Orthognathic Surgery

991
CHAPTER 25  Dentofacial Disharmonies in Adults: Reconstruction and Rejuvenation
142. Yaremchuk MJ: Infraorbital rim
augmentation. Plast Reconstr Surg 107:1585–
1592, discussion 1593-1595, 2001.
143. Yaremchuk MJ: Subperiosteal and
full-thickness skin rhytidectomy. Plast
Reconstr Surg 107:1045–1057, 2001.
144. Yaremchuk MJ: Restoring palpebral fissure
shape after previous lower blepharoplasty.
Plast Reconstr Surg 111:441–450, 2003.
145. Yaremchuk MJ: Improving periorbital
appearance in the “morphologically prone.”
Plast Reconstr Surg 114:980–987, 2004.
146. Yaremchuk MJ: Making concave faces
convex. Aesthetic Plast Surg 29:141–147,
discussion 148, 2005.
147. Yaremchuk MJ: Indications, evaluation and
planning. In Yaremchuk MJ, editor: Atlas of
facial implants, Philadelphia, 2007,
Saunders-Elsevier, pp 3–22.
148. Yaremchuk MJ, Chen YC: Enlarging the
deficient mandible. Aesthet Surg J 27:539–
550, 2007.
149. Yaremchuk MJ, Doumit G, Thomas MA:
Alloplastic augmentation of the facial
skeleton: An occasional adjunct or alternative
to orthognathic surgery. Plast Reconstr Surg
127:2021, 2011.
150. Yousif NJ, Gosain AK, Sanger JR, et al: The
nasolabial fold: A photogrammetric analysis.
Plast Reconstr Surg 93:70–77, 1994.
151. Yousif NJ, Gosain AK, Matloub HS, et al:
The nasolabial fold: An anatomic and
histologic reappraisal. Plast Reconstr Surg
93:60, 1994.
152. Yousif NJ: Changes of the mid face with age.
Clin Plast Surg 22:213, 1995.
153. Zadoo VP, Pessa JE: Biological arches and
changes to the curvilinear form of the aging
maxilla. Plast Reconstr Surg 106:460–466,
2000.

992

26
Obstructive Sleep Apnea: Evaluation
and Treatment
JEFFREY C. POSNICK, DMD, MD
• Rationale for Treatment
• Diagnosis, Characterization, and Assessment
of Obstructive Sleep Apnea Severity
• Obstructive Sleep Apnea during Childhood:
Diagnosis and Management
• Managing the Airway during a Surgical
Procedure in the Individual with Obstructive
Sleep Apnea
• Treatment Options for Obstructive
Sleep Apnea
• Conclusions
Approximately 40% of individuals who are more than 40
years old snore, and half of them snore every night. Among
habitually loud snorers, the incidence of OSA is at least
17% in men and 15% in women. The Foundation estimates
that 16 million of the 20 million Americans with OSA
remain undiagnosed. Affected individuals are often aware
of snoring, daytime sleepiness, poor sleep patterns, and
complaints from bed partners.352 To the educated clinician,
the diagnosis of OSA may seem clear, but the affected indi­
viduals and their families are often unaware.9,106
Young and colleagues carried out a study to determine
the prevalence of sleep-disordered breathing.393-395 With the
use of a random sample of 602 employed men and women
who were between the ages of 30 to 60 years old and who
were studied via overnight polysomnography (PSG), these
authors assessed the frequency of episodes of apnea and
hypopnea per hour of sleep. The authors determined that
this condition affected up to 9% of middle-aged women
and 24% of middle-aged men (i.e., an apnea–hypopnea
index [AHI] of 5 or more and daytime hypersomnolence).185
Both male and female habitual snorers tended to have a
higher AHI of 15 or more.
Although obesity is often given as the cause of OSA,
evidence supports the idea that a significant percentage
of individuals with OSA have an anatomic predisposition
to airway collapse (i.e., retrusive jaws and obstructed
nasal cavities). Clinical studies confirm that maxillary–
mandibular–chin advancement (MMCA), which is often
combined with intranasal procedures (i.e., septoplasty, infe­
rior turbinate reduction, and nasal floor recontouring), is
relatively safe and highly effective for the treatment of OSA
when multiple sites of upper airway narrowing are present.
Published studies consistently document that MMCA is the
most effective surgical alternative to tracheostomy, with
results that are comparable to the therapeutic efficacy of
nasal continuous positive airway pressure (CPAP). This
chapter will review several aspects of OSA, including its
diagnosis, the characterization of its severity and the ratio­
nales for its various treatment options.
Researchers are increasingly finding that a lack of sleep is
detrimental for our health. Sleepiness has been linked to
increased rates of heart disease, obesity, stroke, and even
certain cancers. The exact reasons for these effects are still
largely unknown, but they give support to the theory that
sleep is the time when our bodies naturally repair them­
selves on a cellular level.150 Sleep—or the lack of it—is now
thought to be a complex process that underpins everything
from the ability to learn a new skill to how likely we are to
find a novel solution to a problem.243 It is also considered
a vital part of happiness and one of the best forms of pre­
ventative medicine.288
Sleep disorders include conditions that are character­
ized by repeated pauses in breathing during sleep, which
lead to the fragmentation of sleep and decreases in oxyhe­
moglobin saturation. The physiologic spectrum of sleep-
disordered breathing ranges from partial airway collapse
with increased upper airway resistance, which is manifested
as loud snoring and episodes of hypopnea, to complete
airway collapse and prolonged episodes of apnea. Obstruc­
tive sleep apnea (OSA) is clinically defined by frequent
episodes of apnea and hypopnea as well as symptoms of
functional impairment.13,14,129,130
According to the National Sleep Foundation, some form
of snoring or OSA occurs in 90 million Americans.245,246

993
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
*References 10, 23, 25, 42, 118, 125, 138, 140, 153, 175, 182, 221, 228,
250, 263, 265, 266, 289, 330, 331, 333, 350
Rationale for Treatment
The two major rationales for the treatment of OSA are to
address 1) pathophysiologic derangements and 2) behav­
ioral derangements.263
The pathophysiologic derangements related to OSA are
primarily cardiorespiratory in nature.* They include
increased risks of myocardial infarction, stroke, and sudden
death.153 Sudden death may be caused by tachycardia and
tachyarrhythmias (i.e., atrial fibrillation) as well as by brady­
arrhythmias. The documented high prevalence of athero­
sclerotic coronary artery disease among patients with OSA
is possibly related to endothelial damage, with platelet acti­
vation and the presence of inflammatory mediators also
being involved.153 When OSA is combined with systemic
hypertension, an increased incidence of stroke has been
reported.138,140,392 A higher-than-average occurrence of idio­
pathic dilated cardiomyopathy and more frequent episodes
of ST-segment depression have also been recognized.118,125,153
The physiologic processes that are believed to be involved
in OSA and that predispose patients to these risks include
hypoxemia, negative intrathoracic pressure, and the disequi­
librium of the autonomic nervous system.42
The behavioral derangements caused by OSA may be the
result of excessive daytime sleepiness.161,367 OSA is associ­
ated with nocturnal arousals during sleep that occur in
response to airway collapse and that result in poor sleep.
Excessive daytime sleepiness manifests as sleepiness or
fatigue of such a degree that the individual lacks vigilance
and does not function as well as he or she should during
the day. Other symptoms typically include heavy snoring,
known apnea, headaches, difficulty waking in the morning,
fatigue, sleepiness after eating, memory loss, having diffi­
cultly with work interactions, stressed relationships and
sexual performance complaints. There is a documented
increased incidence of motor vehicle accidents and job-
related injuries among individuals with OSA (e.g., individu­
als with OSA are 10 times more likely to die in an automobile
accident).26,85,103,292 OSA is also known to be a cause of dif­
ficulty with concentration at school or during work activi­
ties. Over time, the hypoxia that is caused by OSA is
believed to result in changes in the neurons of the hippo­
campus and the right frontal cortex of the brain. Neuroim­
aging studies have revealed evidence of hippocampal atrophy
in people who chronically suffer from OSA. Clinically, it is
documented that a greater percentage of patients with OSA
have problems with mentally manipulating nonverbal infor­
mation and with executive processing.100 Interestingly, there
is not a direct correlation between these behavioral derange­
ments and the severity of OSA as measured with the AHI
or with specific levels of oxygen desaturation. It is important
to note that there are multiple causes of excessive daytime
sleepiness other than OSA, including volitional sleep depri­
vation, alcoholism, insomnia, and narcolepsy.
Diagnosis, Characterization, and
Assessment of Obstructive
Sleep Apnea Severity
Pathophysiology
OSA is characterized by symptoms that result from the
recurrent sleep-associated collapse of the pharyngeal airway
and that lead to hypoxemia, hypercapnia, and fluctuations
in intrathoracic pressure caused by increased respiratory
effort, with arousal from sleep required to reestablish airway
patency. When awake, protective mechanisms increase the
activity of the pharyngeal dilator muscles; however, during
sleep, these mechanisms may fail and result in the collapse
of the pharyngeal airway.45,73,120,293,329,346,349,387 This is made
worse by nighttime horizontal and supine sleep position­
ing.244,256 Frequent locations of pharyngeal collapse include
the velopharynx (behind the soft palate), the oropharynx
(behind the tongue), or both.240
Schwab and colleagues have documented an increase in
adipose hypertrophy within the floor of the mouth, the soft
palate, the pharyngeal fat pads, and the lateral pharyngeal
walls in many individuals with OSA.324 In patients with
obesity, there is a direct deposition of fat that causes sub­
mucosal adipose volume expansion within the pharyngeal
walls (thus narrowing the lumen) and the floor of the
mouth (thus causing elevation and retro positioning of the
tongue), thereby diminishing the actual upper airway
breathing space and, in many cases, explaining the greater
extraluminal critical closing pressure documented in patients
with OSA. Evidence supports the concept that many indi­
viduals with OSA have an anatomic predisposition to
airway collapse as a result of retrusive jaws and obstructed
nasal cavities. An individual’s unique baseline skeletal
(i.e., jaw) anatomy may have a dramatic effect on the
size (i.e., the luminal diameter) of the upper airway. It is
now also appreciated that the variability in upper airway
breathing space from one person to the next is influenced
by the subject’s developmental or congenital maxillofacial
skeletal morphology. Deficient maxillomandibular struc­
tural support adds to the environmental causes (i.e., weight
gain) that thicken the pharyngeal soft tissues, thereby
further narrowing the lumen and diminishing the patency
afforded by pharyngeal dilator muscle contraction forces
that work to maintain and open the airway. Genetics plays
a lesser role in the observed volumes of the tongue, the soft
palate, the adenoids, the turbinates, and the tonsillar tissues
seen in individuals with OSA. These soft-tissue structures
are more likely to be affected by acquired conditions such
as weight gain, infections, or allergies. With obesity, there
may also be alterations of pharyngeal muscle orientation
and function. These factors combine to determine overall
upper airway breathing space, pharyngeal muscle function,
and, as a consequence, the occurrence of apnea events
during sleep.
Schwartz and colleagues measured the critical closing
pressures during sleep in individuals with OSA and

994 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
Frieberg and colleagues hypothesized that a progressive
lesion in the afferent and/or efferent nerve pathways caused
by repetitive “snoring trauma” may also contribute to the
collapsibility and obstruction of the upper airway that is
seen in patients with OSA.89-91 Their study evaluated the
hypothesis of the presence of a progressive neurogenic lesion
in the pharyngeal muscles in patients with longstanding
upper airway obstruction. Biopsies of palatopharyngeal
muscle were obtained from patients (n = 21) with habitual
snoring and degrees of upper airway obstruction and com­
pared with those of non-snoring control subjects (n = 10).
The degree of abnormality found was significantly increased
in the study patients as compared with control subjects. The
results of their research support the hypothesis of a progres­
sive local neurogenic lesion that is caused by the “trauma of
snoring” as a possible contributory factor in upper airway
collapsibility.
Sleep electroencephalograms (EEGs) of patients with
OSA will differ from those of individuals with upper airway
resistance syndrome (UARS) and from those of control
subjects.117,128 The arousal response of individuals with OSA
is delayed, despite the fact that increased respiratory effort
is seen during the obstructive phase. This delayed arousal
response has been confirmed by differences in the patterns
of EEG findings. Guilleminault and colleagues hypothe­
sized that a difference in sensory input may be the respon­
sible factor for the divergent responses to the abnormal
breathing patterns that may exist between individuals with
UARS and those with OSA.122 The authors set out to
compare the results of a palatal mucosa two-point discrimi­
nation response in normal subjects (n = 15), those with
OSA (n = 15), and those with UARS (n = 15). The subjects
were matched for age, sex, and body mass index. The 45
subjects were submitted to a two-point discrimination study
of the palatal mucosa during wakefulness. Individuals with
OSA had a clear impairment of their palatal mucosa sensory
input with a significant decrement in two-point discrimina­
tion. Interestingly, the subjects with UARS and the normal
control subjects responded similarly to each other. The
responses seen in individuals with UARS indicate that those
individuals are more capable of transmitting sensory inputs
than individuals with OSA. This may be at least one factor
that explains the difference in arousal response that is been
documented in patients with UARS as compared with those
with OSA.122
For the individual with OSA, as apnea events become
more frequent, hypoxemic and hypercarbic episodes require
increased respiratory effort to ultimately achieve arousal
from sleep. With awakening from the apnea event, there is
a reestablishment of airway patency, and ventilation pro­
ceeds. The individual then returns to sleep, and the cycle
repeats itself. This repetitive pattern of sleep disruption not
only affects the quality of the individual’s life (i.e., behavior
derangements), but it also affects their longevity (i.e., patho­
physiologic derangements).
The basic anatomic factors that reduce the size of the
upper airway include the following:
compared these values to those of controls (i.e., individuals
without OSA).327 Individuals with baseline anatomically
“large-volume” airways are less dependent on pharyngeal
dilator muscles to maintain airway patency than those with
intrinsic “small-volume” anatomic airways. Schwartz and
colleagues showed that control subjects (i.e., individuals
without OSA) typically have critical closing airway values
of less than 0 cm of water, whereas those with severe OSA
have values of more than 8 cm of water. Multiple diagnostic
modalities (e.g., cephalometric x-rays, computed tomogra­
phy [CT] scans, acoustic reflection, magnetic resonance
imaging) confirm that individuals with OSA generally have
“smaller-volume” baseline awake airway lumens as com­
pared with controls.264
According to Fogel and colleagues the pharyngeal muscles
of primary importance fall into three groups87:
1. The muscles that influence the hyoid bone position
(i.e., geniohyoid, sternohyoid)
2. The muscles of the tongue (i.e., genioglossus)
3. The muscles of the soft palate (i.e., tensor palatine
and levator palatine)
The activity of these muscles is normally increased during
inspiration to stiffen and expand (i.e., open) the upper
airway. This counteracts the collapsing influences that
would otherwise occur with inspiratory negative airway
pressure. During expiration, the muscles normally substan­
tially relax while positive pressure is flowing through the
respiratory tree. The tensor palatine is an exception in that
it must maintain a constant level of tone throughout the
respiratory cycle to preserve a patent airway. Fogel and col­
leagues stated that the activity of the pharyngeal dilator
muscles during wakefulness is tightly controlled to maintain
pharyngeal patency.87 In individuals with an anatomically
“small-volume” airway, the activation of this negative-
pressure reflex (i.e., feedback mechanism) to increase the
function of the pharyngeal muscles must occur to prevent
or limit apnea. This reflex has been shown to be diminished
in apnea-prone individuals for both the genioglossus and
the tensor palatine muscles. An individual’s use of specific
medications (e.g., alcohol, sedatives, narcotics) will also
negatively influence the reflex arc, thereby causing the relax­
ation of the muscles and further diminishing airway patency.
At least until the age of 65 years, age is positively cor­
related with OSA severity as demonstrated by an increase
in the AHI.152 This increase is substantially greater in the
presence of baseline maxillomandibular sagittal deficiency.
While a person is awake, neuromuscular mechanisms and
body position (i.e., standing or sitting up) can positively
influence and compensate for the “small-volume” airway.
However, the pharyngeal dilator muscles are less able to
effectively contract during sleep, which results in the more
frequent collapse of the anatomically small breathing space.
The ability of the pharyngeal muscles to compensate for and
prevent apnea events becomes progressively more difficult
with age and in the presence of weight gain.

995
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
superiorly, the epiglottis inferiorly, the maxillomandibular
complex anteriorly, and the spinal column posteriorly. The
upper airway is somewhat artificially subdivided into the
following regions:
1. The intranasal region. This portion of the airway
extends from and includes the external nasal valves,
the internal nasal valves, the turbinates, the nasal
septum, and the adenoids.
2. The retropalatal region. This portion of the airway is
primarily affected by the position of the maxilla (i.e.,
the hard palate), the size and position of the soft
palate, the tonsils, and the parapharyngeal fat pads.
3. The retroglossal region. This portion of the airway is
primarily affected by the position of the mandible,
the size and position of the tongue, the fullness of the
soft tissues in the floor of the mouth, the parapha­
ryngeal fat pads, and the tonsils.
An increased body mass index (BMI), which is also
known as obesity, is a known risk factor for OSA in children,
adolescents, and adults (Fig. 26-1).21,88,241,255,337 Peppard and
1. Regional obesity (i.e., increased volume of the lateral
pharyngeal fat pads, the soft palate, and the floor of
the mouth
2. Baseline (inherent) abnormalities of the maxilloman­
dibular skeletal structures (i.e., the maxilla, the man­
dible, and the nasal septum)
3. Volumetric enlargement of upper airway soft-tissue
visceral structures (e.g., tongue, soft palate, tonsils,
adenoids, inferior turbinates) as a result of congenital
anomalies, allergies, infections, or tumors.
The term pharynx is used to describe the anatomic
region that extends from the esophageal entrance up to the
back of the nose. It is further subdivided according to prox­
imity to the nose, mouth, and throat down to the larynx.
Together, these pharyngeal structures are involved in critical
physiologic functions, including breathing, swallowing,
vocalization/speech, and mastication. Each of these func­
tions is potentially influenced by any one of the upper
airway anatomic components. The upper airway functions
as a continuous cohesive organ; it is commonly defined as
the soft-tissue region that is bounded by the nasopharynx
• Figure 26-1  A, Midline sagittal cross-section head and neck illustration of a 20-year-old man with a normal body mass index to demonstrate
upper airway space and associated maxillofacial anatomy. This individual has a normal upper facial skeleton (cranial vault, orbits, and zygomas),
a normal lower facial skeleton (maxilla and mandible), and normal soft tissues (soft palate, tongue, tonsils, and adenoids). The intranasal cavity,
which includes the turbinates and the septum, is also normal. B, The same individual when he is 50 years old with an elevated body mass
index. The upper and lower facial skeleton remain unchanged with age. The adipose cells, which are scattered throughout and within the
upper airway soft tissues, have now increased in volume. This includes the retropharyngeal and the lateral pharyngeal tissues, the soft palate,
and the floor of the mouth. As a result, the soft palate is long, thick, and in close proximity to the posterior and lateral pharyngeal walls, thereby
diminishing the retropalatal space. As a result of increased adipose volume in the floor of the mouth, the tongue has been displaced superiorly
and posteriorly, thus decreasing the retroglossal airway space. As a result of chronic allergies, the patient’s turbinates have enlarged to cause
increased nasal airway resistance (i.e., diminished intranasal airway space). There is also excess adipose volume in both the submental triangle
and the supraplatysmal locations, thereby resulting in a full neck and a “double chin” appearance. In review, when the patient was 20 years
old, he had normal upper airway space, including the intranasal site; the retropalatal site; and the retroglossal sites. When he was 50 years
old, the upper airway space is considerably smaller, including the intranasal space, the retropalatal space, and the retroglossal space. The
patient depicted here now has documented obstructive sleep apnea.
Normal
tongue
position
Normal soft
palate/uvula
Normal inferior turbinate
Normally
positioned maxilla
Normally
positioned
mandible
Normal intranasal space
Normal
retroglossal
space
Normal
retropalatal
space
Vocal fold
Displaced
tongue
Enlarged
soft palate/
uvula
Excess fat
in pharyngeal
wall
Excess
supraplatysma fat
Excess fat in
submental triangle
Enlarged
inferior turbinate
A
B
Normally positioned
maxilla
Normally positioned
mandible
Diminished
intranasal space
Diminished
retroglossal
space
Diminished
retropalatal space

996 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
long face growth pattern, short face growth pattern, primary
mandibular deficiency, maxillary deficiency with relative
mandibular excess, maxillary hypoplasia associated with
repaired cleft palate), which affect at least 5% of the general
population, also negatively affect the upper airway.212
Unfortunately, these more common patterns of jaw dishar­
mony frequently go unrecognized as significant etiologic
factors for OSA (Figs. 26-2 and 26-3). It is incumbent on
the otolaryngologist, the pulmonologist or sleep specialist,
the pediatrician or internist, the orthognathic or maxillofa­
cial surgeon, and the general dentist or orthodontist to
understand the fundamental relationship between develop­
mental jaw deformities and upper airway obstruction in
each patient who is evaluated.
Not infrequently, the individual with “mandibular prog­
nathism” has undergone a lower jaw set-back treatment to
improve the occlusion. Historically, such procedures have
been preferred by many clinicians for the treatment of skel­
etal Class III patterns. However, it is now known that this
approach is associated with a risk to the airway size and
shape.6,18,41,48,67,68,74,78,84,113,115,171,172,174,314,316,370,386 Demetria­
des and colleagues confirmed the clinical importance of
considering the airway when formulating a treatment plan
for the correction of so called “mandibular prognathism.”69
They described 26 patients who presented with develop­
mental dentofacial deformities that were characterized by
maxillary deficiencies in combination with relative man­
dibular excesses. Each patient underwent mandibular
ramus osteotomies with at least some set-back. The patients
were divided into two groups. The Group 1 patients (n =
13) underwent mandibular setback of at least 5 mm
without simultaneous Le Fort I osteotomies. The Group 2
patients (n = 13) also underwent a degree of mandibular
set-back, but in conjunction with Le Fort I advancement.
All study patients (Groups 1 and 2) underwent preopera­
tive and postoperative lateral cephalometric radiography
and portable PSG. The preoperative and postoperative
radiographs were compared, and any changes that occurred
in the position of the hyoid bone, the distance from the
posterior nasal spine to the palate, the retrolingual space,
and the hypopharyngeal space were measured. The authors
confirmed that mandibular retropositioning of at least
5 mm can significantly decrease the posterior airway space
and cause mild to moderate OSA. The study also suggested
that, when a limited mandibular set-back is carried out
in combination with maxillary Le Fort I advancement,
significant negative effects on the airway are likely to be
prevented.
In summary, anatomic upper airway risk factors for OSA
include the following: 1) regional obesity (i.e., increased
upper airway submucosal adipose tissue deposition);
2) retrusive maxillomandibular skeleton (e.g., hypoplasia of
the maxilla or mandible); 3) alterations in the intranasal
cavity (e.g., septal deviations, hypertrophic inferior turbi­
nates, tight nasal aperture, elevated nasal floor, adenoid
hypertrophy); 4) enlargement of other critical upper-airway
soft-tissue visceral structures (e.g., soft palate, tonsils,
colleagues outlined the cardiovascular risks associated with
OSA for weight gain and weight loss.269,268 Excessive body
weight was found to be positively associated with OSA,262
and the stability of the individual’s weight was also found
to be an important factor. A 10% weight gain predicted a
32% increase in the AHI.319 The same 10% gain in weight
also predicted a six-fold increase in the odds of moderate to
severe OSA developing. Interestingly, a weight loss of 10%
predicted a 26% decrease in the AHI.169 Unfortunately,
studies consistently document that weight loss programs in
patients with OSA frequently fail miserably. Any weight loss
that the individual is able to initially achieve tends to be
temporary.167
When an individual’s BMI is elevated, the volume of fat
in the pharynx and the floor of the mouth also increases. It
is estimated that more than 66% of individuals with OSA
are obese. On the basis of the latest World Health Organiza­
tion statistics, it is estimated that there are more than 1.6
billion overweight adults (from a total population of 6.5
billion) and at least 400 million obese individuals (BMI ≥
25 kg/m2) on Earth.72 Obesity has both a genetic and an
environmental basis.37,63,102,165,237 A review of population
studies suggests that heredity accounts for at least 40% of
the variance in BMI.219,286 Studies have demonstrated a
strong relationship between the BMIs of biologic parents
and their children. Interestingly, no relationship between
the BMI of adoptive parents and their adopted children has
been documented. The best indirect indicator of excessive
fat accumulation in the pharyngeal region and the floor of
the mouth is a person’s BMI.
Studies have also documented that relatives of individu­
als with OSA demonstrate a higher incidence of hypoplastic
maxillae and mandibles, longer soft palates, and wider
uvulas as compared with matched controls.219,326 This also
speaks to the hereditary component of a small pharyngeal
airway space and to an individual’s genetic predisposition
to OSA.295,388
There are specific syndromes and conditions that result
in severe maxillomandibular skeleton dysmorphology and
that also negatively affect the upper airway (e.g., Crouzon
syndrome, Apert syndrome, Treacher Collins syndrome,
Pierre Robin sequence).17,38,270,271,287,341,354,390 It is docu­
mented that more than 50% of individuals with Down
syndrome suffer from OSA.66 Interestingly, a similar per­
centage of individuals with Down syndrome are known
to have a baseline intrinsic developmental jaw deformity
that is characterized primarily by maxillary deficiency.
The surgical correction of the maxillofacial deformities
associated with these syndromes have been documented
to enlarge the upper airway space and to improve and
often resolve breathing difficulties, including OSA (see
Chapters 27, 28, 30 and 31). The surgical management
of velopharyngeal insufficiency (i.e., superiorly based pha­
ryngeal flap or sphincteroplasty) in individuals with a
repaired cleft palate is also known to result in OSA in some
cases.4,39,157,176,187,205,257,258,339,340,343,373,389,396 Interestingly, the
non-syndromal developmental dentofacial deformities (e.g.,

997
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
information should be especially considered for an indi­
vidual with known OSA:
1. The clinician should determine at what specific max­
illofacial skeletal locations (e.g., nasal septum, turbi­
nates, maxilla, mandible), if any, there are negative
effects occurring in the upper airway during sleep or
while awake.
2. If the patient also has a high BMI (i.e., >25 kg/m2),
the clinician should determine at what regional soft-
tissue locations (e.g., nasopharyngeal, palatopharyn­
geal, glossopharyngeal), if any, there is excessive
submucosal adipose and other soft-tissue volume that
may have a negative impact on the airway.
3. The clinician should determine if there are baseline
physiologic dysfunctions of the lungs and chest walls
(e.g., chronic obstructive pulmonary disease) that
negatively affect the airway.
tongue); and 5) inadequate pharyngeal muscular tone (i.e.,
hereditary and environmental factors).320,332,348,378 Each of
these head and neck structural aspects predispose individu­
als to OSA by causing upper-airway narrowing during
wakefulness and airway collapse during sleep. When these
aspects occur in combination, the risk is greatly exacerbated.
There are also specific medical conditions (e.g., myasthenia
gravis, Parkinson disease, amyotrophic lateral sclerosis) as
well as certain medications and drugs (e.g. alcohol, narcot­
ics, sedatives, muscle relaxants) that are known to negatively
affect the neuromotor tone of the chest wall and the pha­
ryngeal musculature and thus predispose an individual
to apnea.
Basic Clinical Evaluation
A thorough medical and sleep history should be taken
and a physical examination completed. The following
• Figure 26-2  Midline sagittal cross-sectional head and neck illustrations of a 16-year-old girl with primary mandibular deficiency, maxillary arch
constriction, and Class II excess overjet malocclusion (see Fig. 19-4). The illustrations demonstrate the upper airway space and the associated
maxillofacial anatomy before and after jaw and intranasal reconstruction. A, Illustration when the patient was 16 years old, before intervention.
The inferior turbinates are hypertrophic as a result of chronic allergies, and the nasal septum is deviated. These findings result in a diminished
intranasal airway space. As part of the developmental jaw deformity, the maxilla is retropositioned, and there is a narrow arch width. Therefore,
the soft palate is posterior, which results in diminished retropalatal space. The mandible is horizontally (sagittally) deficient, with a posterior dis­
placed tongue. As a result, there is diminished retroglossal space. The tonsils, the adenoids, the tongue, and the soft palate are displaced but
otherwise normal. Although the patient is young and has a normal body mass index, the intranasal and jaw deformities result in diminished upper
airway space. The patient has difficulty breathing through the nose while she is awake, and is with heavy snoring at night. Obstructive sleep
apnea has been documented. B, The patient agreed to a comprehensive orthodontic and surgical approach. Lower bicuspid extractions allowed
for the relief of dental compensation. The patient’s surgery included maxillary Le Fort I osteotomy in segments (arch expansion and horizontal
advancement); bilateral sagittal split ramus osteotomies (horizontal advancement); osseous genioplasty (horizontal advancement); and septoplasty
and inferior turbinate reduction. The postoperative illustration indicates maxillofacial changes that resulted from the reconstruction. Now there is
an expanded intranasal, retropalatal, and retroglossal airway space. There is improved nasal breathing during the day and reduced snoring and
apnea events at night.
A
B
Displaced
tongue
Hypertrophic
inferior turbinate
Hypoplastic maxilla
Hypoplastic
mandible
Diminished
intranasal space
Diminished
retroglossal space
Diminished
retropalatal space
Vocal fold
Reduced
inferior turbinate
Maxilla advanced
Mandible advanced
Chin advanced
Enlarged
intranasal space
Enlarged
retroglossal
space
Enlarged
retropalatal space

998 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
data. The collected data confirm that, in humans, the airway
size and length increases until the age of 20 years, at which
time there is a variable period of stability. After this stable
period, the airway at first decreases slowly in size; then, after
the age of 50 years, it decreases more rapidly.322 Li and col­
leagues demonstrated a correlation between the airway area
and the likelihood of OSA.197 There is a high probability of
severe OSA with an airway area of less than 52 mm2; an
intermediate probability if the airway is between 52 mm2
and 110 mm2; and a low probability if the airway area is
more than 110 mm2.190 Cillo and colleagues attempted to
correlate specific cephalometric measurements with the
AHI in a consecutive series of patients (N = 101) who were
documented to have OSA. Unfortunately, no one skeletal
or soft-tissue parameter could be linked to OSA.51 Three-
dimensional CT airway analysis has documented quantifi­
able changes in patients’ oropharynges after specific surgical
4. The clinician should consider the effects of baseline
neuromotor disorders (e.g., Parkinson disease) and
currently
used
medications
(including
non-
prescription drugs and alcohol) that may negatively
affect the airway.
It is also recommended that a subjective questionnaire
be used to assess for OSA. The Epworth Sleepiness Scale
(ESS) is considered the reference standard.86,163,164 The
survey assesses the respondent’s propensity for sleep in eight
different situations. Although the survey is not perfect, it
does provide useful information about the patient’s waking
sleepiness.
An airway analysis that is based on CT scan data may
also be a useful tool to assess upper airway space. A recent
study used three-dimensional computer analysis from cone-
beam CT to present normative upper airway size reference
• Figure 26-3  Midline sagittal cross-sectional head and neck illustrations of a 59-year-old man to demonstrate upper airway space and
associated maxillofacial anatomy before and after jaw, intranasal, and facial surgery carried out primarily to open the airway (see Fig. 26-6).
This patient has documented severe obstructive sleep apnea, including a respiratory disturbance index of 51 events/hour with desaturations
reaching as low as 82%. The patient has an elevated body mass index and a short face growth pattern that is characterized by maxillo­
mandibular vertical and horizontal deficiency. At the time of presentation to this surgeon, he had already undergone “Phase I” procedures
including uvulopalatopharyngoplasty, septoplasty, and inferior turbinate reduction without relief of obstructive sleep apnea. A, Illustration of
the patient’s condition before surgery demonstrates hypertrophic inferior turbinates and septal deviation that result in a diminished intranasal
space. The maxilla is vertically short and horizontally deficient. The soft palate is long and thick as a result of excess fat accumulation. For
all of these reasons, a diminished retropalatal airway space is present. The mandible is horizontally deficient, and the tongue is elevated
as a result of excess fat in the floor of the mouth. The lateral and retropharyngeal walls also show excess fat accumulation. These findings
account for the diminished retroglossal airway space. B, After the patient was referred to this surgeon, he underwent simultaneous pro­
cedures that included maxillary Le Fort I osteotomy (horizontal advancement of 10 mm and vertical lengthening of 5 mm) with interpositional
graft; bilateral sagittal split osteotomies of the mandible (horizontal advancement of 12 mm); osseous genioplasty (horizontal advancement);
redo septoplasty; and anterior neck soft-tissue procedures (cervical flap elevation, fat removal, and platysma muscle plication). The illustra­
tion after maxillary–mandibular–chin advancement demonstrates the enlarged upper airway space, including the intranasal space, the
retropalatal space, and the retroglossal space. A 3-month postoperative attended polysomnogram confirms a respiratory disturbance index
of less than 5 events/hour.
A
B
Displaced
tongue
Hypertrophic
inferior turbinate
Hypoplastic
maxilla
Hypoplastic
mandible
Diminished
intranasal space
Diminished
retroglossal
space
Excess fat in
pharyngeal wall
Diminished
retropalatal space
Enlarged soft
palate/uvula
Reduced
inferior turbinate
Maxilla advanced
Mandible advanced
Chin advanced
Enlarged
intranasal space
Enlarged
retroglossal
space
Enlarged
retropalatal
space
S/P uvulectomy
Vocal fold
Excess
supraplatysma fat
Excess fat in
submental triangle
Reduction of
supraplatysma fat
Reduction of fat in
submental triangle
Diminished
retroglossal
space
Excess fat in
pharyngeal wall
Vocal fold
Enlarged
retroglossal
space

999
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
It is recommended that all sleep studies for a surgical
patient be attended overnight PSG. Parameters reviewed
after attended PSG should include the following:
• Sleep stages (both rapid eye movement and non–rapid
eye movement sleep), including the percentage of
sleep in each.
• Apnea index (AI)
• Hypopnea index
• Awake oxygen saturation, including the lowest levels
and the stratifications of the percentage of time below
specific percentiles (i.e., 90%, 80%, and 70%)
• Heart rate fluctuations (e.g., brachyarrhythmia,
tachyarrhythmia)
• Periodic leg movements
To be most accurate as a diagnostic tool, the PSG
study should be current (i.e., within the previous 6 to 12
months) and, if possible, not a split-night study. Split-night
studies apply CPAP for the second half of the night and
may underestimate the severity of OSA. An alternative
to an attended sleep study is a home sleep study. Home
sleep studies lack all of the monitoring parameters of an
attended overnight PSG. However, advantages of home
sleep studies include reduced costs and the ability to perform
the sleep study in the patient’s native sleeping environment.
Disadvantages include the gathering of fewer sleep param­
eters and possibly reduced reliability.
Assessment of Apnea Severity
By convention, the severity of OSA is classically deter­
mined by the AHI. The term obstructive apnea refers to
apnea despite continued respiratory effort. Apnea is defined
as the cessation of airflow for at least 10 seconds in an
adult or for the equivalent of two breaths in a child. Hypop­
nea is defined as 1) a substantial reduction in airflow (i.e.,
>50%); or 2) a moderate reduction in airflow (i.e., <50%)
with oxygen desaturation of more than 3%; or 3) EEG
evidence of arousal in combination with oxygen desatura­
tion that lasts for at least 10 seconds in an adult or for the
equivalent of two breaths in a child. The AHI is a count of
the number of apneas and hypopneas per hour of sleep.
The respiratory disturbance index (RDI) is also used to
describe OSA. The RDI considers the number of apneas,
hypopneas, and respiratory-effort–related arousals per
hour of sleep. Respiratory-effort–related arousals are EEG
arousals that are not associated with clear-cut apnea or
hypopnea but rather with slight changes in airflow or respi­
ratory effort.
In adults, an AHI of 5 to 15 is regarded as mild OSA,
an AHI of 15 to 30 is considered moderate OSA, and an
AHI of 30 or more is severe OSA. (OSA during childhood
is discussed later in this chapter.) Interestingly, the reliability
of data procured during the sleep study and its interpreta­
tion by sleep specialists has not been verified through intra-
observational or inter-observational studies.
interventions. This type of imaging may also be used to
evaluate changes in the airway after specific medical inter­
ventions (e.g., weight loss).75
Susarla and colleagues used a case–control study that was
designed to analyze the value of the cephalometric upper
airway length (UAL) measurement as an indirect predictor
of the presence and severity of OSA.360,361 The study group
included adults (n = 96) with PSG-documented severe OSA
and a control group of adults (n = 56) with skeletal Class
II malocclusion without known OSA. Although significant
attention has been devoted to describing and measuring
upper airway width, little attention has been devoted to
measuring UAL. The theory behind this study is that an
important component of the airway resistance is the airway
length (i.e., the vertical dimension), which is known to be
directly correlated with airway resistance per Poiseuille’s law:
resistance equals 8 ηL/πr4 (L = length). The results of the
study suggest that the UAL (i.e., the distance between
the posterior hard palate and the most superior aspect of
the hyoid bone on a line parallel to the long access of the
airway) is predictive of the presence of OSA in both men
and women. The study results indicate that a cephalometric
UAL of 72 mm or more in men and 62 mm in women was
diagnostic for OSA with high sensitivity and specificity. It
would appear that both a narrow posterior airway space and
a long UAL predispose individuals to upper airway obstruc­
tion and that both conditions are associated with increased
odds of OSA.
A reasonable predictor of OSA is a clinical triad of symp­
toms that includes loud snoring, apnea witnessed by a bed
partner, and excessive daytime sleepiness. When the sleep
and daytime history is combined with attended PSG, the
patient’s clinical head and neck examination (including
instrumentation), and a focused radiographic analysis, then
an overall picture of the upper airway anatomy and function
can be seen.*
Attended Polysomnography
Overnight PSG conducted in a sleep laboratory remains the
reference standard for the diagnosis of central sleep apnea
or OSA.92,111,155,180,365 PSG requires the use of several moni­
toring parameters, including EEG, electrooculography,
electromyography, electrocardiography, the microphone
measurement of snoring, pulse oximetry, respiratory induc­
tance plethysmography, airflow measurement, and the
recording of the body position. PSG primarily evaluates
sleep-disordered breathing, sleep architecture, and oxygen
desaturations. During PSG, episodes of apnea and hypop­
nea are determined from a reduction in airflow in combina­
tion with oxygen desaturation during a 4- to 8-hour time
frame.
*References 1, 7, 19, 20, 22, 28, 33, 61, 64, 70, 101, 135-137, 146, 151,
156, 168, 190, 206, 210-212, 260, 281, 309, 315, 323, 338, 359, 362,
364

1000 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
have shown that there is rarely a single anatomic site of
blockage (see Figs. 26-1 through 26-3). More commonly,
multiple sites of upper airway obstruction occur during
episodes of hypopnea and apnea. As stated, the potential
upper airway sites of obstruction are somewhat artificially
grouped as 1) intranasal; 2) retropalatal; and (3) retroglos­
sal. In addition to taking a history and a physical examina­
tion, diagnostic studies to further clarify the anatomic levels
of obstruction include the Müller maneuver, which is
observed during nasoendoscopic instrumentation; lateral
cephalometric radiographs taken during end-tidal volume
measurement with the Müller maneuver; helical CT; and
magnetic resonance imaging.
Intranasal Site
When a history of chronic obstructive nasal breathing is
combined with an intranasal clinical examination, instru­
mentation (e.g., speculum, endoscope), and radiography
(e.g., sinus CT scan), the causes of the intranasal obstruc­
tion are generally identified. A thickened, buckled, deviated
septum (bone and cartilage), enlarged (hypertrophic) infe­
rior turbinates, an elevated nasal floor, and narrow lateral
walls (tight nasal aperture) are frequent causes (see Chapter
10). Occasionally, crooked nasal bones, stenotic external
nasal valves (after cleft lip repair), or collapsing internal
nasal valves (previous nasal surgery) may also be responsible.
Enlarged adenoids or nasal polyps may also be causative
factors.
Retropalatal Site
Maxillary hypoplasia either from a known syndrome (e.g.,
syndromal craniosynostosis, Treacher Collins syndrome,
repaired cleft palate) or from a more common developmen­
tal dentofacial deformity (e.g., short face growth pattern,
long face growth pattern) may be responsible. Enlarged
tonsils, excessive lateral parapharyngeal fat pads, and an
enlarged floppy soft palate may also be factors.
Retroglossal Site
A retrusive mandible is a frequent component of develop­
mental jaw deformities. As a result of mandibular retrogna­
thia and microgenia, the tongue is retropositioned and
elevated. Only rarely is the tongue itself enlarged; rather, it
rests in a retro and elevated position as a result of the retru­
sive mandible. Occasionally an enlarged lingual tonsil will
cause retroglossal obstruction. Excess fat deposition in the
floor of the mouth will also elevate and retroposition the
tongue. Enlarged tonsils and lateral parapharyngeal fat pads
may also be contributing factors.
Obstructive Sleep Apnea
during Childhood: Diagnosis
and Management
“The [American Academy of Pediatrics] guidelines contain
the following recommendations for the diagnosis of OSA:
Characterization of Apnea
Central sleep apnea is characterized by a lack of drive to
breathe during sleep that results in insufficient or absent
ventilation with compromised gas exchange. This may
occur as a result of a number of known neuromuscular
disorders, or it may not have a specific cause. OSA occurs
when ongoing respiratory efforts are observed during the
cessation of airflow within the upper airway. Central sleep
apnea, like OSA, is associated with frequent nighttime
awakening; excessive daytime sleepiness; and an increased
risk of adverse cardiovascular outcomes. Central sleep apnea
as classically defined is relatively uncommon (i.e., it is seen
in <5% of patients referred to a sleep clinic).
Interestingly, it is recognized that 10% to 20% of indi­
viduals with known OSA will fail to respond to successful
anatomic surgical expansion of the maxillomandibular
complex. Another difficult to explain subgroup of individu­
als with documented OSA is that group with apparent
normal upper airway morphology (i.e., no significant
narrowing). Complex sleep apnea is a newly recognized
category in the spectrum of sleep apnea syndromes that
helps to explain these outliers. According to Susarla and
colleagues, complex sleep apnea often presents with mor­
phologic features that are typical of obstructive disease
but that are combined with PSG evidence of strongly
chemoreflex-modulated sleep breathing.360 Complex sleep
apnea is distinguished from other forms of OSA by the
following:
• Non–rapid eye movement sleep dominance of
obstructive disease;
• Oscillations of respiration with or without flow limi­
tation; and
• Induction of central apneas or periodic breathing
with the application of positive airway pressure
therapy.
Susarla and colleagues believe that a lack of resolution
of OSA after successful maxillomandibular advancement
surgery may occur if a ventilation control disturbance
either remains or is amplified.360 These individuals with
chemoreflex-sensitive apnea can be identified, because they
are extremely prone to changes in their carbon dioxide
levels. It is important to make an accurate diagnosis, because
these patients can be expected to require further manage­
ment of the central component to their apnea. Helpful
treatment for this unique subgroup may include the use of
nasal oxygen, pharmacologic agents, or positive-pressure–
based adaptive ventilation. Affected individuals require con­
tinued reassessment and management by a knowledgeable
clinical sleep specialist.
Sites of Functional Obstruction
Studies that attempt to localize the site of upper airway
obstruction in an individual with moderate to severe OSA

1001
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
recent American Sleep Disorder Association guidelines,
either the pediatric or adult criteria for OSA may be used
for adolescent patients who are between 13 and 18 years
old at the discretion of the scoring sleep specialist.12-16 It is
also unclear how many events per hour should be consid­
ered significant in the adolescent patient as compared with
pediatric and adult patients.5
Treatment Considerations in Children
Adenotonsillectomy (T&A) is generally considered to
be the standard first-line treatment for a child with
OSA who does not have complex medical conditions
that
would
make
surgery
an
unacceptable
risk.34,121,124,183,188,220,224,230,232-234,298,317,344,351,355,366,384 A child
with OSA should not undergo T&A without receiving a
thorough evaluation of the entire upper airway to confirm
the actual need for an operation. Nevertheless, the overall
cure rate of T&A during childhood is believed to be as high
as 82.9%. Studies indicate that, for children with docu­
mented OSA and a preoperative RDI of less than 19 events/
hour, a T&A will frequently reduce the RDI to less than 5
events/hour. Alternatively, if the preoperative RDI is greater
than 19 events/hour, then the T&A has a low probability
of reducing the RDI to less than 5 events/hour.355 Other
anatomic causes for the child’s OSA should be considered
(e.g., maxillomandibular hypoplasia).
A tight nasal inlet is another common cause of upper
airway obstruction that may be first recognized during
childhood (see Chapter 10). Clinical studies have docu­
mented that maxillary arch expansion will improve a tight
nasal inlet and thereby decrease nasal airway resistance.
Maxillary arch expansion, which is accomplished with the
use of a rapid palatal expansion appliance, is commonly
carried out during childhood with little morbidity.8,27,36,79,399
Unfortunately, rapid palatal expansion will only address the
one site of obstruction and in a limited way. No studies have
confirmed that this approach alone will be effective for
OSA. For children in whom T&A or rapid palatal expan­
sion is required but does not lead to the resolution of OSA,
evaluation to confirm the additional sites of obstruction
should follow and appropriate interventions considered.
The option of the administration of CPAP should be
entertained, but the overall long-term adherence rate
for CPAP is unknown and felt to be problematic in this
population. Skeletal reconstruction is likely to be beneficial
in a child with a craniofacial anomaly that is known to
obstruct the upper airway and in whom OSA has been
documented.17,38,53,270,271,287,341,354,390 For example, maxillary
advancement in a child with either Apert or Crouzon syn­
drome and documented OSA has proven value (see Chapter
30). When a small lower jaw with a retro positioned tongue
(i.e., some children with Treacher Collins Syndrome or
Pierre Robin sequence) is the cause of OSA, then mandibu­
lar advancement can also be helpful (see Chapter 19).
Developmental jaw deformities (i.e., long face growth
pattern, short face growth pattern, and isolated mandibular
(1) all children should be screened for snoring; (2) complex
high-risk patients should be referred to a specialist;
(3) patients with cardiorespiratory failure cannot await elec­
tive evaluation; (4) diagnostic evaluation is useful in dis­
criminating between primary snoring and OSA, the
reference standard being polysomnography; (5) adenoton­
sillectomy is the first line of treatment for most children,
and continuous positive airway pressure is an option for
those who are not candidates for surgery or do not respond
to surgery; (6) high-risk patients should be monitored as
inpatients postoperatively; and (7) patients should be
reevaluated postoperatively to determine whether additional
treatment is required.”12,57,328
“This clinical practice guideline is not intended as a
sole source of guidance in the evaluation of children with
OSA.15,16,35,46,50,108,110,127,170,216,223,235,296 Rather, it is designed
to assist primary care clinicians by providing a framework
for diagnostic decision making. It is not intended to replace
clinical judgment or to establish a protocol for all children
with this condition and may not provide the only appropri­
ate approach to this problem.”223
Manifestations in Children
Snoring and difficulty breathing during sleep are the most
common complaints reported by parents of children with
OSA.54,249,400 However, in contrast with reports of OSA in
adults, excessive daytime somnolence is believed to be less
common in children, with only 7% of 10% of pediatric
patients with OSA experiencing this symptom. Neurocog­
nitive deficits and behavioral manifestations are more fre­
quent in children and may be the result of the chronic
exposure to intermittent hypoxemia and sleep disruption
caused by sleep fragmentation. Children with OSA are
more likely to present with symptoms of hyperactivity, inat­
tentiveness, poor academic performance, and behavioral
problems.30,49,60,112,152,166,229,231,253,254,312 Such symptoms are
often attributed to attention-deficit/hyperactivity disorder;
treatments prescribed for this disorder (e.g., pharmaco­
logic therapy with stimulants) can actually worsen sleep
symptoms.
Diagnostic Criteria in Children
Diagnostic criteria for OSA in adults are typically the
product of consensus and often include an AHI of 5 or
more as documented by nocturnal PSG as well as evidence
of disturbed or unrefreshing sleep, daytime sleepiness, or
other daytime symptoms.313,382 The rationale for specific
AHI diagnostic criteria in children as compared with adults
suffers from less available data and heterogeneity across
studies. Part of the problem is that few studies have been
performed to link specified levels of pediatric OSA with
adverse outcomes. At present, an AHI or RDI of as low as
1 event/hour is used to identify children with OSA. Pedi­
atric criteria for scoring AHI or RDI are used until the age
of 13 years as a matter of routine. According to the most

1002 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
Treatment Options for Obstructive
Sleep Apnea
Recognizing that a significant subgroup of adults who have
been diagnosed with OSA have a chronic illness is essential
when considering treatment options. In general, obese
adults with OSA should be thought of in a similar way
to those with diabetes or hypertension. For these individu­
als, the total elimination of the disease is not generally
feasible.63,147,169,344 The goal of any treatment modality in
this situation is to improve or control the symptoms
and the health risks by reducing the severity. A clear excep­
tion to this way of thinking is in the individual with a
small-lumen upper airway that is primarily the result of
retrognathic jaws. For these individuals, who make up
approximately one third of patients with OSA, the correc­
tion of the jaw deficiency is expected to be successful for
most.29,44,82,144,149,186,197,283,285,311,312
A review of the literature that addresses the management
of OSA confirms that a plethora of publications discuss a
spectrum of medical and surgical treatment options.181,207
More than a dozen “non-surgical” treatment options are
mentioned, including palatal, tongue, and jaw training
exercises; controlled sleep positioning; spray medications to
reduce soft-tissue edema or to improve muscle tone; the use
of a spectrum of oral appliances that have been designed to
protrude the lower jaw; and the use of CPAP delivered
through a variety of occlusive devices over the mouth and
nose. The majority of these treatment recommendations
(with the exception of CPAP) are empiric and frequently
recommended as “simple” options in an attempt to avoid
surgery or the need for CPAP. In addition, more than a
dozen surgical options are offered with the intention of
affecting either a specific region of the pharynx or a tissue
type within the head and neck (e.g., external nasal valves,
internal nasal valves, nasal septum, nasal turbinates, soft
palate, adenoids, uvula, tonsillar pillars, tonsils, tongue,
maxilla, mandible, chin, hyoid bone). Ideally, to ensure
compliance with the recommended treatment, 1) the
medical or surgical approach should have a biologic basis
that is directed at the sites of pathology; 2) a reasonable
probability of success should be anticipated; 3) an accept­
able level of risk should be clarified; and 4) a realistic level
of patient acceptance should be expected.
Bariatric Surgery
Rasheid and colleagues completed a prospective study in a
consecutive series of patients (n = 100) that underwent
gastric bypass for the management of obesity to determine
the effects of the surgery on OSA.290 Before surgery, all
patients underwent PSG. The mean preoperative RDI was
40 ± 4. Thirteen patients had no OSA, 29 had mild OSA,
and 58 had moderate to severe OSA. At 6 months after
surgery, patients’ BMIs had improved (38 ± 1 kg/m2 versus
54 ± 1 kg/m2), and so had their ESS scores (6 ± 1 versus
deficiency) occur frequently in the general population, but
they often go unrecognized as causes of OSA in children
and teenagers (see Chapters 19, 21, and 23). After a devel­
opmental jaw deformity has been recognized in a child,
OSA should be ruled out.126,383 Referral to an orthognathic
surgeon familiar with OSA is recommended if the PSG is
positive (Figs. 26-4 and 26-5).
Managing the Airway during a Surgical
Procedure in the Individual with
Obstructive Sleep Apnea
A question has been raised regarding the risk of intubation
in a morbidly obese individual with a baseline diagnosis of
severe OSA. Neligan and colleagues completed a prospec­
tive study to assess whether severity of OSA, neck circum­
ference, and BMI were risk factors for difficult intubation
in morbidly obese patients.248 Each study patient (n = 180)
underwent preoperative PSG, Mallampati scoring, thyro­
mental distance measurement, mouth opening assessment,
and neck circumference measurement. Each study patient
was scheduled to undergo a surgical procedure that required
orotracheal intubation. A systematic approach to the intu­
bation was developed by the authors that included the
placement of the individual into the “ramp” position to
facilitate intubation by aligning the three axes: the pharyn­
geal axis, the laryngeal axis, and the tracheal axis. The ramp
position was achieved by placing padding below the indi­
vidual’s back to elevate the head, upper body, and shoulders
above the level of the chest. This was judged by positioning
the external auditory meatus at the same horizontal level as
the sternal notch. Of the 180 patients enrolled in the study,
124 were documented by PSG to have severe OSA (mean
AHI, 31.3 events/hour). The median Mallampati score was
2; the mean neck circumference was 43.9 cm; and the mean
Cormack and Lehane grade was 1. The incidence of antici­
pated difficult laryngoscopy, which was defined as a
Cormack and Lehane grade of 3 or 4, was 8.3%. Of the
study patients with documented OSA (n = 124), only six
required three or more intubation attempts, and only 3.3%
were judged as being “difficult to intubate.” A Mallampati
score of 3 or 4 predicted difficult intubation, and a mean
neck circumference of 43.9 predicted difficulty with laryn­
goscopy. The study showed no direct relationship between
the diagnosis or severity of OSA and the difficulty of laryn­
goscopy or intubation. There was no relationship between
neck circumference or BMI and difficult intubation. The
authors believe that their successful management of intuba­
tion requirements in this morbidly obese group related to
their meticulous approach to airway management and their
technique of using the “ramp” position, which aligns the
airway axes and facilitates intubation. Some anesthesiolo­
gists prefer to use either a GlideScope (Verathon Medical,
Bothell, Wash) or an awake fiber-optic nasotracheal laryn­
goscopy technique when faced with a morbidly obese indi­
vidual who requires intubation (see Chapter 11).
Text continued on p. 1008

1003
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
C
©Elsevier Inc.
Or
Or
Or
Orthththththththththth
r ogn
gn
gn
gn
g atatatata hicicicicic Su
Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry; J.C.
C.
C Pos
os
os
os
os
os
os
os
os
osnicicicicici k
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Orththththththththth
r ogn
gn
gn
gn
gn
gn
g atatata hicicicicici Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
r ; J.C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
osnicicicicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
O hththththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatathicicicicicicicicicicicic Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry; J.C.
C.
C. Pos
os
os
os
os
o nicicicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Orthththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatathicicicicicicic Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry; J.C.
C. Pos
os
os
os
os
os
os
os
osnicicicicicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Orththththththththththththththththththththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatatatatatatatatatathicicicicicicicicicici Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C Pos
os
os
o nicicicici k
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Orthththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatathicicicicicicicicicicicici Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry
r ; J.C.
C.
C Pos
os
os
os
os
o nicicicicicick
A
B
• Figure 26-4  A 16-year-old boy was referred by
his pediatrician for surgical evaluation. He had a
history of heavy snoring, restless sleeping, daytime
somnolence, attention-deficit/hyperactivity disorder
and other behavioral problems, and poor school
grades. An attended polysomnogram documented
an apnea–hypopnea index of 30 events/hour. Head
and neck examination confirmed a normal-sized
and functioning soft palate and tongue. The tonsils
and adenoids were not enlarged. The intranasal
cavity was obstructed (septal deviation and inferior
turbinate hypertrophy). The soft palate was resting
close to the posterior pharyngeal wall as a result of
maxillary retrusion. The tongue was retropositioned
as a result of a retrognathic mandible. The patient
had previously undergone 2 years of orthodontics
and achieved a Class I canine and molar occlusion.
The anterior and posterior facial heights were rela­
tively normal. After consultation with his medical and
dental team (general dentist, orthodontist, pediatri­
cian, and sleep specialist), the patient agreed to a
surgical approach. Orthodontic appliances were
placed to protect the periodontium, and he under­
went jaw and intranasal surgery. The patient’s pro­
cedures included maxillary Le Fort I osteotomy
(horizontal advancement +10 mm); bilateral sagittal
split ramus osteotomies (horizontal advancement
+10 mm); osseous genioplasty (horizontal advance­
ment +10 mm); and septoplasty and inferior turbi­
nate reduction. Three months after surgery, he
underwent an attended polysomnogram that con­
firmed the resolution of the obstructive sleep apnea
with an apnea–hypopnea index of 2.6 events/hour.
He no longer snored or experienced restless sleep.
Daytime fatigue improved, as did his behavioral
problems and his schoolwork. A, Frontal views with
smile before and after surgery. B, Oblique facial
views before and after surgery. C, Profile views
before and after surgery.
Continued

1004 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
D
Prior to retreatment
Pre surgery
After treatment
D, Occlusal views before retreatment, with orthodontic appliances in place, and after treatment.
• Figure 26-4, cont’d

1005
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
E
F
10 mm advancement
Enlarged
posterior
airway space
Apnea hypopnea index  2.6/hr
Apnea hypopnea index  30/hr
E, Articulated dental casts indicate analytic model planning. F, Lateral cephalometric radiographs
before and after treatment.
• Figure 26-4, cont’d

1006 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
C
©Elsevier Inc.
Or
Or
Or
Or
Orthththththththththththththththththththththtr ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatatatatatatathicicicicicicicicicicicicicicicicicicicici Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
o nicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Orthththththththththththththththththththththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatatatatatatatatatatatatatatathicicicicicicicicicicicicicicicicicicicic Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
o nicicicicicicicicicicicicicicicicicicicicicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
O ththththththtr ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gnatatatatatatatatatatatatatatatathicicicicicicicicicic Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
osnicicicicicicicicicicicicicicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Orthththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatatatatatatatatatatatatatatatatatatatathicicicicicicicicicicicicicicicicicicicicicicicic Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
osnicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
O ththththththththththththththththththththththththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatatatatatatatatatatatatatatathicicicicicicicicicicicicicicicicicicicicicicicicicicicicicicic Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
o nicicicick
©Elsevier Inc.
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
O ththththththththththththththththththththththththththththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatatathicicicicicicicicicicicicicicicicicicic Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
o nicicicicick
A
B
A
B
• Figure 26-5  A 15-year-old boy was referred by
his pediatrician and arrived with his parents for the
surgical evaluation of documented obstructive sleep
apnea. He had a history of heavy snoring, restless
sleeping, and daytime somnolence. He was diag­
nosed with attention-deficit/hyperactivity disorder
when he was 3 years old, and his school grades are
poor. An attended polysomnogram confirmed an
overall apnea–hypopnea index of 17 events/hour. In
the supine position, his apnea–hypopnea index was
39 events/hour with desaturation to 78%. Head and
neck examination confirmed a normal-sized and
functioning soft palate and tongue. The tonsils and
adenoids had previously been removed, and the
intranasal cavity was obstructed (septal deviation
and inferior turbinate hypertrophy). The soft palate
was resting close to the posterior pharyngeal wall,
and the tongue was retropositioned. Both the
maxilla and the mandible were deficient in horizontal
projection, which explained the reduced airway
space. The anterior facial height was mildly deficient.
The patient previously underwent orthodontics and
had achieved a Class I canine and molar occlusion.
In consultation with medical and dental specialists
(general dentist, orthodontist, pediatrician, and pul­
monologist), the patient agreed to a surgical
approach. Orthodontic appliances were placed to
protect the periodontium, and he underwent jaw
and intranasal surgery. The patient’s procedures
included maxillary Le Fort I osteotomy (horizontal
advancement +10 mm); bilateral sagittal split ramus
osteotomies (horizontal advancement +10 mm);
osseous genioplasty (horizontal advancement); and
septoplasty and inferior turbinate reduction. Three
months after surgery, he underwent an attended
polysomnogram that confirmed the resolution of the
obstructive sleep apnea with an apnea–hypopnea
index of 0.9 events/hour and a maximum desatura­
tion of 92%. He was no longer snoring or experienc­
ing restless sleep. His daytime fatigue, behavioral
problems, and schoolwork all improved. A, Frontal
views with smile before and after surgery. B, Oblique
facial views before and after surgery. C, Profile views
before and after surgery.

1007
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
D
Prior to retreatment
Pre surgery
After treatment
D, Occlusal views before retreatment, with orthodontic appliances in place, and after treatment.
• Figure 26-5, cont’d 
Continued

1008 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
E
F
10 mm advancement
Enlarged
posterior
airway space
Apnea hypopnea index  1/hr
Desaturation 92%
Apnea hypopnea index  39/hr
Desaturation 78%
E, Articulated dental casts indicate analytic model planning. F, Lateral cephalometric radiographs before and after
treatment.
• Figure 26-5, cont’d 
12 ± 0.1). There were also a significant reductions in
minimum desaturations during sleep as well as improve­
ments in sleep efficiency. A shortcoming of the study was
its conclusion at just 6 months after surgery.
A study by Pillar and colleagues describes the long-
term follow up of patients with regard to both weight loss
and upper airway findings after bariatric surgery.273 At 4
months after surgery, there was a significant improvement
in the AI from 45 events/hour to 11 events/hour. Over a
7-year time frame, the AI regressed from a mean of 11
events/hour back up to 24 events/hour; however, the AI
remained at a much lower level (24 events/hour) than it was
before surgery (45 events/hour). In their report, the effec­
tiveness of bariatric surgery was to reduce the mean BMI
from 40 kg/m2 (i.e., morbid obesity) to a mean BMI of
35 kg/m2 (i.e., obesity) at 7 years after surgery. During the
same time frame, the mean AI was reduced from 45 events/
hour down to 24 events/hour. Other researchers have also
studied the long-term effects of bariatric surgery on patient
health.52,97,116,134

1009
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
A sleep medicine specialist consult is often beneficial
for the patient to maximize his or her education about
the disease process and its effects (both behavioral and
pathophysiologic) and to explore the CPAP option. Like­
wise, all patients should be advised of potential surgical
alternatives that may apply to them. An evaluation by a
surgeon who is familiar with current literature and treat­
ment modalities is beneficial to fully explore non-CPAP
options. Clearly, not all surgical options have equal success
for each patient. A frank discussion with a knowledgeable
surgeon regarding the patient’s specific potential benefit-
to-risk ratio for each surgical procedure is essential (see
discussion to follow).
Oral Appliance Option
The objective of an oral appliance (OA) for the treatment
of OSA is to mechanically reposition and hold the mandible
in a protruded (forward) location during sleep.259 As the
mandible moves forward, so does the tongue. An effective
OA must prevent the sealing of the tongue to the posterior
pharyngeal mucosa, thereby limiting obstruction at that
site.374 The upper airway response to oral appliances varies
among individuals. It has been stated that up to 50% of
individuals with OSA who use an oral appliance will
“respond to some extent.”218 Unfortunately, no matter how
technically precise the OA is, it can only affect the retroglos­
sal site.213,325 Most individuals with moderate to severe OSA
have obstruction at multiple sites.377 According to published
research, the median compliance rate with an OA after 1
year is 39% with a range of 4% to 82%, depending on the
study reviewed.96 Frequently stated potential long-term
negative effects of OAs include: tooth movement with
changes in occlusion; injury to the periodontium; excessive
salivation or dry mouth; and temporomandibular disorders
including masticatory muscle discomfort.308,310 Other stated
reasons for non-compliance include the insufficient reduc­
tion of snoring, continued OSA, or social concerns during
use. Almeida and colleagues reviewed a series of patients (n
= 70) who used OAs to treat snoring or OSA for more than
5 years.294 The authors found that 44% of those patients
had suffered unfavorable occlusal, dental, or temporoman­
dibular joint changes. In research that was carried out by
Pancer and colleagues, 14% of study patients (n = 106) were
found to have evidence of occlusal changes with the use of
an OA for the treatment of OSA.261 The most common
pathologic tooth movements were lingual tipping of the
maxillary incisors, proclination of the mandibular incisors,
and anterior shifting of the lower first molars. Although
some patients were unaware of the occlusal changes, many
were acutely bothered by the “shifts” (alterations) in their
bites. Bondenmark and Bondenmark and Lindman observed
patients (n = 32) after 2 years of continuous OA use.31,32
Occlusal changes were documented on lateral head radio­
graphs in the study patients. The authors hypothesized that
temporomandibular joint remodeling had occurred. To
Continuous Positive Airway Pressure Option
The use of CPAP for OSA was first reported in
1981. Since its introduction, it has become the
reference
standard
for
non-surgical
manage­
ment.43,65,66,71,105,107,114,132,148,159,160,178,181,217,236,267,356,357 With
this method, positive pressure can be continuously delivered
through a sealed nasal or mouth mask that the patient wears
while sleeping. The positive pressure has the potential to
pneumatically splint open the whole pharyngeal airway by
preventing the soft palate and the tongue from making a
seal with the posterior pharyngeal mucosa (i.e., it acts as a
counteracting force to the aforementioned collapsing force
in the patient with an anatomic predisposition for airway
obstruction). The pressure required to achieve this goal is
titrated at a sleep laboratory during PSG. CPAP is a sound,
evidence-based treatment option that has been shown to be
effective when it is used correctly and consistently through­
out the night as well as night after night throughout the
patient’s life. If CPAP is used in this way, it will decrease
daytime sleepiness and therefore likely improve the patient’s
mood and quality of life. The discomfort and difficulty
associated with the use of CPAP (e.g., drying of the nasal
and oral mucous membranes, dislodgment during sleep,
noise, inconvenience when transporting the unit, social dis­
pleasure, feelings of claustrophobia) makes long-term com­
pliance a clear problem. Even when defining an acceptable
CPAP compliance rate of just 4 hours per night for 70% of
nights, only a limited percentage of patients (depending on
the study reviewed) who consider themselves users of CPAP
are adherent. This does not take into account the significant
number of those with OSA who either will not consider
trying CPAP or those who have tried it but then refuse
to use it. Furthermore, this “acceptable compliance rate”
represents only approximately 50% of functional sleep
time.77,252,291,318,385 Sleep medicine clinicians continue to
appreciate the complexity of the disorder (i.e., complex
chemoreceptor apnea and apnea-related behavioral derange­
ments), and they now acknowledge the inability of a major­
ity of patients to stick with CPAP for the long term, even
if they do use it for the short term. Nevertheless, all indi­
viduals should be advised of the availability of CPAP and
encouraged to consider it.
The American Heart Association/American College of
Cardiology Foundation released a position statement about
the effects of sleep apnea on cardiovascular disease.133 The
organizations summarized published studies that confirmed
the moderate and variable effects of CPAP therapy for OSA
on blood pressure. They concluded that individuals with
more severe OSA, difficult-to-control hypertension, and
better CPAP compliance are likely to have more substantial
blood pressure reduction with CPAP. They also recom­
mended that, for those hypertensive patients who were
either not willing to use CPAP or not compliant, other
effective methods of managing OSA should be considered
(e.g., MMCA).

1010 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
treatment option, because it is considered by some to be
minimal surgery or a first treatment step (see Figs. 26-3 and
26-6).2,40,58,93,119,189,272,298,334,342 The reason for its limited
success is because it addresses only the retropalatal site, and
it does so in an incomplete way.209 In general, it will shorten
the soft palate, but it may also result in a thicker and nar­
rower retropalatal pharyngeal airway as a result of scarring.
Interestingly, although improvements in snoring generally
occur after UPPP, over time, the AHI actually increases
in approximately 30% of patients. This is called silent
apnea; the relief of the snoring may lead the individual to
falsely believe that his or her apnea has also gone away.
Realistically, UPPP is expected to be therapeutic only for
those with massive soft-tissue redundancy of the pharynx
and without concomitant intranasal and retroglossal
obstruction.95,192,204,336,335,391 When either the adenoids, the
tonsillar tissue, or the soft palate is significantly hypertro­
phic or redundant and causing physical blockage of the
upper airway, surgery to remove this excessive tissue should
be considered. In the absence of a specific syndrome or
anomaly that causes increased tongue volume (e.g., Proteus
syndrome, vascular anomalies, Beckwith-Wiedemann syn­
drome), this is rarely a cause of OSA.47,353 Frequent con­
cerns after intrapharyngeal soft-tissue reduction procedures
(e.g., UPPP, tonsillectomy, tongue reduction) include peri­
operative edema (airway compromise); moderate to severe
pain for 2 to 3 weeks; limited success with a single-site
approach for the resolution of OSA; velopharyngeal reflux;
velopharyngeal insufficiency; pharyngeal scarring (stenosis);
and silent apnea.173,226
If the maxilla and the mandible are retrusive then con­
sideration should be given to the surgical advancement
of these structures to correct the baseline anatomic de­for­
mity .193-195,201,215,277,345,398 MMCA has been shown to enlarge
the pharyngeal and hypopharyngeal airway by physically
expanding the whole facial skeletal framework (see Figs. 26-
4 and 26-7 through 26-14). Because the lateral pharyngeal
walls are dynamic, the skeletal expansion also tightens the
soft tissues; this subsequently decreases lumen collapsibility.
This skeletal approach address’s the “small airway” via an
extrapharyngeal operation with minimal risk of early post­
operative edema-induced upper airway compromise or long-
term pharyngeal dysfunction. This operation is also thought
to enhance the neuromuscular tone of the pharyngeal dilator
musculature (e.g., tensor veli palatini, genioglossus). These
anatomic facts explain the highly successful outcomes that
have been documented after MMCA. Frequent short-term
(perioperative) concerns in the adult patient after MMCA
are most often related to: altered occlusion; dysesthesia
(sensory loss); limited mouth opening; adjustment to the
change in facial appearance; and the downtime required for
recovery (see Chapter 25). If septal deviation or thickening
or inferior turbinate enlargement or hypertrophy results
in significant nasal airway resistance, then these abnormali­
ties can be addressed simultaneously with MMCA (see
Chapter 10).94,191,247,275,276,278 The medical risks associated
review, the use of OAs is not generally therapeutic for mod­
erate to severe OSA, and OAs are often not well tolerated
in the long term.
An often-stated objective of an OA is for use as a thera­
peutic trial to determine if a patient would be a candidate
for lower jaw surgical advancement. If patients respond to
an effective OA, they are said to likely respond in a similar
way to mandibular advancement surgery. This is not neces­
sarily the case, because many OAs are designed to position
the mandible into a full Class III malocclusion. To achieve
the same degree of mandibular advancement, both upper
and lower jaw surgery would be required.
Indications for Upper Airway Surgery and
Spectrum of Options
Surgery for OSA is indicated when applicable conser­
vative therapies are unsuccessful, intolerable, or un­
acceptable to the patient with underlying specific
anatomically correctible abnormalities that are causing the
OSA.76,80,81,139,193-195,198,202,280,282,285,304,307,358,375 Unfortunately,
the use of either CPAP or an OA requires continued per­
sonal application of a mechanical device. Likely for this
reason, neither is consistently well tolerated or found to be
acceptable to the patient in the long run. Indications for
surgery to treat OSA are often stated to be a failure of
medical management in the individual with one of the fol­
lowing symptoms:
• Excessive daytime sleepiness as a result of OSA
• RDI of more than 20 events/hour
• RDI of less than 20 events/hour but with marked
excessive daytime sleepiness
• Oxygen desaturations of less than 90% with apnea
events
• Documented hypertension, arrhythmia, or both
believed to be triggered by OSA
• Negative esophageal pressures (i.e., >−10 cm of water)
• Anatomic abnormalities of the upper airway (i.e., jaw
deformity, fixed intranasal obstructions, chronically
enlarged tonsils, enlarged floppy soft palate) that
result in apnea events
Although tracheostomy may be considered a way of
achieving a “cure” for OSA because it completely bypasses
all obstructions of the upper airway, secondary medical and
social problems as a result of the tracheostomy cannot be
overlooked.242,368,369 In general, this option is only consid­
ered for extreme cases (e.g., newborns or infants with con­
genital deformities such as the severe retrognathia seen with
Treacher Collins syndrome) or as a temporary solution.
Uvulopalatopharyngoplasty
(UPPP)—the
surgical
removal of the uvula, additional parts of the soft palate,
the pharyngeal pillars, and the tonsils—to open the airway
was originally described by Fujita in 1981.98,99 Although
the effectiveness of this approach for the resolution of
OSA is limited, it continues to be an often mentioned
Text continued on p. 1045

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-6  A 59-year-old man was referred by his otolaryngologist/head and neck surgeon to discuss further surgical options for the manage­
ment of documented obstructive sleep apnea. He had already undergone uvulopalatopharyngoplasty, septoplasty, and inferior turbinate reduction.
The procedures helped his snoring, but a postsurgery attended polysomnogram confirmed a respiratory disturbance index of 51 events/hour, with
desaturations reaching as low as 82%. The patient was also seen by a pulmonary sleep specialist and a cardiologist; mild concentric left ventricular
hypertrophy and mild pulmonary hypertension we found. The patient was unable to tolerate continuous positive airway pressure on a regular basis.
He lost 20 pounds and was exercising regularly, but this did not resolve his obstructive sleep apnea. Examination confirmed a short face growth
pattern with maxillomandibular deficiency (decreased vertical height and limited horizontal projection). During his teenage years, the patient had
undergone orthodontic treatment that included four bicuspid extractions. He was now showing signs of periodontal deterioration, and he had a
posterior crossbite on the left side. He underwent evaluation by a periodontist, a restorative dentist, and an orthodontist. He agreed to a compre­
hensive dental rehabilitation approach, with a primary interest in achieving an improved upper airway with the resolution of the obstructive sleep
apnea. The sleep specialist and the otolaryngologist were also supportive of this approach. The patient’s procedures included maxillary Le Fort I
osteotomy (horizontal advancement +10 mm and vertical lengthening +5 mm) with interpositional graft; bilateral sagittal split osteotomies of the
mandible (horizontal advancement +12 mm); osseous genioplasty (horizontal advancement); redo septoplasty; and anterior arch soft-tissue proce­
dures (cervical flap elevation, fat removal and platysma muscle plication). Three months after surgery, an attended polysomnogram was carried
out, which confirmed a respiratory disturbance index of less than 5 events/hour with the lowest desaturations at 90%. Subjectively, the patient
feels that his snoring has resolved, his nighttime sleeping is improved, and his daytime somnolence is greatly diminished. A, Frontal views in repose
before and after surgery. B, Frontal views with smile before and after surgery.
Continued

1012 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
C, Oblique facial views before and after surgery. D, Profile views before and after surgery.
• Figure 26-6, cont’d

1013
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
E
Prior to retreatment after four bicuspid extractions as a teenager
Pre surgery
After treatment
E, Occlusal views before retreatment, with orthodontic appliances in place, and after
treatment.
• Figure 26-6, cont’d 
Continued

1014 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
10 mm maxillary advancement
Mandibular counter
clockwise rotation
Arch expansion
Respiratory disturbance index  3/hr
Respiratory disturbance index  51/hr
F
G
F, Articulated dental casts that indicate analytic model planning. G, Lateral cephalometric radiographs before
and after surgery.
• Figure 26-6, cont’d

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-7  A 51-year-old man was referred by a neurologist to discuss surgical options for the management of documented obstructive sleep
apnea. He had heavy snoring, restless sleeping, and significant daytime somnolence. A recent attended polysomnogram confirmed a respiratory
disturbance index of 41 events/hour with oxygen desaturation of as low as 80%. A continuous positive airway pressure titration study was effective
at 12 cm of pressure; however, the patient was not able to tolerate continuous positive airway pressure. Intranasal examination confirmed a devi­
ated septum and hypertrophic inferior turbinates. The patient’s tonsils and adenoids were minimal in size. The soft palate functioned well, but the
uvula was enlarged. The tongue was of normal size and function. During his teenage years, the patient had undergone orthodontic treatment, and
he had a Class I deep bite. Examination confirmed a short face growth pattern that involved deficient vertical height and limited horizontal projec­
tion. Consultations with a sleep specialist, an internist, a general dentist, an otolaryngologist/head and neck surgeon, and an orthodontist were
carried out. The patient agreed to a surgical approach that included orthodontics as needed to protect the periodontium. The procedures included
maxillary Le Fort I osteotomy (horizontal advancement +10 mm and vertical lengthening +8 mm) with interpositional allograft; bilateral sagittal split
osteotomies of the mandible (horizontal advancement); osseous genioplasty (horizontal advancement); uvulectomy; and septoplasty and inferior
turbinate reduction. After surgery, the patient’s snoring was resolved, his nighttime sleeping improved, and his daytime somnolence was greatly
diminished. A 1-year postoperative polysomnogram confirmed a respiratory disturbance index of 13 events/hour. A, Frontal views in repose before
and after surgery. B, Frontal views with smile before and after surgery.
Continued

1016 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
C, Oblique facial views before and after surgery. D, Profile views before and after surgery.
• Figure 26-7, cont’d

1017
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Prior to treatment
Pre surgery
After treatment
E
E, Occlusal views before retreatment, with orthodontic appliances in place, and after treatment.
• Figure 26-7, cont’d 
Continued

1018 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
F
G
10 mm
advancement
8 mm
lengthening
Respiratory disturbance index  13/hr
Respiratory disturbance index  41/hr
F, Articulated dental casts that indicate analytic model planning. G, Lateral cephalometric radiographs before and after
surgery.
• Figure 26-7, cont’d

1019
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Additional microplate
and screws
I
Iliac graft
Pharyngeal
airway
expansion
H
H, Computed tomography scans reformatted to indicate pharyngeal airway space before and after surgery. I, Close-up
intraoperative view of the left side Le Fort I osteotomy site with plate and screw fixation in place (zygomatic buttress and piriform aperture regions).
Also shown is the corticocancellous iliac graft that was crafted and then inset in the defect; this was followed by additional plate and screw fixation
of the graft.
• Figure 26-7, cont’d 
Continued

1020 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
C
Or
Or
Or
Orththththth
r ogn
gn
gn
gn
gn
gn
gn
gn
gn
gn
gn
g atatatatatatata hicicicicicicicicicicicicici Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C Pos
os
os
os
os
o nicicicicicicicicick
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
Or
O ththththththththththth
r ogn
gn
gn
gn
gn
gn
g atatatatatatatatatatatatathicicicicicicicicicicicicicicicicicic Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
o nicicicicicicicicicicicicicici k
Or
Or
Or
O ththtr ogn
gn
gn
gn
gn
gn
gn
g atatatatatathicicicici Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
osnicicicicicicicicicicicicicicicicicicicicick
Or
Or
Or
O thththth
r ogn
gn
gn
gnatatatatatata hicicic Su
Su
Su
Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
o nicicicicicicicicicicick
Or
Or
Or
Or
Or
O thththth
r ogn
gn
gn
gn
gn
gnatatatatatatathicicicicicici Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
S rg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
osnicicicicicicicicicicicicicicicicicicicicicicicicicicick
Or
Or
Or
Or
O thththth
r ogn
gn
gn
gn
gn
gn
g atatatatatatatatatatathicicicicicicicicicicici Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Su
Surg
r ery
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry
ry; J.C.
C.
C.
C.
C.
C.
C.
C Pos
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
os
osnicicicicicicicicicicicicicicicicick
A
B
• Figure 26-8  A 50-year-old woman
was referred by her general dentist to
an orthodontist and then for surgical
evaluation. She had a mandibular defi­
ciency and a constricted upper jaw
width growth pattern that resulted in a
Class II deep-bite excess overjet mal­
occlusion. Over the years, there was
destruction to the dentition and the
periodontal apparatus with general­
ized bone loss and gingival recession.
She was now under the care of a
restorative dentist and a periodontist.
To resolve the malocclusion, maxillary
expansion and mandibular advance­
ment in combination with orthodontics
were recommended. As part of her
referral to this surgeon, a history was
taken that documented heavy snoring,
restless sleeping, and daytime somno­
lence. An attended polysomnogram
confirmed a respiratory disturbance
index of 42.7 events/hour. There was
intranasal site obstruction as a result
of septal deviation and inferior turbi­
nate enlargement. There was also
retropalatal obstruction caused by
maxillary retrusion and a retroposi­
tioned tongue that resulted from man­
dibular retrusion. The soft palate and
the tongue were of normal size and
function. There were minimum tonsil
and adenoid structures. Continuous
positive airway pressure was tried but
not well tolerated. Surgery was agreed
to in combination with orthodontics to
improve the malocclusion and open
the airway. The procedures that were
carried out included maxillary Le Fort I
osteotomy (horizontal advancement
+7 mm, vertical lengthening +3 mm,
and arch form correction); bilateral
sagittal split osteotomies of the
mandible
(horizontal
advancement
+12 mm); osseous genioplasty (hori­
zontal advancement); septoplasty and
inferior turbinate reduction; and an
anterior approach to the neck (cervical
flap elevation, supraplatysmal defat­
ting, and vertical platysma muscle pli­
cation). Subjectively, there was good
relief of snoring, restless sleeping, and
daytime fatigue. One year after
surgery, an attended polysomnogram
confirmed
the
resolution
of
the
obstructive sleep apnea, with a respi­
ratory disturbance index of 1.9 events/
hour. A, Frontal views in repose before
and after treatment. B, Oblique
facial views before and after treatment.
C, Profile views before and after
treatment.

1021
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Prior to treatment
Pre surgery
After treatment
D
D, Occlusal views before treatment, with orthodontics in progress, and after treatment.
• Figure 26-8, cont’d 
Continued

1022 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
E
F
Maxillary counter
clockwise rotation
Arch correction
Mandibular counter
clockwise rotation
Respiratory disturbance index  1.9/hr
Respiratory disturbance index  42.7/hr
E, Articulated dental casts that indicate analytic model planning. F, Lateral cephalometric radiographs before
and after surgery.
• Figure 26-8, cont’d

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-9  A 25-year-old man was referred by his general dentist to an orthodontist and then to this surgeon for the evaluation of a dentofacial
deformity. Examination confirmed a maxillary deficiency and a relative mandibular excess growth pattern; this resulted in a severe Class III negative
overjet anterior open-bite malocclusion. The maxillomandibular deformities had a negative impact on the patient’s speech articulation, swallowing,
chewing, breathing, and lip closure/posture. The patient’s history confirmed lifelong obstructed nasal breathing, restless sleeping, heavy snoring,
and daytime fatigue. An attended polysomnogram was carried out and documented a respiratory disturbance index of 14 events/hour, with desatu­
rations of as low as 87%. The patient underwent additional evaluations by a sleep specialist, an otolaryngologist, a speech pathologist, a restorative
dentist, and a periodontist. He agreed to a comprehensive surgical and dental rehabilitative approach, and his periodontal treatment was followed
by orthodontic decompensation. The patient’s procedures included maxillary Le Fort I osteotomy in segments (horizontal advancement +10 mm,
arch expansion and minimal clockwise rotation) with interpositional graft; bilateral sagittal split osteotomies of the mandible (horizontal advancement
+4 mm and counterclockwise rotation); osseous genioplasty (horizontal advancement); and inferior turbinate reduction and septoplasty. The patient
experienced relief of his snoring, improvements in his sleep quality, less daytime fatigue, and improved breathing during the day. Interestingly, the
4-month postoperative attended polysomnogram indicated only mild reduction of the sleep indexes. Reevaluation by the sleep specialist recom­
mended the avoidance of supine sleep, with no need for further treatment. A, Frontal views in repose before and after surgery. B, Frontal views
with smile before and after surgery.
Continued

1024 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
C, Oblique facial views before and after surgery. D, Profile views before and after surgery.
• Figure 26-9, cont’d

1025
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Prior to treatment
Pre surgery
After treatment
E
E, Occlusal views before treatment, with orthodontic appliances in place, and after treatment. Note the
pulpal necrosis of the right maxillary lateral incisor, which required root canal therapy and crown coverage.
• Figure 26-9, cont’d 
Continued

1026 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
F
G
Maxillary clockwise
rotation
Mandibular counter-
clockwise rotation
Arch expansion
Apnea hypopnea index  14/hr
Apnea hypopnea index  14/hr
F, Articulated dental casts that indicate analytic model planning. G, Lateral cephalometric radiographs before
and after surgery.
• Figure 26-9, cont’d

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-10  A 37-year-old man was referred to this surgeon with a request to have his chin implant removed because he was dis­
pleased with the aesthetic results. When he was 20 years old, he had undergone a chin augmentation (silicone implant) in an attempt to
camouflage the small lower jaw profile. Ten years later, he underwent four bicuspid extractions and orthodontic alignment to improve the
occlusion. He had undergone a septorhinoplasty procedure, but he was still experiencing continued difficulty breathing through the nose.
During the patient’s referral to this surgeon, an examination confirmed maxillomandibular deficiency. He was recognized as having a short
face growth pattern with decreased lower anterior facial height and limited facial projection. There was an accentuated labiomental “lip
curl” and a “button appearance” of the chin. It was clear that the patient suffered with snoring, restless sleeping, and excessive daytime
fatigue. An attended polysomnogram confirmed a respiratory disturbance index of 16 events/hour, with desaturations of 89%. A titration
study confirmed the need for 12 cm of water pressure to reduce the respiratory disturbance index to 3 events/hour. A, Frontal views in
repose before and after surgery. B, Frontal views with smile before and after surgery.
Continued

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
The use of continuous positive airway pressure was attempted, but the patient found it to be uncomfortable and difficult to use.
Consultations with a sleep specialist, an otolaryngologist, and an orthodontist confirmed the advantage of an intranasal and orthognathic surgical
approach. The patient agreed to perioperative orthodontics and surgery to improve the airway and facial appearance. The patient’s procedures included
maxillary Le Fort I osteotomy (horizontal advancement +9 mm, vertical lengthening +5 mm) and interpositional grafting; bilateral sagittal split osteotomies
of the mandible (horizontal advancement +12 mm); removal of the chin implant; osseous genioplasty (horizontal advancement and vertical lengthening)
with interpositional grafting; reduction of the inferior turbinates; redo septoplasty; and an anterior approach to the neck (cervical flap elevation, suprapla­
tysmal defatting, and vertical platysma muscle plication). As a result of the procedures, the patient experienced relief of his snoring, improved sleep quality,
diminished daytime fatigue, and improved breathing during the day. Six months after surgery, he underwent an attended polysomnogram that indicated
a normal sleep study, with no snoring or apnea events. C, Oblique facial views before and after surgery. D, Profile views before and after surgery.
• Figure 26-10, cont’d

1029
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Prior to retreatment after 4 bicuspid extractions as a teenager
Pre surgery
After treatment
E
E, Occlusal views before retreatment, with orthodontic appliances in place, and after treatment.
• Figure 26-10, cont’d 
Continued

1030 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
F
G
9 mm maxillary advancement
Respiratory disturbance index  3/hr
Respiratory disturbance index  16/hr
Silicone chin implant to be removed
F, Articulated dental casts that indicate analytic model planning. G, Lateral cephalometric radiographs before and after
surgery (note the preoperative chin implant).
• Figure 26-10, cont’d

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-11  A 33-year-old man was referred by his orthodontist for the surgical evaluation of a dentofacial deformity. Examination confirmed
a long face growth pattern with a Class III anterior open-bite malocclusion. During the mixed dentition, the patient underwent growth modification
and orthodontic treatment that included the use of a Frankel appliance, a chin cup, and rapid palatal expansion. By the end of high school, he
was left with a residual anterior open bite, a constricted maxillary arch, and a gummy smile. When he was 29 years old and had a lifelong history
of heavy snoring, difficulty sleeping at night, and daytime fatigue, he underwent a sleep study. The polysomnogram revealed moderate obstructive
sleep apnea with a respiratory disturbance index of 16 events/hour and oxygen desaturations down to 86%. A continuous positive airway pressure
titration study confirmed the need for 10 cm of water pressure to resolve the respiratory events. The current head and neck examination docu­
mented a deviated septum; enlarged inferior turbinates; an elevated nasal floor; narrow pyriform rims; a soft palate close to the pharyngeal wall;
and a retropositioned tongue. The tonsils were not enlarged, and the tongue and soft palate were of normal size. A, Frontal views in repose before
and after surgery. B, Frontal views with smile before and after surgery.
Continued

Orth
r ognathic Sur
u g
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Sur
u g
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
The patient hoped to achieve improved breathing during the day, better sleeping at night, and resolution of his obstructive
sleep apnea. He also wanted correction of his malocclusion, improvements in his lip closure/posture, and an enhanced profile and smile. He agreed
to a comprehensive orthodontic and surgical approach. With the orthodontic relief of his dental compensation, intranasal, orthognathic, and facial
surgery was carried out. The patient’s procedures included maxillary Le Fort I osteotomy in three segments (horizontal advancement +8 mm, vertical
shortening −4 mm, and arch expansion); bilateral sagittal split osteotomies of the mandible (horizontal advancement +12 mm and counterclockwise
rotation); osseous genioplasty (horizontal advancement and vertical shortening); reduction of the inferior turbinates, septoplasty, and recontouring
of the nasal floor; and an anterior approach to the neck (cervical flap elevation, supraplatysmal defatting, and vertical platysma muscle plication).
He experienced the relief of his snoring, improvement in his quality of sleep, the ability to breathe through the nose during the day, and less daytime
fatigue. He had not yet undergone a formal posttreatment polysomnogram. C, Oblique facial views before and after surgery. D, Profile views before
and after surgery.
• Figure 26-11, cont’d

1033
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Prior to retreatment
Pre surgery
After treatment
E
E, Occlusal views before retreatment, with orthodontic appliances in place, and after treatment.
• Figure 26-11, cont’d 
Continued

1034 SECTION 3  Classic Patterns and Presentations of Dentofacial Deformity
F
G
Maxillary counter
clockwise rotation
Mandibular counter
clockwise rotation
Arch expansion
F, Articulated dental casts that indicate analytic model planning. G, Lateral cephalometric radiographs before
and after surgery.
• Figure 26-11, cont’d

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-12  A 32-year-old man was referred by his internist and otolaryngologist/head and neck surgeon to discuss further surgical options
for the management of document obstructive sleep apnea. An attended polysomnogram confirmed a respiratory disturbance index of 56 events/
hour, with oxygen desaturations reaching as low as 84%. The patient’s sleep efficiency was reduced to 46%. He underwent a split study that
confirmed the need for 8 cm of continuous positive airway pressure to significantly reduce the respiratory disturbance index. He was unable to
effectively use the continuous positive airway pressure device as a result of claustrophobia, excessive noise, and poor mask fit. Since his early
childhood years, the patient was known to have a jaw deformity with malocclusion. He underwent 2 years of orthodontic treatment when he was
12 to 14 years old; this resulted in improvement of the occlusion but residual jaw deformity. Examination confirmed a short face growth pattern
with maxillomandibular deficiency (decreased vertical height and limited horizontal projection). The tonsils were not inflamed, but they were mod­
erately enlarged, and the uvula was mildly long and floppy. The tongue was of normal size, the septum was straight, and the inferior turbinates
were enlarged. A, Frontal views in repose before and after surgery. B, Frontal views with smile before and after surgery.
Continued

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
The patient underwent evaluation by a restorative dentist, an orthodontist, a sleep specialist, an otolaryngologist/head
and neck surgeon, and an internist. His primary motivations were to achieve an improved airway and to resolve his obstructive sleep apnea. He
was also interested in improved profile aesthetics and long-term dental health. We discussed potential benefits of tonsillectomy and of the reduction
of the size of the soft palate, but he preferred a skeletal approach, thus reserving the option of soft-tissue reduction if needed as a secondary
procedure. With orthodontic appliances in place, the patient’s procedures included maxillary Le Fort I osteotomy (horizontal advancement +10 mm
and vertical lengthening +4 mm) with interpositional allogenic graft; bilateral sagittal split osteotomies of the mandible (horizontal advancement +12);
osseous genioplasty (horizontal advancement); and inferior turbinate reduction. He experienced relief of his snoring, improvement in his quality of
sleep, better breathing during the day, and less daytime fatigue. Three months postoperatively, he underwent an attended polysomnogram. Inter­
estingly, after surgery, he chose to sleep with his lips taped together out of the belief that this improves sleep hygiene, including air humidification.
Thus, the sleep study was carried out with the patient’s lips taped together. An overall respiratory disturbance index of 15 events/hour was docu­
mented, with average desaturations to 95%. C, Oblique facial views before and after surgery. D, Profile views before and after surgery.
• Figure 26-12, cont’d

1037
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
F
G
Respiratory disturbance
index  15/hr
Respiratory disturbance
index  56/hr
Pre surgery
After treatment
E
E, Occlusal views before and after treatment. F, Articulated dental casts that indicate analytic model planning.
G, Lateral cephalometric radiographs before and after surgery.
• Figure 26-12, cont’d

Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
A
B
• Figure 26-13  A 43-year-old man was referred by a restorative dentist to an orthodontist and then for surgical evaluation of a dentofacial deformity
characterized by maxillomandibular deficiency. Despite orthodontic treatment (including four bicuspid extractions when the patient was a teenager),
there remained a Class III negative overjet bilateral posterior cross-bite malocclusion. A degree of labial bone loss and gingival recession was
appreciated. Earlier during his life, the patient’s nose was broken during a sports injury, and he had since experience chronic obstructive breathing.
Examination confirmed a deviated septum and inferior turbinate enlargement. The tonsils, the tongue, and the soft palate were essentially normal;
the uvula was somewhat enlarged. He admitted to heavy snoring, restless sleeping, and excessive daytime fatigue. A sleep study confirming a
respiratory disturbance index of 37 events/hour with desaturations reaching a low of 86%. The patient was fitted with a continuous positive airway
pressure device (8 cm of water pressure per hour) as temporary treatment while his orthodontics were initiated. After the orthodontic relief of dental
compensation, surgery was carried out. The patient’s procedures included maxillary Le Fort I osteotomy in two segments (horizontal advancement
+10 mm, vertical lengthening −2 mm, and arch expansion) with allogenic interpositional grafting; bilateral sagittal split osteotomies of the mandible
(horizontal advancement +13 mm and counterclockwise rotation); osseous genioplasty (horizontal advancement); inferior turbinate reduction and
septoplasty; and an anterior approach to the neck (cervical flap elevation, supraplatysmal defatting, and vertical platysma muscle plication). After
surgery, there was an immediate relief of the patient’s snoring as well as improvements in his quality of sleep, his ability to breathe through his
nose, his concentration, and his daytime fatigue. The 6-month postoperative attended polysomnogram confirmed a reduction in the respiratory
disturbance index to 10 events/hour. A, Frontal views in repose before and after surgery. B, Frontal views with smile before and after surgery.

1039
CHAPTER 26  Obstructive Sleep Apnea: Evaluation and Treatment
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
Orth
r ognathic Surg
r ery; J.C. Posnick
C
D
C, Oblique facial views before and after surgery. D, Profile views before and after surgery.
• Figure 26-13, cont’d 
Continued