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REVIEW ARTICLE

Management of obstructive sleep apnea: A dental perspective

Ariga Padma, Ramakrishnan N^, Vinod Narayanan*

Departments of Prosthodontics,
*Oral and Maxillofacial
ABSTRACT
Surgery, Saveetha University, Sleep disordered breathing is a term which includes simple snoring, upper airway resistance
162 Poonamallee High Road,
Chennai - 600 077, syndrome, and obstructive sleep apnea (OSA). Simple snoring is a common complaint
^Consultant Sleep Medicine, affecting 45% of adults occasionally and 25% of adults habitually and is a sign of upper
NITHRA, 19, Periyar Road, T airway obstruction. Snoring has also been identified as a possible risk factor for hypertension,
Nagar, Chennai, India
ischemic heart disease, and stroke. The role of dentistry in sleep disorders is becoming more
significant, especially in co-managing patients with simple snoring and mild to moderate OSA.
The practicing dental professional has the opportunity to assist patients at a variety of levels,
starting with the recognition of a sleep-related disorder, referring patients to a physician for
evaluation, and assisting in the management of sleep disorders. Obesity is the main predisposing
factor for OSA. In nonobese patients, craniofacial anomalies like micrognathia and retrognathia
may also predispose to OSA. Diagnosis of OSA is made on the basis of the history and physical
examination and investigations such as polysomnography, limited channel testing, split-night
testing, and oximetry. Nocturnal attended polysomnography, which requires an overnight stay
in a sleep facility, is the standard diagnostic modality in determining if a patient has OSA. As far
as treatment is concerned, the less invasive procedures are to be preferred to the more invasive
options. The first and simplest option would be behavior modification, followed by insertion of
oral devices suited to the patient, especially in those with mild to moderate OSA. Continuous
positive airway pressure (CPAP) and surgical options are chosen for patients with moderate
to severe OSA. The American Academy of Sleep Medicine (AAOSM) has recommended oral
appliances for use in patients with primary snoring and mild to moderate OSA. It can also be
used in patients with a lesser degree of oxygen saturation, relatively less day time sleepiness,
lower frequency of apnea, those who are intolerant to CPAP, or those who refuse surgery. Oral
appliances improve the blood oxygen saturation levels as they relieve apnea in 20-75% of
Received : 31-12-06 patients. They reduce the apnea–hypopnea index (AHI) by 50% or to < 10 events per h. Oral
Review completed : 05-06-07 appliances also reduce the AHI to normal in 50-60% patients.
Accepted : 09-06-07
PubMed ID : 17938499 Key words: Dental implications, obstructive sleep apnea, oral appliances

Sleep disordered breathing (SDB) is a term which includes
simple snoring, upper airway resistance syndrome (UARS),
and sleep apnea. Patients present with various symptoms,
although almost all complain of snoring, witnessed
breathing pauses, and excessive day time sleepiness. Simple
snoring is a common complaint affecting 45% of adults
occasionally and 25% of adults habitually and is a sign of
upper airway obstruction.[1] Snoring has also been identified
as a possible risk factor for hypertension, ischaemic heart
disease, and stroke.[2]
The role of dentistry in sleep disorders is becoming more
significant, especially in co-managing patients with
simple snoring and mild to moderate obstructive sleep
apnea (OSA). The practicing dental professional has the
Correspondence:
Dr. Ariga Padma,
E-mail: padma-ariga@hotmail.com
201
opportunity to assist patients at a variety of levels, starting
with the recognition of a sleep-related disorder, referring
them to a physician for evaluation, and assisting in the
management of sleep disorders. Almost every discipline
in dentistry needs to be aware of sleep disorders and their
potential impact.
In normal weight adults, when there is an increased
inspiratory effort exerted during sleep, without the cessation
of airflow that leads to brain or electroencephalogam (EEG)
arousals, it is termed UARS. Patients are described as
‘arousing,’ when they shift from a deeper to a lighter stage of
sleep or have an actual awakening. The definitive diagnosis
of UARS is made when nocturnal esophageal pressure
monitoring demonstrates crescendo changes in intrathoracic
pressures followed by frequent arousals or microarousals.
Hypertension may be an important sequel of this disorder
as a result of the autonomic and cardiovascular changes
induced by the negative intrathoracic pressure.
Indian J Dent Res, 18(4), 2007
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Obstructive sleep apnea
Sleep apnea is probably the most prevalent of all the sleep
disorders and is classified as central, obstructive, or mixed;
it may be mild, moderate, or severe.[3] In central sleep apnea
(CSA) there is a diminution of oxygen entry into the lungs
due to the respiratory (chest) muscles failing to act as a result
of a central nervous system disorder. OSA, the most prevalent
of all the apneas, is a disturbance in normal sleep patterns
and when combined with excessive day time sleepiness
is termed obstructive sleep apnea syndrome (OSAS). It is
characterized by repeated increases in resistance to airflow
(blockage) within the upper airway, causing obstruction. As
a result there is blood oxygen (oxyhemoglobin) desaturation
and carbon dioxide accumulation and, in long standing
cases of the syndrome, headache, systemic hypertension,[4]
dysrhythmias, depression,[5] stroke,[6] and angina.[7] A patient
with a combination of CSA and OSA is said to have mixed
sleep apnea. Sleep apnea syndrome differs fundamentally
from other common dental diseases, in that it can result in
life threatening cardiac or pulmonary diseases.[8]
EPIDEMIOLOGY
It has been reported that 10% of men and 5% of women in the
30-40 year age-group are habitual snorers; prevalence of
snoring increases with age, reaching at least 20% for men
and 15% for women in the 50-60 year age-group. Day time
sleepiness is reported by at least 5% of men and 8% of
women in the general population. The prevalence of OSAS
is around 4% for men and 2% for women in the age-group
of 30-60 years.[9]
ETIOLOGY
The upper airway is basically a soft tissue tube, the patency
of which is maintained, in part, by muscular groups,
including the tensor veli and genioglossus. Snoring is often
the result of the base of the tongue obstructing the upper
airway. The upper airway consists of the nasopharynx,
oropharynx, and the hypopharynx. The oropharynx includes
the tongue, teeth, maxilla, mandible, the hard and soft
palate, uvula, tonsils, and the hyoid bone, which is involved
in the muscular action of the oral cavity. When a patient
falls asleep in the supine position, the muscle relaxation
causes the base of the tongue to approach the posterior wall
of the pharynx. With the consequent reduced air flow, the
patient the patient must increase the speed of the airflow
to maintain the required oxygen supply to the lungs. This
increase in airflow velocity causes vibration of soft tissues,
which produces snoring.
It is suggested that collapse of the lateral pharyngeal walls
is also a cause for airway obstruction in patients with
OSA. The lateral pharyngeal wall consists of muscles
(hyoglossus, styloglossus, palatoglossus, palatopharyngeus,
and pharyngeal constrictors), tonsillar tissues, and fat pads.
Indian J Dent Res, 18(4), 2007
Padma, et al.
It has been shown that the total volume of fat is greater
in patients with OSA. An increase in the thickness of the
lateral pharyngeal wall predisposes to the development of
OSA.[10]
OSA is characterized by a partial or complete obstructive
collapse of the upper airway during non-REM or REM
sleep. As a result of these respiratory events, which deplete
certain stages of non-REM and REM sleep, patients have
an agitated sleep and present abnormal breathing patterns
during sleep.
Predisposing factors
Obesity is the main predisposing factor for OSA.[11] In
nonobese patients, craniofacial anomalies like micrognathia
and retrognathia[12,13] may also predispose to OSA. Other
orofacial features that may predispose to OSA, include
enlarged palatine tonsils, enlarged uvula, high-arched
palate, nasal septal deviation, longer anterior facial height,[14]
steeper and shorter anterior cranial base,[15] inferiorly
displaced hyoid bone,[16] disproportionately large tongue, a
long soft palate,[17] and decreased posterior airway space.[18]
In addition to obesity, age,[19] ethnic background,[20] genetic,
and gender predilection,[21] habits like consumption of
alcohol,[22] smoking,[23] and sedatives may aggravate existing
OSA. Alcohol relaxes the airway muscles, making it more
prone to obstruction. Obese patients with an increased neck
circumference (collar size greater than 16-17 inches) or those
with a high body mass index (BMI > 25) who sleep in the
supine position are potential candidates for OSAS.[24] When
supine obese patients present with restricted chest bellows
disease, the diaphragm is displaced to a higher and flatter
position, decreasing the inspiratory strength of the diaphragm.
This results in a mechanical reduction in lung capacity (as
in REM sleep) where muscles adjacent to the airway are
most hypotonic, resulting in blood oxygen desaturation. To
maintain a normal tidal volume the accessory respiratory and
abdominal muscles also need to act.
Anatomically, a block could occur as a result of excess
fat or inflamed tissues in the upper airway. The presence
of tumors could also lead to a pathological blockage, and
environmental factors like allergies and infections can
influence the response of the airway dilators and hence the
size of the airway.[25]
CLINICAL FEATURES
Patients with OSAS may have memory problems, excessive
day time sleepiness, difficulty in concentrating,[26] night
drooling of saliva, depression,[27] irritability, xerostomia,
gasping for breath at night, and witnessed apneas. Poor
work performance, occupational accidents and a reduction
in social interactions and other aspects of quality of life[28]
appear to be associated with untreated OSA. There have
been reports of exacerbations of epilepsy,[29] asthma,[30] and
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Obstructive sleep apnea
hypertension[4] in patients with untreated or undiagnosed
OSA. Motor vehicle accidents in untreated OSAS patients
is reported to be two or three times higher than in matched
control drivers.[31]
DIAGNOSIS
Diagnosis of OSA can be made on history, examination,
polysomnography, limited channel testing, split-night
testing, and oximetry. Nocturnal attended polysomnography,
which requires an overnight stay in a sleep facility is
the standard diagnostic modality in determining if a
patient has OSA. This study records sleep staging like
electroencephalography (EEG), electrooculography (EOG),
electromyography (EMG), and physiological variables like
sleep positioning, respiratory activity, oxygen saturations,
blood pressure, and ECG. Unattended polysomnographic
tests, which are done with four to six channel sleep study,
include measuring the nasal airflow using the snoring
microphone, thoracic and abdominal effort channels, ECG,
EOG, and pulse oximetry.
Split-night polysomnography refers to a single night of
attended sleep testing; in addition to aiding in diagnosis, it
has a therapeutic component, namely the nasal continuous
positive airway pressure (CPAP) titration, which helps
in assessment of a positive airway pressure, also serves to
maintain the patency of the patient’s airway on the night of
the test. Split-night testing has also been used to demonstrate
the changes in sleep disordered breathing caused by an
adjustable airway dialator at different positions of mandibular
advancement.[32]
Portable sleep studies (polysomnography and continuous
positive airway titration) are helpful for postoperative
patients who cannot come to the sleep centre after surgery.
Oximetry testing alone is quite portable, cost-effective, and
a useful diagnostic tool to evaluate response to treatment
after surgery or airway dilator placement in patients with
known OSA.
Apnea is defined as the cessation of airflow—a complete
obstruction for at least 10 sec—with a concomitant 2 to 4%
drop in arterial oxygen saturation. Hypopnea is a reduction
in airflow of at least 30 to 50% with a drop in oxygen
saturation. The apnea-hypopnea index (AHI) is the average
number of apneas and hypopneas per hour of sleep.
The severity of OSA is classified on the basis of the patient’s
AHI index into three categories:[33]
1. Mild OSA (5 to 15 events per h),
2. Moderate OSA (15 to 30 events per h)
3. Severe OSA (more than 30 events per h)
Patients with mild to moderate OSA are candidates for
placement of appropriate oral devices.
203
Padma, et al.
Pretreatment medical assessment
Prior to fabrication of oral devices, details pertaining to the
patient’s name, age, gender, change in weight, allergies, nasal
congestion, neck size, alcohol consumption, frequency of
smoking, sedatives, and sleep position should be noted; it
is also necessary to find out whether the patient awakens
gasping for air or stops breathing during sleep and whether
he/she feels refreshed after sleep, or tired and sleepy during
work / meetings. Epworth sleepiness scale is a validated
questionnaire which indicates a patient’s level of day
time sleepiness.[34] Scores range from 0 to 3, and measure
the likelihood of the patient dozing off while watching
television, driving, or reading: 0 = would never doze, 1
= slight chance of dozing, 2 = moderate chance of dozing,
and 3 = high chance of dozing. The blood pressure, blood
sugar, and body mass index (BMI) are also recorded prior
to treatment.
Airway evaluation
The condition of the tongue and its size and relation to
the oral cavity in a relaxed state should be observed. The
tonsil size should be graded on an universally recognized
standard (Grades1-4).[35] The Mallampati score[36] (Grades
1-4) can be used as a predictor for determining the severity
of sleep apnea, particularly in cases where an enlarged
tongue may seem to be the cause for airway obstruction.
The nasal turbinates[37] are also evaluated as they may
be a cause for airway obstruction and mouth breathing.
It has been demonstrated that an increase in BMI along
with increased tonsillar size and higher Mallampati score
indicates a greater potential for OSAS.[36] The assessment of
the effect of mandibular repositioning, both vertically and
horizontally, on the airway can be done using a wax bite
or a device called the George Gauge.[38] Another technique
termed acoustic reflexion[39] evaluates the site of airway
restriction and the effect mandibular repositioning may
have on the size of the airway.
Pretreatment dental assessment
This includes dental history and an oral examination
focusing on occlusion, periodontal status, tooth mobility,
parafunctional habits, wear facets (generalized / isolated),
DMFT, charting, recording of the sensitivity of teeth, tori,
and the amount of overbite and overjet present. The dental,
skeletal midlines, and temperomandibular joint (TMJ) status
have to be recorded prior to treatment planning.
Imaging
The ideal upper airway imaging modality for patients
with OSA should be noninvasive, inexpensive, permit
supine imaging, allow for three-dimensional volumetric
reconstructions of the upper airway and the surrounding
tissues, and not expose the patient to ionizing radiation.
A number of imaging modalities like acoustic reflexion,
fluoroscopy, nasopharyngoscopy, cephalometry, MR
imaging, and both conventional and electron-beam CT
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Obstructive sleep apnea
scanning have been used to assess the airway. MR imaging
is probably the best, if not an ideal, imaging modality. At the
very least, a patient should have radiographs of the teeth and
surrounding tissues to rule out any pathology. A panoramic
radiograph is useful because of its ability to display a
wide variety of structures in a single view with minimum
irradiation. When specific problems like TMJ dysfunction
are present and an oral appliance is being planned, specific
imaging of the TMJ should be done. Cephalometrics could
be used if the practitioner wishes to evaluate the airway
dimension, evaluate cranial or skeleted structures, or plan
for orthognathic surgery; for example, SNA and SNB angles
and posterior airway space are decreased and PNS-P (length
of soft palate) are increased in OSAS.
TREATMENT OPTIONS
The sleep medicine team defines possible treatment options
for adult patients with OSA, based on the severity of the
sleep disorder, preference of the patient, the patient’s
general health, and the preference and experience of the
team members. Less invasive treatment options are selected
wherever possible. The first and simplest option is behavior
modification; this would be followed by insertion of oral
devices suited to the patient, especially in those with mild
to moderate OSA. CPAP and surgical options are chosen for
patients with moderate to severe OSA.
Behavior modification
Behavior modification suggestions include changing the
sleep position from the supine position to the side position;
this can be accomplished by placing a tennis ball in the
centre of the back of their pajamas or by positioning a
pillow such that they cannot roll on to their back (positional
training). The avoidance of alcohol and sedatives for 3 h
before sleep has been recommended, because they have a
depressing effect on the central nervous system; they may
also act as muscle relaxants, reducing airway patency. In
obese patients, weight loss should be recommended; when
the BMI becomes 10% more than ideal, the loss in airway
space becomes significant.[40]
Oral appliances
Oral appliances were used by Robin[41] to treat glossoptosis in
infants with micrognathia as early as 1905. There is sporadic
mention of dental devices for prevention of snoring in patent
records before 1980. In 1990, adjustable mandible-advancing
oral appliances became the predominant form of dental therapy
for SDB, signaling the entry of dentistry into mainstream sleep
medicine. In 1991, The American Academy of Sleep Dentistry
was formed for the education and certification of dental sleep-
disorders specialists. In 1995, controlled studies indicated
similar effectiveness of, and greater patient preference for,
oral appliances compared with CPAP in mild to moderate
OSA. In 2000, a section on oral appliances was created in the
Academy of Sleep Medicine.[42]
Indian J Dent Res, 18(4), 2007
Padma, et al.
Oral devices are basically thermoplastic materials with
retainers and supports and are usually custom made.
a. Mandibular repositioning or advancement devices (MRD/
MAD) [Figure 1] which may be titratable, e.g., Herbst
appliance[43]/ snoreguard[44]/ silencer.[45] They function
by engaging one or both of the dental arches to modify
mandibular protrusion; they require dental impressions,
a centric relation record, and protrusive record.
b. Tongue repositioning or retaining devices (TRD), e.g.,
SnorEx.[46]
c. Soft-palate lifters.[26]
d. Tongue trainers.[26]
e. A combination of oral appliance and CPAP in the new
products deliver pressurized air directly into the oral
cavity and eliminates the use of head gear or nasal
mask and avoids the problems of air leaks and the
claustrophobia associated with CPAP treatment.[47]
The American Academy of Sleep Medicine (AAOSM) has
recommended oral appliances for use in patients with primary
snoring and mild to moderate OSA. It can also be used in
patients with a lesser degree of oxygen saturation, relatively
less day time sleepiness, lower frequency of apnea, those who
are intolerant of CPAP, or those who refuse surgery.[48]
Patient evaluation
Patient evaluation prior to treatment requires a skilled
multidisciplinary team. The Association of American Sleep
Disorders has published guidelines about the appropriate use
of oral appliance therapy and defines the respective roles
of the physician and the dentist in this type of care.[48] The
initial patient assessment, differential diagnosis of sleep
complaints, and overnight diagnostic monitoring by the
sleep specialist determine the indications for treatment.
This physician determines the patient’s suitability for an
oral appliance. The dentist can also identify a patient with
symptoms of snoring and OSA and refer him/her for medical
and sleep evaluation.
RATIONALE OF ORAL APPLIANCES AND HOW
THEY WORK
Oral appliances are worn only during sleep and work to
Figure 1: Mandibular advancement device
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Obstructive sleep apnea Padma, et al.

enlarge the airway by moving the tongue (anteriorly) or the
mandible to enlarge the airway. Whether they change the
airway shape or increase the cross-sectional area of the upper
airway is not clear. It is hypothesized that these appliances
may also affect upper airway muscle tone and thus decrease
their collapsibility. Movement of the tongue or mandible
anteriorly can increase the cross-sectional size of the airway[49]
and hence oral appliances help in increasing the airway
size.[50] Activation of the upper airway dilator muscles by the
appliance could cause a decrease in airway collapsibility and
this may contribute to preservation of airway patency during
sleep,[51] although the increase in airway size may be the most
important factor preventing airway occlusion.
A tongue-retaining device is a custom-made soft acrylic
appliance that covers the upper and lower teeth and has
an anterior plastic bulb. It uses negative suction pressure
to hold the tongue in a forward position inside the bulb.
By holding the tongue in a forward direction through its
attachment to the genial tubercle, it stabilizes the mandible
and hyoid bone, thus preventing retrolapse of the tongue.
These devices, reverse pharyngeal obstruction both at the
level of the oropharynx and the hypopharynx, thereby
enlarging the airway and reducing snoring and the related
apnea.[52] Soft palate trainers and tongue posture trainers
are rarely used.[26]
posttreatment nocturnal polysomnography to evaluate
individual oral appliances.[54]
Oral appliances improve the blood oxygen saturation levels
as they relieve apnea in 20-75% of patients. They reduce
AHI to < 10 events per h or bring about 50% reduction in
AHI. Oral appliances also reduce the AHI to normal in 50-
60% of patients. Lateral cephalometric radiographs [Figures
2 and 3] which show the measurements of the neck and
pharynx could be used to predict posttreatment AHI with
good accuracy.[55]
In the near future, three-dimensional CT or MRI imaging
reconstruction could be used to predict changes in airway
size and tongue position with individual oral appliances,
which would closely correlate to treatment response
measured by nocturnal polysomnography.
Mechanical variables that influence treatment efficacy and
which may be adjusted in individual appliances, include jaw
protrusion distance and angle of mouth opening. Efficacy
may also affected by head[56] and body posture[57] during
sleep. Most authors suggest that for adjustable MRDs, 50 to

Factors which predict the response of the sleep disorder

to oral appliances include the age of the patient, marital
situation, abstinence from stimulants such as caffeine and
alcohol, change in weight over 12 months or weight loss,
lowering of BMI < 25, percent obesity, initial severity of the
AHI scores (5-15), supine sleeping position, and the patient’s
tolerance and motivation. Positionality and percent obesity
account for 83% of the response to treatment.[53]

Efficacy
Designs of oral appliances vary and it is advisable to evaluate
the patient before and after insertion of the appliance. Figure 2: Pretreatment cephalogram—mandibular advancement
device
The treatment goal should be a decrease of about 50%
of the initial AHI or to less than 10 events per hour.
Table 1 summarizes a number of studies using pre- and

Table 1: Literature review on evaluation of oral appliances

using pre- and post treatment nocturnal polysomnography
Author Device type, Criteria Success
No. of patients for success rate %
Cartwright, 1991 TRD, 15 AHI ≤ 20 and 57
≥ 50% decrease
in AHI
Eveloff, 1994 MRD, 15 AHI< 10 53
Ferguson, 1996 MRD, 27 AHI < 10 48
Menn, 1996 MRD, 23 AHI ≤ 20 and 69
≥ 50% decrease
in AHI
Schonhofer, 1997 TRD, 23 N/A 26
TRD - Tongue repositioning or retaining devices, MRD - Mandibular Figure 3: Posttreatment cephalogram—mandibular advancement
repositioning devices, AHI - Apnea–hypopnea index device

205 Indian J Dent Res, 18(4), 2007

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Obstructive sleep apnea
75% maximal jaw protrusion maximizes efficacy without
causing obvious TMJ problems.[58] It has also been suggested
that maximal jaw protrusion may increase the AHI.[59]
Evaluation of blood pressure of patients before and after
treatment with oral appliances could also indicate their
efficacy. It is reported that effective oral appliance therapy for
OSAS patients with hypertension can lead to a significant fall
of about 3.4 mm in mean arterial blood pressure, associated
with a reduction of AHI.[60] This translates into a reduction
in the risk of stroke by 20% if this fall in blood pressure
were maintained for two to three years.[61] The fall in blood
pressure with the use of oral appliances was observed to
be maximum in the early morning, which is the peak time
for risk of myocardial infarction[62] and stroke.[63] A drop in
the blood pressure at this time, it is suggested, will provide
further protection against these adverse cardiovascular events.
Subjective efficacy reported by patients using oral appliances
include reduction in snoring in 80-100%, elimination of
snoring in 16-65%,[51] and a decrease in day time sleepiness
as assessed by multiple sleep latency test (MSLT);[64] Patients
also report improved memory, mood, and concentration and
less difficulty in driving.
The main advantages of using oral appliances are that there is
good patient compliance and the appliances are noninvasive
and relatively inexpensive; they can also be easily carried
anywhere by the patient.
SIDE EFFECTS AND COMPLICATIONS
Dental malocclusion (21%), TMJ pain (15%), and TMJ
dislocation (<5%) are the side effects of MRDs. Other
side effects include excessive salivation, tongue dryness,
tooth pain, posterior open bite, and insomnia. The overall
incidence of side effects with MRDs is reported to be 25-
60%, though these side effects were often mild and resolved
with adjustment of the device.[58] Long-term changes in
the TMJ with MRD use have not been studied, although
joint degeneration is a theoretical concern.[65] Tongue
abrasion, oral mucosal dryness, excessive salivation, and
gagging are some of the reactions with a TRD.[46] The overall
incidence of side effects was 25-75% for the TRD, resulting
in noncompliance in patients. Complications with oral
appliances include limited degree of lateral freedom during
jaw movements. Recalls are necessary at a minimum at 2
weeks, 1 month, and thereafter every 6 months.[66] The
appliances are retained tightly by the remaining dentititon
and place almost orthodontic like forces on the teeth. They
may also become loose or can distort or break and hence
maintenance is mandatory.
Future studies
Newer oral appliances allow greater lateral jaw movement,
cover all of the dentition, and provide better retention.
Adjustable (titratable) appliances allow the clinician to
Indian J Dent Res, 18(4), 2007
Padma, et al.
titrate the amount of mandibular protrusion in order to
obtain an adequate treatment response. Patients report high
levels of compliance with oral appliance therapy, which
can be objectively confirmed with an intraoral compliance
monitor. Several studies are currently underway to study
the effects of adjustable oral appliances vs CPAP in the
treatment of OSA. One of these appliances (Klearway)
was effective in reducing the AHI to < 15 per h in 71% of
patients.[55] There should be continued exploration of the
problems in compliance and the long-term side effects
of these appliances to assist in predicting the treatment
response. Late recurrences of symptoms and snoring, in the
absence of weight gain or any other obvious cause, do occur
and require monitoring of therapy.
Sleep bruxism
The AASOM has classified sleep bruxism (SB) as a parasomnia
and defined it as an undesirable physical phenomenon that
occurs during sleep.
Bruxism has been defined as an oral parafunctional activity
that can occur when an individual is asleep or when awake.
SB is an involuntary oro-mandibular movement, with tooth
grinding or clenching, occurring during sleep, regardless of
cause. Bruxism has been classified as primary (idiopathic)
and secondary (iatrogenic) forms. Primary forms of bruxism
include day time clenching and sleep bruxism, in the absence
of a medical cause. Secondary forms of bruxism are associated
with either neurologic, psychiatric, or sleep disorders or
with the administration or withdrawal of drugs. SB occurs in
stage I and II of non-REM sleep, whereas apnoea/hypopneic
events occur mainly in REM sleep.[67] As a result there are
no abnormal respiratory events in SB patients, as indicated
by polysomnographic studies. Patients with SB may not
have OSAS. On the other hand, patients with OSAS may
have SB, which may occur as a result of sleep arousal or
fragmental sleep patterns. An epidemiological study in the
general population reported that OSA is more prevalent in
patients with tooth grinding than in patients without the
habit (1.4%).[68] Maxillary occlusal splints which are used to
manage bruxism can aggravate the AHI in patients with OSA.
Interestingly, there are also reports that when a mandibular
occlusal splint was used, the AHI did not differ from baseline
values.[69]
Continuous positive airway pressure
CPAP continues to be the ideal treatment for patients
with moderate to severe OSA.[70] It is highly effective in
approximately 62% of patients. CPAP is noninvasive and acts
by continuously pumping room air under pressure through
a sealed face- or nose mask into the upper airway and the
lungs. Its success lies in its ability to act as a pneumatic
splint to increase upper airway caliber. A study by Kuna et
al.[71] and Schwab et al.[72] showed that upper airway dilation
with CPAP is greater in the lateral dimension than in the
anterior-posterior dimension. This suggests that the lateral
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Obstructive sleep apnea
pharyngeal walls (retropalatal and retroglossal) are more
compliant than the tongue or soft palate. Although CPAP is
the treatment of choice in patients with moderate to severe
OSA, it has a poor patient compliance because of problems
with portability, cost, pump noise, dryness of the airway
passage, and nasal leaks with mask discomfort.[73] Out of 70%
of the patients attempting to use CPAP equipment, only 20%
use it throughout the night.[74]
Surgical options
It is estimated that 1.5% of patients with OSA have a space-
occupying lesion that can be directly attributed to their
sleep-related upper airway obstruction.[75] In such cases,
surgical extirpation is potentially corrective. In 98.5% of
adult patients with OSA, no such lesion is identifiable and
apnea results from abnormal anatomy of the upper airway
and its supporting structures. Nasal obstruction can result
from bony and cartilaginous anatomic abnormalities or
from soft tissue changes. The dimensions of the pharynx
are determined by: (1) soft tissues, such as the tonsils, that
directly abut the air column; (2) the underlying foundation
of muscles that compose the pharynx and whose orientation
directly affects the dimensions and configuration of the
pharyngeal lumen; and (3) the location of the insertions
and origins of these muscles in the craniofacial bones of
the patient. On the basis of diagnostic pharyngeal imaging
patterns of pharyngeal obstruction, narrowing or collapse
have been classified as Type 1, narrowing or collapse in
retropalatal region only as Type II, narrowing or collapse in
both retropalatal and retrolingual regions as Type III, and
narrowing or collapse in retrolingual region only.[76]
Upper airway surgical approaches for the treatment of OSAS
fall into three categories: (1) classic produces that directly
enlarge the upper airway, (2) specialized procedures that
enlarge the upper airway by modifying soft tissue elements
and/or the skeletal anatomy, and (3) tracheotomy for control
of OSA by means of bypassing the pharyngeal portion of the
upper airway. Most procedures tend to address either the
retropalatal or the retrolingual portion of the pharyngeal
airway. The procedures may be applied individually,
synchronously with other procedures, or sequentially with
other procedures, depending on the nature of the anatomic
problem at hand.
Procedures that modify only soft tissue elements include
the following operations:
(1) Uvulopalatopharyngoplasty (UPPP), a procedure that
enlarges the retropalatal airway through excision of the
tonsils if present, trims and reorients the posterior and
anterior tonsillar pillars, and excises the uvula and posterior
portion of the palate. Laser-assisted uvulopalatoplasty
(LAUP) is a procedure to enlarge the retropalatal airway, in
which the uvula and posterior margin of the soft palate are
ablated with carbon dioxide laser. Although theoretically
the tonsils can be ablated using this technology, LAUP,
207
Padma, et al.
as commonly reported, does not include tonsil ablation.
Unlike other procedures described in this section, LAUP
can be carried out under topical and local anesthesia in
an outpatient setting. Unvulopalatopharyngoglossoplasty
(UPPGP) is an operation that incorporates modified UPPP
with limited resection of the tongue base, enlarging both
retropalatal and retrolingual portions of the airway. (2)
Laser midline glossectomy (LMG) and lingualplasty are
two procedures that create an enlarged retrolingual airway
by laser extirpation of a 2.5 cm × 5 cm midline, rectangular
strip of the posterior half of the tongue. Laser lingual
tonsillectomy, reduction of the aryepiglottic folds, and
partial epiglottectomy are performed in selected patients.
Lingualplasty differs from LMG in that additional tongue
tissue is extirpated posteriorly and laterally to that portion
excised in LMG, and lingualplasty reportedly results in a
higher response rate. Other procedures involve skeletal
alteration, including mandibular advancement with
a bilateral sagittal split mandibular ramus osteotomy,
genioglossal advancement with hyoid myotomy and
suspension (GAHM), and maxillomandibular advancement
(MMA). These procedures enlarge the retrolingual portion,
or both retrolingual and retropalatal portions, of the upper
airway. The average response rate in postoperative patients
was a 50% decrease in the AHI.[77]
MMA surgically moves the maxilla and mandible anteriorly,
along with their muscular attachments. This increases the
tension in the muscles, particularly those which form part of
the lateral pharyngeal wall, and thus prevents its collapse. A
standard advancement of 10-15 mm is carried out by Le Fort 1
osteotomy of the maxilla and bilateral saggital split osteotomy
of the mandible. The success rates of MMA is 96%.[78,79]
OTHER DENTAL CONSIDERATIONS
The dentist may be the first to recognize a patient’s sleep
disorder by witnessing repeated apneic events in patients
undergoing intravenous sedation for dental treatment; this
may occur in patients with OSAS who are known to have
a compromised airway aggravated by airway obstruction
after administration of sedating drugs.[80]
Surgical extractions which may involve reflecting a
mucoperiosteal flap, may predispose the patient to developing
subcutaneous emphysema on using CPAP during the first
two postoperative nights.[81] Hence surgical procedures
involving reflecting mucoperiosteal flaps may best be
avoided in OSA patients using CPAP. Gastroesophageal
reflux (GER) associated with the enhanced diaphragmatic
excursions needed to fight a partial airway obstruction
during sleep can progressively scar the soft palate mucosa,
and inflamed scar tissue can further decrease the size of
the upper airway. These patients are at an increased risk of
experiencing aspiration and chemical pneumonitis. Patients
with OSA may have an impaired swallowing reflex which
Indian J Dent Res, 18(4), 2007
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Obstructive sleep apnea
may affect recording of the centric relation accurately.[82]
Medications used in weight loss therapy, e.g., sibutramine,
is associated with xerostomia and have sympathomimetic
properties likely to cause an increase in blood pressure or
heart rate.[83] Xerostomia is a potential side effect of several
medications such as antidepressants, antihypertensives,
and anticholinergics. These patients should be prescribed
artificial saliva to help in complete denture retention, should
have fluoride applications to avoid the incidence of caries,
and must maintain good oral hygiene. Patients should also
be advised to avoid cariogenic food and beverages. Smoke
is an airway irritant and results in mucosal edema, which
may contribute to an increase in the secretions obstructing
the upper airway.[23] Patients should, therefore, be cautioned
against the ill effects of smoking. Calcified carotid atheromas
appear more often on panoramic radiographs of patients
with sleep apnea.[84] Such patients may be referred for further
vascular evaluation. A small percentage of patients with
OSA have symptomatic hypothyroidism as a codiagnosis.[85]
Maxillary occlusal splints have been found to aggravate
respiratory disturbances and hence clinicians should
question patients about snoring and sleep apnea before
fabricating night guards / splints for TMJ disorders.[69]
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How to cite this article: Padma A, Ramakrishnan N, Narayanan V.
Management of obstructive sleep apnea: A dental perspective. Indian J Dent
Res 2007;18:201-9.
Source of Support: Nil, Conflict of Interest: None declared.
Indian J Dent Res, 18(4), 2007