and the mandible is the result of the forces
acting on them.
Harvold (Harvold et al., '72) has shown that obstruction of the nares in
monkeys is followed by the recruitment of muscles to lower the mandible
and spread the lips to establish an oral airway. The same changes can be
seen in man. The suprahyoids contract and the masseters, internal ptery-
goids and temporalis relax, permitting the mandible to rotate in a clock-
wise direction. Upon swallowing, many mouth breathers do not elevate
324
Rubin
Figure 1. The long face syndrome. Note incompetent lip posture.
their mandible to bring the upper and lower posterior teeth into contact
(Ricketts, '68b). As a result, they are at risk to develop the long face
Syndrome. It is believed that the absence of these interdental contacts,
estimated to occur normally over 1,000 times per 24 hours, permits exces-
Sive vertical alveolar development and eruption of the posterior segments.
Pathological examples support this concept. Cerebral palsy patients
have a characteristically steep mandibular plane and excessive anterior
face height. Scoliosis patients who wore a Milwaukee brace with a chin
rest developed a reduction in their mandibular plane angle and deepening
of their overbite as the brace enhanced the action of the mandibular
elevators (Alexander, '66).
Linder-Aronson (75) has shown cephalometrically that the mandibular
325

Facial Deformity
Figure 2. Excessive appearance of maxillary anteriors.
plane angle flattened when mouth breathers became nasal breathers after
adenotonsillectomy.
The writer believes that the case for nasal airway obstruction as a
major cause of high angle malocclusion has been convincingly established
through clinical research. In an unpublished study of fetal skulls (Rubin,
'74), no high angles were found. Balyeat and Bowen (34) reported a very
low incidence of dentofacial abnormalities in Oklahoma Indians. Sincock
('63) confirmed this finding in the Chippewa Indians.
326







Rubin
Thus, the epidemiology infers that high angle malocclusion is an ac-
quired characteristic, possibly caused by reduced, biologically effective
forces being expressed between the mandible and maxilla. The cause may
be central nervous system damage, peripheral myoneuropathy or mouth-
breathing secondary to obstruction of the nasal airway. Bushey has re-
ported the case of monozygotic twins, in which only the one who had
nasal obstruction developed the long face syndrome (Bushey, '65).
The major cause of nasal airway obstruction in the young child is
allergic rhinitis (Sale, '76). While there is a genetic inclination to develop
allergies, there are reports that prophylaxis of allergic disease in infancy
can alter the course of allergic symptoms for a lifetime. Glaser (62) has
reported that among infants with familial allergic histories, four times as
many children who are fed cow's milk during their first year develop
respiratory allergies by age six than those placed on hypoallergenic soy
bean milk. This observation, which has been confirmed by others (Sale,
'76), may be a major benefit to children of allergic parents. It suggests
that an attempt should be made to avoid an allergic reaction during the
first year of life to permit the allergic response mechanism to become
quiescent. •
Cow’s milk, the basis of most baby formulae, contains three times as
much large molecular protein as human milk and is the major allergen
affecting the newborn (Sale, '76). Dr. Frank Oski (79), Chief of Pediat-
rics, New York University Hospital, estimates that up to 25% of infants
suffer from allergic and related disorders from cow's milk. Clearly,
breastfeeding is best for children and especially desirable when either
parent has an allergic history. If breastfeeding is impossible, as is rarely
the case, hypoallergenic formula based on soybeans should be used when
a familial allergic history is present. -
The early introduction of adult food, before the gastrointestinal tract
loses its porosity at approximately six months of age, frequently causes
allergic reactions in children. Orange juice, eggs and cereal are common
food allergens in infancy (Sale, '76). Some pediatricians introduce foods
at two months of age. The tendency to add these foods in the first months
of life, in response to parental request, must be resisted. Primitive soci-
eties use breast milk as the only food source for a year or longer with
excellent nutritional results.
Breastfeeding has other advantages. The colostrum in the breast milk is
rich in antibodies, conferring immunity to the infant against viral and
other diseases. The infant does not produce its own immunoglobulin for a
few months after birth. The mother's antibodies and the porosity of the
infant’s gastrointestinal tract combine to protect the child. Cow’s milk
becomes a two-sided disadvantage. It contains no antibodies, and its ex-
cessive protein sensitizes many children.
327
Facial Deformity
At three months of age many pediatricians begin dipropyltryptamine
immunization. This introduces foreign protein, and many infants have
allergic reactions to these injections. The breastfed infant has some anti-
body protection from the mother’s milk and can afford to delay the
immunization program until six months of age or later.
After the first year of life, airborne particles replace foods as the major
cause of allergy in children (Sale, '76). Proper humidification to reduce
the number of floating particles, air cleaners, elimination of house dust
and removal of pets are some of the steps to be taken to promote nasal
airway health.
The adenoids and tonsils, which are frequently the target of the blame
for airway obstruction, often are enlarged in response to the health of the
anterior nose and sinuses. Therefore, allergy must be controlled before
adenotonsillectomy is performed. Untreated allergic children often are
seen to have recurrence of the lymphoid tissue after surgery.
Vasomotor rhinitis and septal deviation are other causes of nasal ob-
struction and can be corrected early with surgery. It has been demon-
strated that careful surgery on the nasal Septum in growing patients does
not have an adverse effect on growth (Pirsig, '78). Gray and Brogan ('72)
report that early rapid maxillary expansion is effective in correcting septal
deformity and improving the airway in over 80% of cases. They recom-
mend expansion around age 3 to 7 years even when no crossbite exists
(Gray and Brogan, '72). Cryosurgery for chronic vasomotor (nonallergic)
rhinitis is being performed increasingly with success (Principato, '79).
The orthodontist is uniquely qualified to monitor the growing face. He
should consult with his colleagues in pediatrics, obstetrics, otolaryngology
and allergy to promote optimal facial growth. When he observes a patient
developing excessive anterior face height because of nasal airway obstruc-
tion, he should arrange appropriate referrals.
Dr. Charles Berman ('78) recently wrote, “Natural law did not divide
man into three parts: dental, medical and psychological. If society chose
this division for the purposes of health care delivery, then each profes-
sional group bears a special responsibility to be sufficiently informed
about the others so that integrated total health care is an achievable
goal.”
It is not enough to look in the mouth and see large tonsils or to see
extensive epipharyngeal lymphoid tissue on a cephalometric X-ray and
order an adenotonsillectomy. Dr. Berman continues, “Although we have
generations of the best-trained dentists in the world, few have ever evalu-
ated... the nose. How can we discuss these problems with a parent or
physician if we have never performed rhinoscopy?”
Equally as important, we must learn to communicate with our col-
leagues in medicine. Just as no dentist would obediently respond to a
328
Rubin
request from a physician to extract all remaining teeth for some vague
medical reason, no physician should be expected to do an adenotonsillec-
tomy upon an orthodontist’s request without a proper evaluation. There
is a better way. The following letters are offered as examples of construc-
tive communication between dentists and physicians.
Re: Mary Jones
Dear Otolaryngologist:
As Mary Jones' orthodontist, I have been observing her growth and
development for the past few years. I have noticed that she is a consis-
tent mouth breather and I am concerned about her future craniofacial
development. It has been established that mouthbreathing can cause a
facial deformity characterized by an openbite and excessive lower face
height.
I have asked Mrs. Jones to arrange an appointment with you to deter-
mine the location of her nasopharyngeal airway obstruction.
I am looking forward to hearing from you as we both try to help this
nice patient.
With a copy of this letter, I am notifying her general dentist of this
referral.
Sincerely,
cc: Patient’s dentist
Re: Chris Somers
Dear Pediatrician:
I am ready to begin Chris Somers’ orthodontic treatment and want to
share with you some views about his facial growth.
Chris has a long face and a very steep plane of his mandible. He has a
long history of mouthbreathing and is uncomfortable when he breathes
through his nose on command.
His lateral headplate shows a large adenoid mass in the epipharynx.
Although there is a history of a T and A, it is very possible that this
posterior superior tissue was not removed. Alternatively allergy may
be present to explain the continued presence of pharyngeal lymphoid
tissue. There is a familial allergic history.
I believe he should have a careful examination of his nasal airway from
nares to pharynx to establish the causes of his airway obstruction.
329
Facial Deformity
Chris' orthodontic treatment and its stability will be seriously compro-
mised if he continues to be a mouth breather.
His parents are very interested in pursuing this aggressively. If you are
in agreement with these findings I would like you to refer him to an
otolaryngologist or allergist for examination and evaluation.
I am enclosing his lateral headplate for your use. Please let me hear
from you if you have any questions.
Sincerely,
Enclosure
The result is that respectful cooperation is promoted which permits the
patient to obtain the best treatment with all the unimportant obstacles
removed.
As our profession witnesses great strides in mechanical efficiency, it is
time to reexamine the etiology of those conditions that perplex us. It is
unlikely that the problems of incompatibility of tooth size and jaw size
will ever be prevented. But the case for prevention of many cases of the
long face syndrome has been established. We must be aggressive in im-
parting our knowledge to primary care physicians and dentists so that our
young patients can experience favorable growth throughout their early
years. Age two may be a little late for the orthodontist to evaluate
whether the patient is at risk to develop the long face syndrome.
We must go beyond our own journals to learn about those factors that
are profoundly affecting our patients. It should not be long before Oto-
rhinolaryngology for Orthodontists and Allergy for Orthodontists are in
the curriculum of orthodontic education and prominent among continuing
education courses.
The American Association of Orthodontists' Public Information Pro-
gram advocates a dental examination at age three and an orthodontic
examination at age seven. This is obsolete. The orthodontist’s interest
should begin prenatally with the developing fetus and continue until need
for treatment has been removed.
It is unlikely that prevention can influence significantly intra-arch dis-
crepancies and most anteroposterior problems. However, it is apparent
that many vertical dysplasias, which include some of the most difficult
cases to treat, can be prevented with proper early care.
330
Rubin
REFERENCES
Alexander, C. The effects of tooth position and maxillofacial vertical growth
during scoliosis treatment with the Milwaukee Brace: an initial study. Am. J.
Orthodont. 52:161-189, 1966.
Balyeat, R. M. and R. Bowen. Facial and dental deformities due to perennial
nasal allergy in childhood. Int. J. Orthodont. 20:445, 1934.
Berman, C. Preface. J. Prevent. Dent. 5:8, 1978.
Bushey, R. S. Alterations in certain anatomical relations accompanying the
change from oral to nasal breathing. M.S. Thesis, University of Illinois, Chi-
cago, 1965.
Glaser, J. The prophylaxis of allergic disease in infancy. Pediatrics; 29.835, 1962.
Gray, L. P. and W. F. Brogan. Septal deformity malocclusion and rapid maxillary
expansion. The Orthodontist, 4:1-13, 1972.
Harvold, E. P., G. Chierici and K. Vargervik. Experiments on the development
of dental malocclusions. Am. J. Orthodont. 61:38-44, 1972.
Jones, K. L., D. W. Smith, C. N. Ulleland, et al. Pattern of malformation in
offspring of chronic alcoholic mothers. Lancet, 1:1267-1271, 1973.
Kendrick, F. J. and C. T. G. King. Oral anomalies induced in the rat by meclizine
hydrochloride. Oral Surg., Oral Med. and Oral Path. 18:690-696, 1964.
Linder-Aronson, S. Effects of adenoidectomy on the dentition and facial skeleton
over a period of five years. In: Transactions of the Third International Ortho-
dontic Congress. C. V. Mosby Co., St. Louis, pp. 85-100, 1975.
Meredith, H. V. Growth in head width during the first twelve years of life.
Pediatrics, 12:411-429, 1953.
Nelson, W. E., V. C. Vaughan and R. J. McKay. Textbook of Pediatrics. W. B.
Saunders, Philadelphia, pp. 23-42, 1969.
Oski, F. Personal communication, 1976.
Pirsig, W. Septal plasty in children: influence on nasal growth. Rhinology,
MV:193-204, 1978.
Principato, J. J. Chronic vasomotor rhinitis: cryogenic and other surgical modes
of treatment. Laryngoscope, 89:619-638, 1979.
Quinn, G. W. Airway interference and its effect upon the growth and develop-
ment of the face, jaws, dentition and associated parts. N. Carol. Dent. J.
60:28-31, 1978.
Ricketts, R. M. Respiratory obstruction syndrome. In: Forum on the Tonsil and
Adenoid Problems in Orthodontics. Am. J. Orthodont. 54:495-514, 1968a.
Ricketts, R. M. Esthetics environment and the law of lip relation. Am. J. Ortho-
dont. 54:272-289, 1968b.
Rubin, R. M. Unpublished data, 1974.
Safra, M. J. and G. P. Oakley. Association between cleft lip with or without cleft
palate and prenatal exposure to diazepam. Lancet, 7933:478-480, 1975.
Sale, C. S. Children’s Colds. Medical Book Publishers, Norfolk, 1976.
Schendel, S. A., J. Eisenfeld, W. H. Bell, B. N. Epker and D. J. Mishelevich.
The long face syndrome: vertical maxillary excess. Am. J. Orthodont.
70:398-408, 1976.
331
Facial Deformity
Sincock, H. A. (Quoted by E. E. Carpenter). Letters, Inter. Corres. Soc. Aller.
26th Series:48, 1963.
Subtelny, J. D. Workshop on tonsillectomy and adenoidectomy. Supplement 19,
Ann. of Oto., Rhino. Laryng. 84:250-254, 1974.
Thompson, D’Arcy, W. On Growth and Form. Cambridge University Press,
1961.
Tomes, C. S. On the developmental origin of the v-shaped contracted maxilla.
Monthly Rev. Dent. Surg. 1:2, 1872.
332
UNIVERSITY OF MICHIGAN
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OO64 1870
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