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CRANIO®
The Journal of Craniomandibular & Sleep Practice

ISSN: 0886-9634 (Print) 2151-0903 (Online) Journal homepage: http://www.tandfonline.com/loi/ycra20

Sleep and airway assessment: A review for

dentists

Ahmed I. Masoud, Gregory W. Jackson & David W. Carley

To cite this article: Ahmed I. Masoud, Gregory W. Jackson & David W. Carley (2016): Sleep and
airway assessment: A review for dentists, CRANIO®, DOI: 10.1080/08869634.2016.1228440

To link to this article: http://dx.doi.org/10.1080/08869634.2016.1228440

Published online: 19 Sep 2016.

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Download by: [Cornell University Library] Date: 20 September 2016, At: 07:39
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CRANIO®: The Journal of Craniomandibular & Sleep Practice, 2016

http://dx.doi.org/10.1080/08869634.2016.1228440

SLEEP

Sleep and airway assessment: A review for dentists

Ahmed I. Masoud BDS, MSa,b,c , Gregory W. Jackson DDS, MSDb and David W. Carley PhDd

a Department of Orthodontics, Faculty of Dentistry, King Abdulaziz University, Jeddah, Saudi Arabia; bDepartment of Orthodontics, College of
Dentistry, University of Illinois, Chicago, IL, USA; c Graduate Program in Neuroscience, University of Illinois, Chicago, IL, USA; dDepartments of
Biobehavioral Health Science, Medicine and Bioengineering, University of Illinois, Chicago, IL, USA

ABSTRACT KEYWORDS
Introduction: Dentists can be the first professionals to recognize a patient's potential sleep problem since Sleep apnea;
they typically have more frequent contact with their patients than do physicians. It is important that dentists sleep-disordered
have a reasonable understanding of sleep disorders and how to assess their patients if they suspect such a breathing; airway analysis;
cephalogram; CBCT;
problem so that a timely referral can be made or treatment can be provided as appropriate. adenoids

Objective: To review the key literature relevant to sleep-disordered breathing (SDB) characteristics and
diagnosis, including history, examination, and investigation with an emphasis on radiographic airway analyses.

Conclusion: The authors present a concise explanation of SDB conditions and an outline for thorough patient
examination and evaluation, including radiographic airway analyses. Limited two-dimensional and three-
dimensional norms exist for adult patients with no SDB and even less so for children. Much more research is
needed, particularly in the pediatric population.

1.Introduction emphasis on radiographic airway analyses. This was done

A good night's sleep is essential to restoring the body and
mind. For the estimated 40 million Americans who
experience symptoms of sleep-disordered breathing (SDB),
a good night's sleep also has the power to save their lives.
[1] Dentists can be the first professionals to recognize a
patient's potential sleep problem since they are usually in
contact with their patients more frequently than are
physicians. Furthermore, orthodontists are involved in
comprehensive treatment of the facial skeleton and the
occlusion. This requires an understanding of all relevant
functional entities, including the upper airway. The
development of the facial morphology and malocclusion is
significantly affected by the upper airway and the mode of
respiration. Orthodontists regularly obtain records that can
help in early assessment of the upper airway, in addition to
assessing the risk for sleep apnea.[2,3] Furthermore, a clear
knowledge of airway changes in adults is important for
orthodontic and orthognathic surgical treatment planning.[4]
The objective in this paper was to review the key lit-
erature relevant to SDB characteristics and diagnosis,
including history, examination, and investigation, with an
to help provide dentists with a concise explanation of SDB
and means by which a thorough patient assessment can be
performed. Dentists can then refer symptomatic patients in
a timely manner to a sleep medicine specialist who can
definitively assess the patient's condition. If a patient is
diagnosed with the disorder, he or she may return to the
dentist to receive treatment. Also, a large number of patients
being treated for sleep apnea with continuous positive
airway pressure are not compliant with that treatment and
may seek out their dentist to discuss potential benefits from
alternative treatment.[5]
2. Definitions and anatomy
Sleep is defined behaviorally as a normal and temporary
suspension of consciousness. Electrophysiologically, sleep
is defined by specific brain wave criteria, whereby the human
descends into successive stages of sleep that are defined
by electroencephalogram (EEG) criteria. Additional signals,
including the electrooculogram (EOG) and the
electromyogram (EMG), are necessary to accurately define
rapid eye movement (REM) sleep.[6] The Airway is the
conductive path air follows to get into and out of the lungs and allows

CONTACT Ahmed I. Masoud aemasoud@kau.edu.sa

© 2016 Informa UK Limited, trading as Taylor & Francis Group
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2 AI Masoud et al.

for gas exchange. The mouth and nose are the normal 3.2 Sleep-disordered breathing (SDB)
entry and exit ports. Entering air then passes through the
SDB includes an array of airway dysfunctions that occur
phar-ynx, continues through the larynx, down the trachea,
during sleep. These include significant snoring, upper
the bronchi, and finally into the bronchioles and alveoli.
airway resistance syndrome (UARS), both central and
The Upper airway is the portion of the respiratory tract
obstructive sleep apnea (CSA and OSA), and other sleep-
that extends from the nares or the mouth, down the
related hypoventilation and hypoxemia disorders.
pharynx to and including the larynx.[7] The Pharynx is
[1,16–18] SDB is common, and in the United States,
divided into three segments. The first is called the
approximately 10–20% of the population is affected,
nasopharynx, which lies behind the nasal cavity, above
although the majority of those affected remain undi-
the soft palate. It contains the pharyngeal tonsils, or adenoids, in its posterior wall.
agnosed.[1,19,20] These disorders all lead to disturbed
The second segment is the oropharynx, which is encom-
sleep patterns. Insufficient or fragmented sleep confers
passed by the soft palate above and the epiglottis below.
increased risks for hypertension, myocardial infarction,
It contains the palatine tonsils, generally referred to as
strokes, diabetes, sleepiness related accidents, and all-
the tonsils. The last is the hypopharynx or laryngopharynx.
causes mortality.[19,21,22] SDB has also been linked to
It extends from the upper border of the epiglottis to the
mild cognitive impairment and dementia.[1] Additional
lower margin of the cricoid cartilage.[8]
consequences in children include attention-deficit/hyper-
Skeletal support of the upper airway includes the spine
activity disorder and other behavioral manifestations, dis-
and the basilar portion of the occipital bone posteriorly,
turbances in cognitive development, failure to thrive, and
the cranial base and vomer superiorly, the nasal septum
increased utilization of health care services.[16,23]
anterosuperiorly, the jaws and hyoid bone anteriorly, and
the pterygoid hamuli and medial pterygoid plates laterally.
[3,4] The adenoid tissue usually extends from the bony 3.3 Snoring
recess at the region of the spheno-occipital suture inferiorly
Snoring is the rasping sound that occurs when breathing
along the posterior pharyngeal wall.[3] The airway valves
is partially obstructed during sleep and upper airway soft
include the nares, soft palate, tongue, and epiglottis.[9]
tissues are vibrating.[24] As the diameter of the airway is
reduced, the air velocity increases, leading to a higher
3. Normal breathing and sleep-disordered negative pressure, an increase in turbulence, and vibration
breathing of soft tissues. This tissue vibration occurs most commonly
3.1 Normal breathing in the soft palate but can also occur in the lateral walls of
the pharynx or the base of the tongue. When the soft
During exhalation and breathing pauses, blood oxygen
palate vibrates, it acts like a flag and causes a sound that
decreases and carbon dioxide increases. This increases
is heard during snoring. Snoring is typically inspiratory;
activation of central chemoreceptors in the brain and
However, a small expiratory component sometimes can
peripheral chemoreceptors in the carotid body, which, in be heard.[25]
turn, facilitate initiation of a breathing effort.[10] The brain
Snoring can either be associated with other forms of
then sends signals to spinal motor neurons con-trolling
SDB or it can stand as a distinctly separate disease (pri-
the diaphragm, the external intercostals, and the accessory
mary or habitual snoring), which might be an independent
muscles of inspiration, which create a vacuum leading to risk factor for cardiovascular diseases.[26] Trauma from
gas exchange.[11,12] The normal awake breathing rate
long-term snoring can also lead to deterioration of the soft
in adults typically ranges from 12 to 20 breaths per min,
palate.[14,24] There are three types of snoring: nasal,
while children are on the higher end of the spectrum and
oral, and oronasal, which usually require different
may exceed 20 breaths per min.[13] treatment modalities.[25]
The pharynx contains the soft palate. It can contract
forcefully and elevate to act as a check valve during swal-
3.4 Upper airway resistance syndrome (UARS)
lowing to prevent regurgitation of fluids into the nose.
It relaxes partially during normal breathing to allow air- UARS was defined by Guillerminault et al. as a condition
flow through the nasopharynx during both inhalation and in which there is a combination of daytime sleepiness and
exhalation. Generally, normal muscle tone while awake demonstrated upper airway flow limitation with increased
keeps the airway patent for breathing. When muscle tone respiratory effort. Such events are transient and are
in the soft palate and the tongue protrudor muscle, the resolved by an arousal just following peak end inspiratory
geniusglossus, reduces physiologically with sleep onset, esophageal pressure.[27]
the airway size decreases, doubling upper airway Diagnosing UARS is not as clear-cut as diagnosing sleep
resistance even in healthy individuals.[14,15] apnea, and UARS is often mislabeled with a different
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CRANIO: The Journal of Craniomandibular & Sleep Practice 3
diagnosis. Individuals with UARS often do not have
frequent apneas, hypopneas, or desaturations. However,
respiratory effort-related arousals (RERAs) are a
common finding.[28]
3.5 Sleep apnea
Sleep apnea is a disease characterized by recurrent
episodes of breathing pauses (apneas) or decreases in
airflow (hypopneas) during sleep, resulting in arousals,
fragmented sleep, and disturbance in normal sleep
architecture.[29] Apneic events result in hypoxemia (low
oxygen in the blood), hypoxia (low oxygen in the tissues),
and hypercapnia (increased blood carbon dioxide ).
Patients may experience 30–300 events of greater than
10 s breathing pauses per night. Because of chil-dren's
different physiology, lower functional residual capacity,
and higher baseline respiratory rate, clinically relevant
apneas may not last this long. Apneas of three to four
seconds duration can be accompanied by blood oxygen
desaturations in children. However, children are more
likely to have hypopneas than clear-cut apneas.
[15,18,30,31] There are two types of sleep apnea: CSA
and OSA.
3.6 Central sleep apnea (CSA)
CSA is the least common form of sleep apnea, which
accounts for less than 5% of all apneas. The prevalence
of CSA is negatively correlated with age, occurring in
younger children more than older children.[32] In central
apneas, there is absence of nasal and oral airflow
associated with a transient loss of inspiratory effort.[31]
Breathing pauses occur because the brain temporarily
stops sending signals to the muscles that control breathing
with no blocking necessary. CSA often occurs in people
who have medical conditions such as congestive heart
failure. Other reasons include high altitudes, narcotics,
and obesity. The large majority of CSA patients also
experience OSA. The CSA may not be noted until the OSA is treated.[33]
3.7 Obstructive sleep apnea (OSA)
Obstructive apneas are characterized by an absence of
oral and nasal airflow despite persistent inspiratory efforts.[31]
Breathing pauses occur because of recurrent episodes of
airway obstruction.[29] OSA is much more common than
CSA, affecting approximately 17% of adults in the United
States, with the disease affecting men more than women.
[19,34] In children, OSA prevalence is 1–5.7%, equally
distributed between males and females.[23,35,36] More
recently, the prevalence of childhood obesity has gone up
to 60% (this diagnosis is based on charts developed by
the Centers for Disease Control and Prevention (CDC) in
2000). This has led to an increase in awareness of
pediatric sleep disorders such as obesity-related OSA.
Timely diagnosis and management of pediatric OSA may
prevent associated comorbidities.[36]
3.8 Airway obstruction
People who have airflow limitation or who have OSA may
suffer from the following airway obstructions:
(1) Nasal obstruction by a stuffy nose, turbinate
hypertrophy, nasal polyps, or a deviated
septum. Other examples in infants include cho-
anal atresia, nasolacrimal cysts, and nasal
aperture stenosis.[18,26]
(2) Excessive throat tissue: enlarged palatine, lin-
gual, or pharyngeal tonsils, excess fat or fluid,
and rarely, cysts or tumors, all of which can be
surgically removed.[26,37]
(3) Long, thick, soft palate and/or uvula.[25]
(4) Large or retropositioned tongue.[25,38]
(5) Laryngeal pathology, which is also a surgically
curable cause of obstruction. The five most
common laryngeal pathologies are nodules,
edema, polyps, laryngeal cancer, and vocal
fold paralysis.[39]
(6) Poor muscle tone in the tongue, throat, soft
palate, or upper airway.[25]
4. Diagnosis of SDB and specifically OSA
4.1 History
(1) Symptoms of OSA [19,22,23,40]:
• Snoring
• Reported cessation of breathing
• Gasping for air
• Teeth clenching and grinding associated with
sleep bruxism
• Increased urine production and enuresis
associated with hormonal dysregulation
• Disturbed sleep and nighttime awakening
• Morning headaches
• Waking up with a dry or sore throat
• Daytime sleepiness and sleeping during the
day
• Irritability
• Impaired concentration
Additional symptoms in children:
• Poor academic performance
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4 AI Masoud et al.
• Hyperactivity and unusual daytime behavior
(2) Risk factors for OSA [30,41,42]:
• Family history
• Narrow airway for any reason
• Obesity
• Increased neck circumference (ÿ42 cm for
men and ÿ 37 cm for women)
• Being male (fourfold increase in probability)
• Being older (twofold increase in probability
when over 52 years)
• Alcohol (due to muscle relaxation)
• Smoking (due to inflammation and fluid
retention)
• Prolonged sitting: long periods sitting lead to
fluid retention. When the individual reclines,
fluids shift from the legs and narrow the
airway.
Sleep questionnaires
Sleep questionnaires can be used to assess symptoms
and risk factors. Sleep questionnaires are subjective
tools to describe psychometric qualities in the field of
sleep medicine and are concerned with the symptoms of
OSA and SDB.[43] In adults, the Berlin questionnaire is
the most commonly used, followed by the Wisconsin
sleep questionnaire.[44] Pediatric sleep questionnaires
also exist and are mainly parent report tools. Among the
best-constructed pediatric sleep questionnaires are the
Sleep Disturbance Scale for Children, the Sleep Disorders
Inventory, and the Pediatric Sleep Questionnaire.[43] To
assess daytime sleepiness and the possible need for
medical attention, the Epworth Sleepiness Scale is used
in both adults and children.[43,44]
4.2 Examination
(1) Obesity
The body mass index (BMI) positions the individual into
one of four weight status categories: underweight, healthy
weight, overweight, and obese. BMI can be calculated
using the equation: BMI = weight (kg)/[height(m)]2 . For
adults, a patient is considered obese when the BMI is 30
or above.[41] For children, once the BMI is calculated, it
can be compared to age and sex specific BMI measures
using charts published by the CDC (Figures 1 and 2). A
child is considered obese when he/she is at or greater
than the 95th percentile.[23,45] The BMI is probably the
most commonly used measure to identify obesity.
However, the type of body fat distribution seen in obese
and overweight SDB patients has led to the propositions
that a large neck circumference and a high waist-to-hip circumference
are stronger predictors of SDB, compared with weight-
based measures such as the BMI. Presently, there is no
body habitus measure that is considered the most pre-
dictive for SDB.[34]
(2) Craniofacial morphology
to. Midface hypoplasia or micrognathia. A thorough
physical examination should include evaluation of facial
characteristics. Some authors have proposed a
relationship-ship between midface hypoplasia or
micrognathia and OSA.[18] These findings can then be
later confirmed by radiographic cephalometric
measurements such as the nasolabial angle, SN-Orbitale,
SNA, and the maxillary depth for the maxilla and SNB,
facial angle, and the man-dibular length for the mandible.
It is important to note that it is the midface hypoplasia or
the micrognathia that showed a relationship with OSA
and not the skeletal classification, which, conversely,
showed variability when related to OSA.[46]
b. Features of the long-face syndrome (adenoids
facies) associated with mouth breathing [47]
(1) Excessive anterior facial height
(2) Steep mandibular plane
(3) Narrow alar base
(4) Lip incompetence
(5) Tongue positioned downward and forward
(6) Long and narrow maxillary arch
(7) Anterior dental open bite
(8) Posterior dental crossbite
(9) Retroclined upper and lower incisors
(3) Growth evaluation
OSA can lead to failure to thrive. Failure to thrive refers
to infants and children whose growth deviates from the
norms for their age and gender on the CDC growth charts
(Figures 3 and 4). Growth failure is shown mainly by
decreased weight or rate of weight gain, but in more
severe cases, height and head circumference may be
affected and should be charted as well. Any child who
drops below the 5th percentile on multiple occasions or
two major percentile lines on a growth chart is thought to
exhibit failure to thrive.[48,49]
The hypothesized etiology for failure to thrive with
OSA is increased work of breathing, with subsequent
increase in baseline caloric expenditure. Decreased
production of growth hormone during fragmented sleep
may contribute further to poor growth.[18]
(4) Tongue and pharyngeal size
To evaluate the tongue and pharyngeal size, the
Mallampati classification can be used. The Mallampati
classification was developed in 1985 to determine the
degree ofratio
difficulty of direct laryngoscopy by the ability to visualize the
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CRANIO: The Journal of Craniomandibular & Sleep Practice 5

Figure 1. Body mass index-for-age percentiles for boys.

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6 AI Masoud et al.

Figure 2. Body mass index-for-age percentiles for girls.

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CRANIO: The Journal of Craniomandibular & Sleep Practice 7

Figure 3. Height-for-age and weight-for-age percentiles for boys.

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8 AI Masoud et al.

Figure 4. Stature-for-age and weight-for-age percentiles for girls.

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CRANIO: The Journal of Craniomandibular & Sleep Practice 9
Figure 5. Mallampati classification for tongue and pharyngeal size. Adapted from Juang et al. [51] with permission.
faucial pillars, the soft palate, and the base of the uvula.
It relates the size of the tongue to the pharyngeal size.
The patient should be sitting and the tongue should be
protruded to the maximum when using the Mallampati
classification.[50]
Grading the tongue and pharyngeal size according to
this classification is shown in Figure 5 and is as follows [51]:
Class I: Soft palate, fauces, pillars, and uvula are visible.
Class II: Soft palate, fauces, and uvula are visible.
Class III: Soft palate and base of uvula are visible.
Class IV: Soft palate is not visible at all.
• For every 1-point increase in the Mallampati score, the
odds of having OSA increased more than two-fold.
[52]
(5) Palatine tonsils
Palatine tonsils are what are usually referred to as tonsils.
If enlarged, they can affect the airway. To evaluate the
pal- atine tonsils, a standardized tonsillar hypertrophy
grading scale (Figure 6) can be used:
(0) Tonsils are entirely within the tonsillar fossa.
(1+) Tonsils occupy less than 25% of the lateral
dimension of the oropharynx as measured between the
anterior tonsillar pillars.
(2+) Tonsils occupy less than 50% of the lateral
dimension of the oropharynx.
(3+) Tonsils occupy less than 75% of the lateral
dimension of the oropharynx.
(4+) Tonsils occupy 75% or more of the lateral
dimension of the oropharynx.[18]
(6) Enlarged adenoids
The adenoids, which are also referred to as the pharyngeal
tonsils, are important to assess in order to rule out enlarged
adenoids as a potential cause for sleep apnea. Adenoids
get enlarged because they trap germs that enter the body,
and they can swell as they try to fight off an infection.[53]
This swelling can interfere with breathing and delay growth,
and studies have shown that growth velocity is restored
after adenotonsillectomy.[54] The standardized height and
weight, insulin-like growth factor 1 (IGF-1), and insulin-like
growth factor binding protein 3 (IGFBP-3) were also shown
to increase significantly after adenotonsillectomy.[55]
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10 AI Masoud et al.
Figure 6. Standardized palatine tonsillar hypertrophy grading scale. Adapted from Chan et al. [18] with permission.
Symptoms associated with enlarged adenoids
include [56]:
• Bad breath
• Difficulty breathing through the nose
• Breathing through the mouth (dry mouth and cracked
lips)
• Breathing noisily
• Talking as if the nostrils are pinched (persistent runny
nose or nasal congestion)
• Snoring
• Sleep apnea
• Ear infections or middle ear fluid that might make
ear tube surgery necessary
Examination for enlarged adenoids [53]:
• Examination of ears, nose, and throat
• Feeling the neck near the jaw for lymph nodes
• Radiographic examination
The American Academy of Otolaryngology lists the
following as indications for tonsillectomy and
adenoidectomy : recurrent throat infections, recurrent
suppurative chronic otitis media with effusion,
unresponsive peri-tonsillar abscess, presumed unilateral tonsil hypertrophy
neoplastic, unresponsive chronic sinusitis, hypertrophy
causing severe dysphagia, hypertrophy causing dental
malocclusion or adversely affecting orofacial growth, and
SDB.[57, 58]
The maximum size of the adenoids and tonsils is
reached at about 5 years of age, after which they began
to shrink.[53, 59] It is worth mentioning that the Scammon's
curve shows lymphoid tissues to start decreasing in size
after reaching their maximum size at about the age of 12.
However, the Scammon's curve did not include tonsils
and adenoids. It was based on the lymphoid tissues of the
appendix, spleen, thymus, and intestine.[59]
4.3 Investigation
(1) Sleep studies [60]
Sleep studies can either be done in a laboratory setting
using in-laboratory polysomnography (PSG) or at home
using portable monitors (PMs). A PSG is the current gold
standard for evaluating SDB. The bedroom where the
PSG takes place is typically more like a comfortable hotel
room rather than a hospital room. A PSG generates
several records of activity during several hours of sleep,
usually six to eight, and these records can include:
(1) EEG measuring brain waves
(2) EOG measuring eye movement
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CRANIO: The Journal of Craniomandibular & Sleep Practice 11
Table 1. AHI (or RDI) cut off points for sleep apnea in adults and
children.
Normal Mild OSA Moderate OSA Severe OSA
Adults Less than 5 5–14 15–30 >30
Children Less than 1 1–4 5–10 >10
(3) Electrocardiogram (ECG) measuring heart rate and
rhythm
(4) Chin EMG
(5) Anterior tibialis EMG activity to identify leg
movement
(6) Respiratory effort and rate using chest and
abdominal bands
(7) Oral and nasal airflow
(8) Additional monitors that sense oxygen and carbon
dioxide levels in the blood
Some of the drawbacks of PSG include: high cost, time
consuming, technically complex, and scarcity of sleep
laboratories specializing in children.[36,61] Records
obtained from PMs depend on the sophistication of the
device and can range from logging nighttime movement or
blood oxygen levels to records that are identical to a PSG.
The American Academy of Sleep Medicine (AASM)
recommends that, at minimum, PMs should record airflow,
respiratory effort, and blood oxygenation.[61] It is debatable
whether or not home sleep studies in the patient's normal
environment are more representative of the true disease
compared to sleep studies done in a controlled laboratory
environment.[62]
Apnea-hypopnea index (AHI)
The most crucial data generated from a sleep study is the
apnea-hypopnea index (AHI). An apnea is a cessation of
nasal and oral airflow. In general, it is scored when there is
at least 90% reduction in airflow compared to the pre-
event baseline for 10 s in adults, or two breaths in children.
In hypopneas, as opposed to apneas, airflow is evident but
reduced. A hypopnea is an event with at least a 30% drop
in a pre-event baseline associated with either at least 3%
oxygen desaturation or an arousal.[63]
Respiratory disturbance index (RDI)
Sometimes also referred to as the respiratory distress
index, the respiratory disturbance index (RDI) is used less
frequently than the AHI. It includes the total number of
apneas, hypopneas, and RERAs per hour of sleep. A
RERA is an event that does not meet apnea or hypopnea
criteria but leads to an arousal. [63,64] Another definition
for the RDI is the number of apneas and hypopneas per
hour of recording time. This definition is used with limited sleep
studies that do not include an EEG such as when using a
PM at home.[65]
Sleep apnea can be mild, moderate or severe. Table 1
shows the AHI (or RDI) cut off points for sleep apnea
severity in adults [60,66] and children. [67]
(2) Lateral cephalometric radiographs
Lateral cephalometric radiographs are taken routinely in
orthodontic practice. Normally, only limited and subjective
evaluations are done of the airway.[3] However, on a lateral
cephalometric radiograph, the following regions can be
evaluated objectively (Figure 7). Limited norms for these
regions of non-OSA adult patients are available, and even
less so for children:
to. Hyoid bone: The hyoid bone is connected to the
tongue, the pharynx, the mandible, and the cra-nium
through muscles and ligaments, and is part of the
oropharyngeal complex. It is the only bone in the
body that has no bony joints. It main-tains the
airway, helps in swallowing, and prevents regurgitation.
[68] The distance of the hyoid to the mandibular
plane (HMP) and the measurements obtained from
the hyoid triangle are among the ways to assess the
hyoid bone position.
Yo. HMP: The perpendicular distance between
the hyoid bone and the mandibular plane
(gnathion (Gn) through gonion (Go)). Adult
norms were around 23.5 mm for males and
18.5 mm for females. Patients with severe
OSA have an increased HMP, and HMP has
been positively correlated with the RDI in
adults and children. One thing to consider is
that the mandibular plane angle may affect
the results obtained.[69–71]
ii. Hyoid triangle: A triangle constructed by
joining three points:
• Retrognathion (RGn): Most inferior posterior point
on the mandibular symphysis
• Hyoidale (H): Most superior anterior point on the body
of the hyoid bone
• C3: Most inferior anterior point on the 3rd cervical
vertebrae
The vertical position of the hyoid bone (HHÿ) is
determined by dropping a perpendicular from hyoidale to
the plane C3-RGn. An Increase in HHÿ and a decrease in
C3-H (airway depth) correlate with a narrower airway.
Table 2 shows standard hyoid triangle measurements in
children reported by Bibby and Preston in 1981.[72]
b. Posterior airway space (PAS): The PAS, also
referred to as the retrolingual space, is the
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12 AI Masoud et al.

Figure 7. Lateral cephalometric radiograph airway analysis. A: the distance between the outermost point of convexity of the adenoid
shadow and the sphenobasioocciput. N: the distance between the sphenobasiocciput and the posterior end of the hard palate. PNS:
posterior nasal spine. Q: tip of the soft palate. RPA: retropalatal airway space. PAS: posterior airway space. UAL: upper airway length.
HMP: hyoid to mandibular plane. C3: most inferior anterior point on the 3rd cervical vertebrae. H: most superior anterior point on the
body of the hyoid bone. RGn: most inferior posterior point on mandibular symphysis. H': determined by dropping a perpendicular from
H to the plane C3-RGn. Go: gonion. Gn: Gnathion. Eb: base of the epiglottis. TT: tip of the tongue. B: point B. S: seal. Ba: basion. SO:
mid-point of distance sella-basion. ad1 : intersection of line PNS-Ba and the posterior pharyngeal wall. ad2 : intersection of line PNS-
SO and the posterior pharyngeal wall.

Table 2. Standard hyoid triangle measurements in children. tongue and the posterior pharyngeal wall is the
Distance Mean (mm) S.D.
PAS.[69]
C3-RGn 67.2 6.6 After ruling out OSA using a questionnaire, Lee et al.
C3-H 31.76 2.9 found that the normal PAS in adults was about 15 mm in
H-RGn 36.83 5.83
H H' 4.8 4.64
males and 12.5 mm in females.[69] Will et al. measured
PAS in adult patients with OSA and found it to be 9–9.5
mm.[70] Pirilä-Parkkinen et al. ruled out SDB in children
narrowest PAS at the level of the tongue base.[73] between 4 and 12 years of age using a question-naire
The PAS can be evaluated with a line drawn from and found a PAS of 12 mm.[74]
point B through Go. This line intersects the base
c. Retropalatal airway space (RPA): The RPA is the
of the tongue and the posterior pharyngeal wall.
The linear measurement between the base of the narrowest PAS at the level of the soft palate.[73] TO
Machine Translated by Google
CRANIO: The Journal of Craniomandibular & Sleep Practice 13
predictive RPA cut off value for OSA adult patients
is between 10 and 11 mm.[75,76]
d. Upper airway length (UAL): The UAL is the dis-
tance in millimeters, parallel to the long axis of the
airway, between a horizontal plane tangent to the
superior aspect of the hyoid bone and a horizontal
plane tangent to the posterior palate. Upper airway
length represents the longest length in the mid-
sagittal plane. The UAL is directly proportional to
airway resistance; the longer the airway length, the
more airway resistance there is. Susarla et al.
suggested that above 72 mm for males and 62 mm
for females was the best threshold as a diagnostic
test for OSA.[77]
and. Uvula length (PNS – P): The uvula length is
measured from the posterior nasal spine (PNS) to
the tip of the soft palate (P). It is also referred to as
the length of the soft palate. Authors report the
stand-ard PNS-P in normal adult patients to be about
35 mm.[69,76] Other researchers measured the
uvula length in OSA adult patients and found it to be
around 45 mm.[70,78] Pirilä- Parkkinen et al.
reported a uvula length of approximately 28 mm in
normal children.[74]
F. Uvula thickness (UT): The UT is the thickest part
of the uvula. Muto et al. found the uvula thickness to
be 9.7 mm in adult females with normal mandibles
(no retrognathism or prognathism).[69,76]
Pirilä-Parkkinen et al. found the uvula thickness to
be roughly 8 mm in normal children. A hyperplastic
appearance of the uvula may be a result of vibration
or inflammation when snoring. On the other hand, it
might also be an anatomical feature that predisposes
patients to SDB.[74]
g. Adenoids: Linder-Aronson found a high level of
correlation between the results of subsequent rhi-
noscopy and radiographic cephalometric
measurements in the assessment of adenoid size.[79]
Linder-Aronson and Leighton used PNS-ad1
and PNS-ad2 to measure the nasopharyngeal air-
way (Figure 7).[59] Standard measurements for PNS-
ad1 and PNS-ad2 in normal children were about 21
mm and 16 mm respectively.[74]
The adenoid – nasopharynx ratio (A/N ratio) can be
used to assess the size of the adenoids. A is the distance
between the outermost point of convexity of the adenoid
shadow and the sphenobasioocciput. N is the distance
between the sphenobasiocciput and PNS. The A/N ratio
upper airway.[87,88] These factors, in addition to extreme
correlated well with nasal endoscopic examination
individual variability and other obstacles such as head
findings. When the mean choanal obstruction ratio was
posture, the stage of respiration and swallowing, tongue
88.5, the mean A/N ratio was found to be 0.87.[80]
position, and the mandibular position, have hindered the
However, some have proposed that adenoid measurements based
development of CBCT airway volume norms.[84,89]
on the size of the airway tended to have more specificity
compared to measurements based on the adenoid size.[81]
The McNamara line, similar to PNS-ad1 and PNS-ad2 , es
a measurement based on the size of the airway and is the
minimum distance from the adenoid to the soft palate.
When this distance was 5 mm or less, this was an indicator
of possible airway impairment.[82]
h. Tongue: The tongue is an important structure to
evaluate because it can drop and block the airway.
Common tongue measurements used include the
tongue length and the tongue height. The tongue
length is measured from the tongue tip (TT) to the
base of the epiglottis (Eb). The tongue height is the
maximum tongue height along a perpendicular line
from TT-Eb to the dorsum of the tongue.[46]
(3) Cone beam computed tomography (CBCT)
Although lateral cephalometric radiographs can be used
to assess the airway, they remain a two-dimensional
representation of the three-dimensional anatomy. Other
limitations include differential magnification and over-
lapping of structures, which can make landmark
identification challenging.[83] Meanwhile, the airway can
be viewed three-dimensionally using magnetic resonance
imaging (MRI), medical computed tomography (CT), and
cone beam computed tomography (CBCT). CBCT
differentiates between soft tissue structures and empty
spaces such as the airway with high resolution and pro-
duces airway volume measurements that are nearly 1–1
of the real volume.[84,85] That, in addition to the other
advantages CBCT has over medical CT and MRI such as
lower radiation, lower costs, easier access, and shorter
acquisition times has made CBCT the method of choice
for upper airway analysis.[9,84,86,87] Semi-automated
computer programs can calculate the airway length ,
small -est cross-sectional area, largest cross-sectional
area, total volume, and other desired measurements (Figure 8).[4]
Three-dimensional imaging of the airway can also provide
information about the exact location and nature of airway
obstruction in OSA patients, which is important to obtain
an effective treatment plan even in the presence of a PSG.
[9]
When CBCT is used to analyze the upper airway, the
analysis is influenced by several factors. In addition to
image quality, three-dimensional upper airway analysis
depends on segmentation accuracy (manual or semi-
automatic), image thresholding (fixed, interactive, or
variable), and the selected anatomical boundaries of the
Machine Translated by Google
14 AI Masoud et al.
Figure 8. Cone beam computed tomography airway analysis
showing total airway volume and minimal cross-sectional area.
One of the key papers published on CBCT airway volume
norms was by Schendel et al. in 2012. Although the
factors listed above were not all explicitly listed or
controlled, they established normative data for airway
size and shape using a sample size of 1300 individuals
with age groups from 6 to 60 years. Additionally, they
showed that the airway size and length increased from
age 6 to 20, remained relatively stable until age 50, and
then decreased dramatically after 50.[4] It is important to
note that Schendel et al. did not include the nasopharynx in theReferences
The nasopharynx becomes critical in children since ade-
noidectomy/tonsillectomy is the first line of treatment in
children with OSA.[23]
As opposed to the airway volume, the airway minimal
cross-sectional area (MCSA) has been shown to be
mean- ingful. Li et al. found that, although weakly
correlated, the retroglossal and retropalatal CSAs in CT
scans were predictive of RDI in adults.[90] Avrahami and
Englender looked to associate the MCSA in CT scans
with OSA in adults. They found that subjects with severe
OSA had an MCSA of less than 50 mm2
. Subjects with moderate OSA
had an MCSA between 60 mm2 and 100 mm2, and control
subjects had an MCSA over 110 mm2 .[91] Ogawa et al.
used CBCT in adults and found relatively similar MCSA
numbers for OSA subjects.[92]
5. Conclusion
The authors presented a review of SDB and an outline for
diagnosis. Before treatment planning in a patient
suspected of having SDB, the dentist should perform a
thorough history and examination, and a formal diagnostic
investigation should take place, if necessary. An
investigation could be done inconclusively using radio-
graphic airway analyzes or definitively by referring for a
sleep study. The majority of OSA research is conducted
in adults, and much more research is needed in the
pediatric population.
Contributors
Ahmed I. Masoud, Performed the literature review,
prepared references and citations, prepared figures and
tables, and wrote the paper. Gregory W. Jackson, Helped
prepare the abstract and provided references. David W.
Carley, Revised the paper, checked grammar and spelling,
and made sure all statements stated were in agreement
with what is believed in the field of sleep medicine.
Human and animal rights statement
This article does not contain any studies with human or
animal subjects performed by any of the authors.
Disclosure statement
No potential conflict of interest was reported by the authors.
ORCiD
Ahmed I. Masoud http://orcid.org/0000-0003-2854-1872
airway volume.
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