|Year : 2007 | Volume
| Issue : 4 | Page : 201-209
|Management of obstructive sleep apnea: A dental perspective
Ariga Padma1, N Ramakrishnan2, Vinod Narayanan3
1 Department of Prosthodontics, Saveetha University, 162 Poonamallee High Road, Chennai - 600 077, India
2 Consultant Sleep Medicine, NITHRA, 19, Periyar Road, T Nagar, Chennai, India
3 Department of Oral and Maxillofacial Surgery, Saveetha University, 162 Poonamallee High Road, Chennai - 600 077, India
Click here for correspondence address and email
|Date of Submission||31-Dec-2006|
|Date of Decision||05-Jun-2007|
|Date of Acceptance||09-Jun-2007|
| Abstract|| |
Sleep disordered breathing is a term which includes simple snoring, upper airway resistance syndrome, and obstructive sleep apnea (OSA). Simple snoring is a common complaint affecting 45% of adults occasionally and 25% of adults habitually and is a sign of upper airway obstruction. Snoring has also been identified as a possible risk factor for hypertension, 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 patients. They reduce the apnea-hypopnea index (AHI) by 50% or to < 10 events per h. Oral appliances also reduce the AHI to normal in 50-60% patients.
Keywords: Dental implications, obstructive sleep apnea, oral appliances
|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
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.  Snoring has also been identified as a possible risk factor for hypertension, ischaemic heart disease, and stroke. 
|How to cite this URL:|
Padma A, Ramakrishnan N, Narayanan V. Management of obstructive sleep apnea: A dental perspective. Indian J Dent Res [serial online] 2007 [cited 2014 Dec 18];18:201-9. Available from: http://www.ijdr.in/text.asp?2007/18/4/201/35833
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 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.
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.  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,  dysrhythmias, depression,  stroke,  and angina.  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. 
| 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. 
| 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. 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. 
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.
Obesity is the main predisposing factor for OSA.  In nonobese patients, craniofacial anomalies like micrognathia and retrognathia , 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,  steeper and shorter anterior cranial base,  inferiorly displaced hyoid bone,  disproportionately large tongue, a long soft palate,  and decreased posterior airway space.  In addition to obesity, age,  ethnic background,  genetic, and gender predilection,  habits like consumption of alcohol,  smoking,  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.  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. 
| Clinical Features|| |
Patients with OSAS may have memory problems, excessive day time sleepiness, difficulty in concentrating,  night drooling of saliva, depression,  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  appear to be associated with untreated OSA. There have been reports of exacerbations of epilepsy,  asthma,  and hypertension  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. 
| 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. 
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: 
- Mild OSA (5 to 15 events per h),
- Moderate OSA (15 to 30 events per h)
- Severe OSA (more than 30 events per h)
Patients with mild to moderate OSA are candidates for placement of appropriate oral devices.
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.  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.
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).  The Mallampati score  (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  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.  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.  Another technique termed acoustic reflexion  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.
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 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 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. 
Oral appliances were used by Robin  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. 
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  / snoreguard  / silencer.  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. 
c. Soft-palate lifters. 
d. Tongue trainers. 
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. 
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. 
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.  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 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  and hence oral appliances help in increasing the airway size.  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,  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.  Soft palate trainers and tongue posture trainers are rarely used. 
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. 
Designs of oral appliances vary and it is advisable to evaluate the patient before and after insertion of the appliance. 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 posttreatment nocturnal polysomnography to evaluate individual oral appliances. 
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 [Figure - 2],[Figure - 3] which show the measurements of the neck and pharynx could be used to predict posttreatment AHI with good accuracy. 
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  and body posture  during sleep. Most authors suggest that for adjustable MRDs, 50 to 75% maximal jaw protrusion maximizes efficacy without causing obvious TMJ problems.  It has also been suggested that maximal jaw protrusion may increase the AHI. 
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.  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.  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  and stroke.  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%,  and a decrease in day time sleepiness as assessed by multiple sleep latency test (MSLT);  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.  Long-term changes in the TMJ with MRD use have not been studied, although joint degeneration is a theoretical concern.  Tongue abrasion, oral mucosal dryness, excessive salivation, and gagging are some of the reactions with a TRD.  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.  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.
Newer oral appliances allow greater lateral jaw movement, cover all of the dentition, and provide better retention. Adjustable (titratable) appliances allow the clinician to 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.  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.
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.  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%).  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. 
Continuous positive airway pressure
CPAP continues to be the ideal treatment for patients with moderate to severe OSA.  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.  and Schwab et al.  showed that upper airway dilation with CPAP is greater in the lateral dimension than in the anterior-posterior dimension. This suggests that the lateral 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.  Out of 70% of the patients attempting to use CPAP equipment, only 20% use it throughout the night. 
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.  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. 
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, 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. 
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%. ,
| 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. 
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.  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 may affect recording of the centric relation accurately.  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.  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.  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.  Such patients may be referred for further vascular evaluation. A small percentage of patients with OSA have symptomatic hypothyroidism as a codiagnosis.  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. 
| References|| |
|1.||Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances. American Sleep Disorders Association. Sleep 1995;18:511-3. [PUBMED] |
|2.||Waller PC, Bhopal RS. Is snoring a cause of vascular disease: An epidemiological review. Lancet 1989;1:143-6. [PUBMED] |
|3.||Brown LK. Sleep apnea syndromes overview and diagnostic approach: Mt. Sinai J Med 1994;61,99-112. |
|4.||Nieto FJ, Young TB, Lind BK, Shahar E, Samet JM, Redline S, et al . Association of sleep disordered breathing, sleep apnea and hypertension in a large community based study. JAMA 2000;283:1829-36. [PUBMED] [FULLTEXT] |
|5.||Baran AS, Richert AC. OSA and depression. CNS Spectr 2003;8:128-34. [PUBMED] |
|6.||Palomaki H. Snoring and the risk ischaemic myocardial or brain infarction. Stroke 1991;22:1021-5. |
|7.||Levi WS, Blackshean JL. Freduchson DA, Caplan J. OSA manifestations as suspected angina -report of three cases. Mayo Clin Proc 1994;69;244-8. |
|8.||Gula LJ, Krahn AD, Skares AC, Yee R, Hein GJ. Clinical relevance of arrythmias daily sleep - Guidance for clinicians. Heart 2004;90:347-52. |
|9.||Swedish Medical Research Council, Diagnosis and management of obstructive sleep apnea syndrome. A State of the Art conference in Stockholm 1994. |
|10.||Schwab RJ, Gupta KB, Gefter WB, Metzger LJ, Hoffman EA, Pack AI. Upper airway soft tissue anatomy in normal and patients with sleep disordered breathing: Significance of the lateral pharyngeal walls. Am J Respir Crit Care Med 1995;152:1673-89. [PUBMED] |
|11.||Strobel RJ, Rosen RC. Obesity and weight loss in obstructive sleep apnea: A critical review. Sleep 1996;19:104-15. [PUBMED] |
|12.||Imes NK, Orr WC, Smith RO, Rogers RM. Retrognathia and sleep. JAMA 1977;237:1596-7. [PUBMED] |
|13.||Miles PG, Vig PS, Weyant RJ, Forrest TD, Rockette HE Jr. Craniofacial structure and obstructive sleep apnea syndrome: A qualitative analysis and meta-analysis of the literature. Am J Orthod Dentofacial Orthop 1996;109:163-72. [PUBMED] [FULLTEXT] |
|14.|| Bacon WH, Kreiger J, Turlot JC, Stierle JL. Craniofacial characteristics in patients with obstructive sleep apnea syndrome. Cleft Palate J 1988;25:374-8. |
|15.||Lowe AA, Fleetham JA, Adachi S, Ryan CF. Cephalometric and computed tomographic predictors of obstructive sleep apnea severity. Am J Orthod Dentofacial Orthop 1995;107:589-95. [PUBMED] [FULLTEXT] |
|16.||Jamieson A, Guilleminault C, Partinen M, Quera-Salva MA. Obstructive sleep apnea patients have craniomandibular abnormalities. Sleep 1986;9:469-77. [PUBMED] |
|17.|| Lowe AA, Gionhaku N, Takeuchi K, Fleetham JA. Three dimensional CT reconstructions of tongue and airway in adult subjects with OSA. Am J Orthod Dentofacial Orthop 1986;90:364-74. |
|18.||Solow B, Skov S, Ovesen J, Norup PW, Wildschiψdtz G. Airway dimensions and head posture in obstructive sleep apnea. Eur J Orthod 1996;18:571-9. |
|19.||Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep disordered breathing among middle aged adults. N Engl J Med 1993;328:1230-5. [PUBMED] [FULLTEXT] |
|20.||Liu Y, Lowe AA, Zeng X, Fu M, Fleetham JA. Cephalometric comparisons between Chinese and Caucasian patients with obstructive sleep apnea. Am J Orthod Dentofacial Orthop 2000;117:479-85. [PUBMED] [FULLTEXT] |
|21.||Kapsimalis F, Kryger MH. Gender and obstructive sleep apnea syndrome, Part 2: mechanisms. Sleep 2002;25:499-506. [PUBMED] |
|22.||Scrima L, Broudy M, Nay KN, Cohn MA. Increased severity of obstructive sleep apnea after bedtime alcohol ingestion: Diagnostic potential and proposed mechanism of action. Sleep 1982;5:318-28. [PUBMED] |
|23.||Wetter DW, Young TB, Bidwell TR, Badr MS, Palta M. Smoking as a risk factor for sleep-disordered breathing. Arch Intern Med 1994;154:2219-24. [PUBMED] |
|24.||Cartwright RD. Effect of sleep position on sleep apnea severity. Sleep 1984;7:110-4. [PUBMED] |
|25.||Marks MB. Stigmata of respiratory tract allergies. The Upjohn Co: Kalamazoo, MI; 1977. |
|26.||Schlosshan D, Elliott MW. Sleep, part 3: Clinical presentation and diagnosis of the obstructive sleep apnoea hypopnoea syndrome. Thorax 2004;59:347-52. [PUBMED] [FULLTEXT] |
|27.||Baran AS, Richert AC. Obstructive sleep apnea and depression. CNS Spectr 2003;8:128-34. [PUBMED] |
|28.||Goncalves MA, Paiva T, Ramos E, Guileminault C. Obstructive sleep apnea syndrome, sleepiness and quality of life. Chest 2004;125:2091-6. |
|29.||Britton TC, O'Donoghue M, Duncan JS, Hirsch NP. Exacerbation of epilepsy by obstructive sleep apnoea. J Neurol Neurosurg Psychiatry 1997;63:808. |
|30.||Bohadana AB, Hannhart B, Teculescu DB. Nocturnal worsening of asthma and sleep-disordered breathing. J Asthma 2002;39:85-100. [PUBMED] |
|31.||Horne JA, Reyner LA. Sleep related vehicle accidents. BMJ 1995;310:565-7. [PUBMED] [FULLTEXT] |
|32.||Raphaelson MA, Alpher EJ, Bakker KW, Perlstrom JR. Oral appliance therapy for obstructive sleep apnea syndrome: Progressive mandibular advancement during polysomnography. Cranio 1998;16:44-50. [PUBMED] |
|33.||Sleep-related breathing disorders in adults: Recommendations for syndrome definition and measurement techniques in clinical research-the report of an American Academy of Sleep Medicine task force. Sleep 1999;22:667-89. |
|34.||Johns MW. A new method for measuring daytime sleepiness: The Epworth sleepiness scale. Sleep 1991;14:540-5. [PUBMED] |
|35.||Fairbanks DN, Fujita S. Snoring and obstructive sleep apnea. 2 nd ed. Raven Press: New York; 1994. |
|36.||Friedman M, Tanyeri H, LaRosa M, Landsberg R, Vaidyanathan K, Pieri S, et al . Clinical predictors of obstructive sleep apnea. Laryngoscope 1999;109:1901-7. |
|37.||Bailey DR, Attanasio R. Dentistry's role in the management of sleep disorders. Recognition and management. Dent Clin North Am 2001;45:619-30. |
|38.||George T. A new instrument for functional appliance bite registration. J Clin Orthod 1992;2:721-3. |
|39.||Breathing disorders in sleep. Clin Chest Med 1992;13:383-554. |
|40.||Smith PL, Gold AR, Meyers DA, Haponik EF, Bleecker ER. Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985;103:850-5. |
|41.||Robin P. Glossoptosis due to atresia and hypertrophy of the mandible. Am J Dis Child 1934;48:541-7. |
|42.||Ivanhoe JR, Attanasio R. Sleep disorders and oral devices. Dent Clin North Am 2001;45:733-58. |
|43.||Clark GT, Arand D, Chung E, Tong D. Effect of anterior mandibular positioning on obstructive sleep apnea. Am Rev Respir Dis 1993;147:624-9. |
|44.||Ferguson KA, Ono T, Lowe AA, al-Majed S, Love LL, Fleetham JA. A short term controlled trial of an adjustable oral appliance for the treatment of mild to moderate obstructive sleep apnoea. Thorax 1997;52:362-8. |
|45.||Schmidt-Nowara WW, Meade TE, Hays MB. Treatment of snoring and obstructive sleep apnea with a dental prosthesis. Chest 1991;99:1378-85. |
|46.||Schonhofer B, Stoohs RA, Rager H, Wenzel M, Wenzel G, K φhler D. A new tongue advancement technique for sleep -disordered breathing: Side effects and efficacy. Am J Respir Crit Care Med 1997;155:732-8. |
|47.||Hart NT, Duhamel J, Guilleminault C. Oral positive airway pressure by the OPAP dental appliance reduces mild to severe OSA. Sleep Res 1997;26:371. |
|48.||Practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances. American Sleep Disorders Association. Sleep 1995;18:511-3. |
|49.||Ferguson KA, Love LL, Ryan CF. Effects of a mandibular and tongue protrusion on upper airway size. Am J Respir Crit Care Med 1997;155:1748-54. |
|50.||Ferguson KA, Love LL, Ryan CF. Effect of mandibular and tongue protrusion on upper airway size during wakefulness. Am J Respir Crit Care Med 1997;155:1748-54. |
|51.||Rogers RR. Oral appliance therapy for the management of sleep disordered breathing. Sleep Breath 2000;4:79-84. |
|52.||Cartwright RD, Samelson CF. The effects of a nonsurgical treatment for obstructive sleep apnea. The tongue-retaining device. JAMA 1982;2248:705-9. |
|53.||Cartwright R. What's new in oral appliances for snoring and sleep apnea: An update. Sleep Med Rev 2001;5:25-32. |
|54.||Hokema A, Stegenga B, deBont LG. Efficacy and co-morbidity of oral appliances in the treatment of obstructive sleep apnea-hypopnea: A systematic review. Crit Rev Oral Biol Med 2004;15:137-55. |
|55.||Liu YH, Lowe A, Fleetham J, Park YC. Cephalometric and physiological predictors of the efficacy of an adjustable oral appliance for the treatment of obstructive sleep apnea. Am J Orthod Dentofac Orthop 2001;120:639-47. |
|56.||Jan MA, Marshall I, Douglas NJ. Effect of posture on human airway dimensions in normal humans. Am J Respir Crit Care Med 1994;149:145-8. |
|57.||Pae E, Lowe AA, Sasaki K, Price C, Tsuchiya M, Fleetham JA. A cephalometric and electromyographic study of upper airway structures in the upright and supine positions. Am J Orthod Dentofacial Orthop 1994;106:52-9. |
|58.||Schmidt-Nowara W, Lowe A, Wiegand L, Cartwright R, Perez-Guerra F, Menn S. Oral appliances for the treatment of snoring and obstructive sleep apnea: A review. Sleep 1995;18:501-10. |
|59.||Jamieson AO, Thomson WK, Forester MD, Becker PM. Progressive mandibular protrusion during sleep in sleep apnea: A pilot study with an adjustable anterior mandibular positioner. Sleep Res 1994;23:445. |
|60.||Gotsopoulos H, Kelly JJ, Cistullii PA. Oral appliance therapy reduces blood pressure in obstructive sleep apnea: A randomized controlled trial. Sleep 2004;27:934-41. |
|61.||MacMahon S, Peto R, Cutler J, Collins R, Sorlie P, Neaton J, et al . Blood pressure, stroke and coronary heart disease. Prospective observational studies corrected for the regression dilution basis. Lancet 1990;335:765-74. |
|62.||Cohen MC, Rohtla KM, Lavery CE, Muller JE, Mittleman MA. Meta-analysis of the morning excess of acute myocardial infarction and sudden cardiac death. Am J Cardiol 1997;79:1512-6. |
|63.||Elliot WJ. Circadian variation in the timing of stroke onset: A meta-analysis. Stroke 1998;29:992-6. |
|64.||Carskadon MA, Dement WC, Milter MM, Roth T, Westbrook PR, Keenan S. Guidelines for the multiple sleep latency test (MSLT): A standard measure of sleepiness. Sleep 1986;9:519-24. |
|65.||Loube DI. Oral appliance treatment for obstructive sleep apnea. Clin Pulm Med 1998;5:124-8. |
|66.||Ivanhoe JR. Treatment of upper airway sleep disorder patients with dental devices. Clinical Maxillofacial Prosthetics. Quintessence: Chicago; 2000. p. 215-31. |
|67.||Lavigne GJ Manzini C. Bruxism. principles and practices of sleep medicine. 3 rd ed. WB Saunders: 2000. p. 773-85. |
|68.||Ohayon MM, Li KK, Guilleminault C. Risk factors for sleep bruxism in the general population. Chest 2001;119:53-61. |
|69.||Gagnon Y, Mayer P, Morisson F, Romprι PH, Lavigne GJ. Aggravation of respiratory disturbances by the use of an occlusal splint in apneic patients: A pilot study. Int J Prosthodont 2004;17:447-53. |
|70.||Ferguson KA, Ono T, Lowe AA, Keenan SP, Fleetham JA. A randomized crossover study of an oral appliance versus nasal continuous positive airway pressure in the treatment of mild-moderate sleep apnea. Chest 1996;109:1269-75. |
|71.||Kuna ST, Bedi DG, Ryckman C. Effect of nasal airway positive pressure on upper airway size and configuration. Am Rev Respir Dis 1988;138:969-75. |
|72.||Schwab RJ, Pack AI, Gupta KB, Metzger LJ, Oh E, Getsy JE, et al . Upper airway and soft tissue structural changes induced by CPAP in normal subjects. Am J Resp Crit Care Med 1996;154:1106-16. |
|73.||Hoffstein V, Viner S, Mateika S, Conway J. Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits and side effects. Am Rev Respir Dis 1992;145:841-5. |
|74.||Kribbs NB, Pack AI, Kline LR, Smith PL, Schwartz AR, Schubert NM, et al . Objective measurements of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis 1993;147:887-95. |
|75.||Rojewski TE, Schuller DE, Clark RW, Schmidt HS, Potts RE. Videoendoscopic determination of the mechanism of obstruction in obstructive sleep apnea. Otolaryngol Head Neck Surg 1984;92:127-31. |
|76.||Fujita S. Pharyngeal surgery for obstructive sleep apnea and snoring. Snoring and Obstructive Sleep Apnea, Raven Press: 1987. p. 101. |
|77.||Riley R, Powell N, Guilleminault C. Obstructive sleep apnea syndrome: A review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993;108:117. |
|78.||Prinsell JR. Maxillomandibular advancement surgery in site specific treatment approach for obstructive sleep apnea in 50 consecutive patients. Chest 1999;116:1519-29. |
|79.||Waite PD, Shashidar MS. Maxillomandibular advancement surgery: A cure for obstructive sleep apnea syndrome. Oral Maxfac Surg Clin North Am 1995;7:327-44. |
|80.||Veis RW. Snoring and obstructive sleep apnea from a dental perspective. J Calif Dent Assoc 1998;26:557-65. |
|81.||Kramer NR, Fine MD, McRae RG, Millman RP. Unusual complication of nasal CPAP - subcutaneous emphysema following facial trauma. Sleep 1997;20:895-7. |
|82.||Termato S, Sudo E, Matsuse T, Ohga E, Ishii T, Ouchi Y, et al . Impaired swallowing reflex in obstructive sleep apnea syndrome. Chest 1999;116:17-21. |
|83.||Aertburn DE, Crane PK, Veenstra DL. The efficacy and safety of sibutramine for weight loss: A systematic review. Arch Intern Med 2004;164:994-1003. |
|84.||Friedlander AH, Friedlander IK, Yueh R, Littner MR. The prevalence of carotid atheromas seen on panaromic radiographs of patients with obstructive sleep apnea and their relation to risk factors for atherosclerosis. J Oral Maxillofac Surg 1999;57:516-22. |
|85.||Moore K, Esther M. Current medical management of sleep related breathing disorders. Oral Maxillofac Surg Clin 2002;14:297-304. |
Department of Prosthodontics, Saveetha University, 162 Poonamallee High Road, Chennai - 600 077
[Figure - 1], [Figure - 2], [Figure - 3]
[Table - 1]
|This article has been cited by|
||Stroke and Obstructive Sleep Apnea: A Review
| ||Daniel A. Barone,Ana C. Krieger |
| ||Current Atherosclerosis Reports. 2013; 15(7) |
||Stroke and obstructive sleep apnea: A review
| ||Barone, D.A. and Krieger, A.C. |
| ||Current Atherosclerosis Reports. 2013; 15(7) |
||Treatment of Patients With Simple Snoring [Tratamiento del paciente con ronquidos simples]
| ||Fiz, J.A. and Morera Prat, J. and JanÃ©, R. |
| ||Archivos de Bronconeumologia. 2009; 45(10): 508-515 |
||Pharyngeal airflow analysis in obstructive sleep apnea patients pre-and post-maxillomandibular advancement surgery
| ||Huynh, J. and Kim, K.B. and McQuilling, M. |
| ||Journal of Fluids Engineering, Transactions of the ASME. 2009; 131(9): 0911011-09110110 |
||Treatment of Patients With Simple Snoring
| ||José Antonio Fiz,Josep Morera Prat,Raimon Jané |
| ||Archivos de Bronconeumología ((English Edition)). 2009; 45(10): 508 |
||Tratamiento del paciente con ronquidos simples
| ||José Antonio Fiz,Josep Morera Prat,Raimon Jané |
| ||Archivos de Bronconeumología. 2009; 45(10): 508 |
||Pharyngeal Airflow Analysis in Obstructive Sleep Apnea Patients Pre- and Post-Maxillomandibular Advancement Surgery
| ||John Huynh,Ki Beom Kim,Mark McQuilling |
| ||Journal of Fluids Engineering. 2009; 131(9): 091101 |
||Optimal treatment of obstructive sleep apnea and excessive sleepiness
| ||Russell Rosenberg,Paul Doghramji |
| ||Advances in Therapy. 2009; 26(3): 295 |
||Optimal treatment of obstructive sleep apnea and excessive sleepiness
| ||Rosenberg, R. and Doghramji, P. |
| ||Advances in Therapy. 2009; 26(3): 295-312 |
| Article Access Statistics|
| Viewed||12747 |
| Printed||451 |
| Emailed||35 |
| PDF Downloaded||1696 |
| Comments ||[Add] |
| Cited by others ||9 |