|Year : 2015 | Volume
| Issue : 2 | Page : 37-43
Obstructive Sleep Apnea: An Overview of the Disorder, Consequences, and Treatment Options
Sameer Pralhad Narkhede, Karthik Shetty, Sushma Sonawane, Nitin Gadhiya, Vivek P Soni
Department of Orthodontics, D. Y. Patil University, School of Dentistry, Nerul, Navi Mumbai, Maharashtra, India
|Date of Web Publication||17-Dec-2015|
Sameer Pralhad Narkhede
Department of Orthodontics, D. Y. Patil University, School of Dentistry, Nerul, Navi Mumbai - 400 706, Maharashtra
Source of Support: None, Conflict of Interest: None
Obstructive sleep apnea (OSA) is a potentially disabling condition characterized by disruptive snoring, repeated episodes of complete or partial pharyngeal obstruction during sleep resulting in nocturnal hypoxemia, frequent arousals, and excessive daytime sleepiness. Among adults, sleep apnea is more common than asthma. Recognized as a separate clinical entity nearly 35 years ago, OSA still remains substantial but frequently ignored public health threat. Although recognized for centuries, its importance for individuals and society has only recently been appreciated. Because individuals with narrow airways and/or craniofacial anomalies may have increased risk for OSA/hypopnea syndrome, dentistry can play a pivotal role in the identification and possible treatment of patients with this syndrome. This article makes an attempt to review some of the basic aspects of this sleep-related disorder, its diagnosis, pathophysiology, various treatment options, and consequences in adults as well as children.
Keywords: Continuous positive airway pressure, mandibular advancement device, sleep apnea, snoring
|How to cite this article:|
Narkhede SP, Shetty K, Sonawane S, Gadhiya N, Soni VP. Obstructive Sleep Apnea: An Overview of the Disorder, Consequences, and Treatment Options. Indian J Oral Health Res 2015;1:37-43
|How to cite this URL:|
Narkhede SP, Shetty K, Sonawane S, Gadhiya N, Soni VP. Obstructive Sleep Apnea: An Overview of the Disorder, Consequences, and Treatment Options. Indian J Oral Health Res [serial online] 2015 [cited 2020 May 25];1:37-43. Available from: http://www.ijohr.org/text.asp?2015/1/2/37/172017
| Introduction|| |
Apnea is defined as complete cessation of nasal airflow for more than 10 s.  Apnea severity is categorized by the frequency of apnea events that occur per hour. This number is called the apnea index.  It is not unusual for a patient with severe apnea to have as many as 300 episodes per night. There are three basic types of sleep apneas: Central, obstructive sleep, and mixed apnea. 
Obstructive sleep apnea (OSA) is a common disorder that is characterized by recurrent upper airway obstruction during sleep. OSA is a widely prevalent problem with significant medical, psychological, and social consequences. , OSA is characterized by a number of symptoms, of which intermittent upper airway obstruction during sleep, socially handicapping snoring, and daytime sleepiness are the most common. After the upper airway obstruction, blood oxygen saturation is reduced and carbon dioxide is accumulated and in long-standing cases of the syndrome, headache, hypertension, cardiac and pulmonary complications often ensue. ,,, Moreover, the automobile accident rate in OSA patients is reported to be 2-3 times higher than in matched control drivers.  Work performance, family and social interaction, and other aspects of quality of life also appear to be compromised in many patients. There is partial or complete cessation of air flow associated with oxyhemoglobin desaturation leading to increased effort to breath. 
OSA is relatively common in the general population. It has been reported that 20% of middle-aged men and 10% of middle-aged women are habitual snorers and the corresponding prevalence of OSA is 4% among men and 2% among women.  Middle-aged obese men are at particular risk but the disorder is also present in women and young children. Estimates of OSA prevalence in Asian population are similar (2-4%). 
The morbidity of OSA relates principally to the cardiovascular system.  Rigorous epidemiologic studies have shown that sleep apnea is a risk factor for the development of arterial hypertension, independent of associated obesity, alcohol intake, sex, and age. ,,, Animal studies have shown that apnea causes arterial hypertension which is reversible with treatment.  OSA patients have significantly more hypertension, ischemic heart disease, and cerebrovascular disease than individuals without OSA. , However, OSA patients have a high incidence of other coexisting cardiovascular risk factors such as obesity, hyperlipidemia, increased age, smoking history, and excessive alcohol intake, which potentially confounds the identification of an independent association of OSA with cardiovascular disease.  The relationship between OSA/hypopnea syndrome (OSAHS) and stroke is still under discussion, not well-defined.
| Physiology and Pathophysiology|| |
The physiopathology and etiology of OSA are not yet fully understood, but certainly an interaction between anatomic and neuromuscular alterations seems to determine the collapse of the pharynx. Broadly, the factors which determine upper airway patency during sleep are upper airway muscle activity, neuromuscular coordination, and the size relationships of the upper airway and surrounding tissues. 
Negative airway pressure is generated by the activity of the diaphragm and intercostal muscles during inhalation. To a large extent, the patency of the upper airway is dependent on the action of oropharyngeal muscles. These dilator and abductor muscles are normally activated in a rhythmic mode in coordination with each inspiration. When the negative pressure exceeds the force produced by these muscles, the pharynx will collapse, occluding the airway.  Frequently, sleep apnea patients have constricted upper airways that increase the pharyngeal resistance during inspiration. This in turn necessitates an increase in pharyngeal dilator muscle contraction to maintain airway patency. Such an increase has been shown in OSAHS patients during wakefulness  but decrease in contraction is seen during sleep, thus contributing to the development of obstructive apnea.  Interestingly, when compared with normal, OSAHS patients show greater pharyngeal dilator muscle contraction during sleep, suggesting that an imbalance between negative airway pressure and dilator muscle contraction is responsible for the obstruction, rather than a primary deficiency in muscle contraction. A sustained increase in dilator muscle contraction in OSAHS could predispose these muscles to fatigue,  possibly aggravating the tendency to pharyngeal occlusion.
Tongue muscle activity and its interaction with upper airway size and respiration have been recently reviewed in depth.  Contraction of the genioglossus muscle moves the base of the tongue ventrally. Since the position of the anterior wall of the pharynx is determined in part by the tongue, contraction of the genioglossus muscle enlarges the volume of the oropharynx. Neuromuscular coordination ensures that contraction of the upper airway dilating muscles precedes the inspiratory onset of diaphragm activity.  This provides a stable intraluminal pressure during inspiratory efforts. Abnormal size relationships between the upper airway and its surrounding skeletal and soft tissues predispose to upper airway occlusion during sleep.
Although the precise pathogenesis of upper airway obstruction during sleep remains uncertain in OSA patients, a number of abnormal craniofacial and upper airway structures have been reported, such as retrognathism of the maxilla and mandible, increased lower facial height, elongated soft palate, enlarged tongue, decreased posterior airway space, and inferiorly positioned hyoid bone.
| Diagnosis|| |
The historically research-based laboratory studies are still considered the primary standard for the diagnosis of sleep apnea.  The laboratory recording technique is called polysomnography (PSG). As a tool, PSG has been essential in the diagnosis for sleep-disordered patients and in the enhancement of our understanding of both normal sleep and its disorders.  PSG is a complex procedure that should be performed by a trained technologist using electrodes and other sensors. A routine clinical PSG includes the monitoring of brain electrical activity (electroencephalogram), electro-oculography and electromyography, effort to breathe (generally from both thoracic and abdominal sensors), nasal and oral airflow, oxygen saturation (oximetry), electrocardiography, and body position.
The major PSG measurement used to determine if a patient is clinically diagnosed with sleep-disordered breathing has been the frequency of the respiratory events per hour of sleep. This measure provides the major index of severity of the disorder and generally is a combination of the number of apneas and hypopneas per hour of sleep. The apnea-hypopnea index (AHI), or more recently the respiratory disturbance index (RDI), has been shown to be a reproducible measure within a patient as well as a predictor of associated cardiovascular disease.  The severity of the accompanying oxygen desaturation and sleep fragmentation during PSG are combined with the clinical symptoms to assess the immediate consequences to the individual from the sleep disordered breathing.
It is now accepted that a diagnosis of clinically significant OSAHS should be accompanied by compatible signs and symptoms, and not based simply on an arbitrary AHI/RDI threshold. , The syndrome should be defined when an index of abnormal obstructed breathing events, or arousals caused by them, exceeds a threshold in a patient with clinical features or symptoms related to the abnormal respiratory pattern during sleep. A recent suggestion by Kryger  stated that patients with daytime sleepiness who have more than 5 abnormal respiratory events per hour of sleep should be treated.
Although the pharynx has been visualized with several techniques, including cineradiography, fiberoptic bronchoscopy, acoustic reflectance, and forced expiratory maneuvers, the techniques of computerized tomography (CT) scanning , and lateral cephalometry , are more common. Recent reports with CT scanning have suggested that the airway in such subjects is narrower than in normal controls. , Although the cause of these changes remains obscure, the importance of craniofacial morphology upon the upper airway dimensions remains undefined.
Traditional cephalometry is used extensively in clinical orthodontics to quantify skeletal and soft-tissue dysplasias before the initiation of therapy. Numerous authors , have quantified specific airway parameters, although the obvious limitations of any two-dimensional cephalometric study are recognized. The significant advantages of cephalometry are its easy access, low cost, and minimal radiation. Cephalometrically sleep apnea subjects show a posteriorly positioned maxilla and mandible, a steep occlusal plane, overerupted maxillary and mandibular teeth, proclined incisors, a steep mandibular plane, a large gonial angle, high upper and lower facial heights, and an anterior open bite in association with a long tongue and a posteriorly placed pharyngeal wall.  Three-dimensional CT measurements provide a detailed analysis of the relationship of upper airway and its surrounding soft-tissues. Both CT and magnetic resonance imaging can be used for volumetric measurements of upper airway. Patients with OSA show large tongue and soft palate. 
| Treatment|| |
The guideline for treating mild cases of OSA include increasing the hours of night sleep to eight, weight reduction, sleep posture training, avoiding any central nervous system depressants including prescription medications and alcohol  and oral appliances, which can be very effective in treating mild cases.
| Nonspecific Therapy|| |
These measures should be included in patients with very mild apnea whose main complaint is snoring. Overweight persons can benefit by losing weight.  Individuals with apnea should avoid alcohol 4-6 h prior to bedtime and also sleeping pills, which might collapse the airway during sleep and prolong the apneic periods. Positional therapy can be used to treat patients whose OSA is related to body positioning during sleep.
| Specific Therapy|| |
Surgical procedure and medication
The specific therapy for sleep apnea is based on medical history, physical examination, and the results of PSG. Medications are generally not effective in the treatment of sleep apnea. Historically, surgical procedures  used for the management of OSA have included intranasal procedures, reduction glossectomies, uvulopalatopharyngoplasty procedures, and tracheostomy. Mandibular advancement surgeries and distraction osteogenesis for mandible are also advocated. For children, once the diagnosis of OSAHS has been established, the first line of treatment is the surgical removal of the enlarged tonsils and/or adenoids. However, the effectiveness of this treatment needs to be further established. Surgery may be appropriate for patients who cannot comply with or are not appropriate candidates for conservative therapies or continuous positive airway pressure (CPAP) alone. The type of surgery performed should be based upon the specific pathophysiology of a patient's condition. Careful and thorough preoperative examination by radiography, imaging, and direct visualization is needed to identify the airway obstruction sites and to select the appropriate surgery.
| Positive Airway Pressure Therapy|| |
The first reported use of nasal CPAP (nCPAP or CPAP) for OSAHS in adults was by Sullivan et al. in 1981.  Their device consisted of intranasal tubes attached to a blower unit. In 1983, the nasal mask delivery system, similar to contemporary systems was introduced.  Fundamentally, the application of a therapeutic level of CPAP results in immediate relief in the upper airway obstruction. This benefit has been attributed to the CPAP functioning as a "pneumatic splint" for the upper airway.  Additional physiologic benefits of CPAP application includes improvement in the function of pharyngeal dilator muscles, ventilator drive, and upper airway morphology. CPAP rarely results in serious side effects. However, about 25% of patients may develop nasal congestion with chronic use.  The introduction of automatically adjusting CPAP devices (auto-CPAP) over the past several years represents a significant advancement in CPAP technology since its inception in 1981. The device continuously adjusts the applied airway pressure to an "optimum" level throughout the night and appears to improve compliance. Disadvantages of CPAP are many patients find the mask uncomfortable, claustrophobic, or embarrassing. Since CPAP is not a cure and must be used every night for life, noncompliant patients experience a full return of OSA and related symptoms. The sound of the machine may be disruptive. Side effects may include: Difficulty in exhaling, inability to sleep, nasal congestion, sore eyes, sore or dry throat, headaches, abdominal bloating, chest muscle discomfort, nosebleeds and mask-related problems such as rash, skin abrasions, and conjunctivitis (from air leakage).
| Oral Appliances|| |
Oral appliances which are used for the treatment of OSA were originally derived from an orthodontic functional appliances, , which basically position the mandible forward. They have been variously modified with the aim of increased effectiveness and patient compliance for intra-oral use. The appliances can be broadly classified into:
- Tongue repositioning devices such as the tongue retaining device
- Mandibular advancement devices (MADs) which work by holding the lower jaw and the tongue forward during sleep
- Devices designed to lift the soft palate or reposition the uvula; however, uvula lifters are not in use now due to discomfort.
Tongue retaining devices
It is a bubble-shaped device made of soft polyvinyl. The patient's teeth rest in custom fitted grooves which are extended to form a "bubble" that sticks out from between the lips. The patient positions his teeth in the grooves, sticks his tongue forward into the bubble until suction grabs, and holds the tongue in place [Figure 1]. Positioning the tongue forward may eliminate any obstruction caused by the base of the tongue.
Mandibular advancement devices
MAD essentially consists of a plastic mold of the teeth. Advancement of the lower teeth moves the mandible forward and opens the airway, preventing its collapse during sleep. The advantages of MAD are its relative simplicity, reversible nature, and cost effectiveness. Complications of MAD could be loosened teeth, joint pain, muscle aches, tissue sores, inability to touch the posterior teeth together when the appliance is first removed in the morning, permanent tooth movement, and excessive salivation. ,
Few of the appliance designs of other MADs are:
Klearway oral appliance
The Klearway oral appliance  utilizes a maxillary orthodontic expander to sequentially move the mandible forward. Klearway is a fully adjustable oral appliance [Figure 2] used for the treatment of snoring and mild to moderate OSA. Small increments of mandibular advancement are initiated by the patient and this prevents rapid jaw movements that cause significant patient discomfort.
Modified Herbst appliance
This appliance design links upper and lower splints [Figure 3] with a piston-post and sleeve adjustable telescopic mechanism on each side.  It prevents side-to-side motion, but since the mandible is held closed with small orthodontic rubber bands, opening the jaws is fairly easy.
Thornton adjustable positioner
The Thornton adjustable positioner  allows for progressive advancements of the jaw [Figure 4] via an anterior screw mechanism at the labial aspect of the upper splint. This appliance has a separate section for the mandible and maxilla.
Parker mandibular positioner
The Parker Mandibular positioner [Figure 5] links the upper and lower splints with bilateral orthodontic expanders. This appliance is made of a thermoplastic material which must be heated in hot tap water every night before it is placed in the mouth.
The elastic mandibular advancement
The elastic mandibular advancement [Figure 6] is the thinnest and least bulky of all the appliances. It is similar to clear acrylic orthodontic retainers, and moves the jaw forward in fairly significant steps, and can be difficult to tolerate.
This appliance [Figure 7] incorporates titanium precision attachments at the incisor level, allowing sequential 2 mm advancement of up to 8 mm, lateral movement of 6 mm, 3 mm bilaterally, and vertical pin height replacements. It is the only appliance that allows adjustment in not only an antero-posterior, but also in an "open and closed" position.
Oral positive airway pressure
It is a "combination" therapy which combines a nonadjustable MRD with nCPAP. Instead of using nasal nCPAP, which delivers air pressure through a mask over the nose or the nose and mouth, the air pressure is delivered through a small conduit [Figure 8] that fits across the roof of the patient's mouth.
A magnetic appliance for the treatment of snoring was given by Bernhold and Bondemark.  The appliance consisted of a maxillary and a mandibular occlusal acrylic splint. In each splint, four cylindrical neodymium-iron-boron magnets were embedded and oriented to produce intermaxillary forces that pulled the mandible forward.
| Conclusion|| |
Sleep breathing disorders are potentially life-threatening; therefore, the diagnosis and treatment of these diseases are the domain of the medical profession. The prevailing opinion is that patients should be treated only with a referral by a physician. As orthodontists, we have a significant role in the diagnosis of sleep apnea and the oral appliance therapy to improve the quality of life to the apneic patients. Oral appliances play a major role in the nonsurgical management of OSA and have become the first-line of treatment in almost all patients suffering from OSA. However, future randomized control trials are needed to compare the effectiveness of different oral appliances. Of all the oral modalities of treatment, CPAP is considered to be the most effective for the management of OSA.
| References|| |
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.
Veis RW. Snoring and obstructive sleep apnea from a dental perspective. J Calif Dent Assoc 1998;26:557-65.
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.
Ferguson KA, Fleetham JA. Sleep-related breathing disorders 4. Consequences of sleep disordered breathing. Thorax 1995;50:998-1004.
Guilleminault C, van den Hoed J, Mitler MM. Clinical overview of the sleep apnea syndrome. In: Guilleminault C, Dement WC, editors. Sleep Apnea Syndrome. New York: Alan R. Liss Inc.; 1978. p. 1-12.
Hoffstein V, Chan CK, Slutsky AS. Sleep apnea and systemic hypertension: A causal association review. Am J Med 1991;91:190-6.
Shepard JW Jr. Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 1992;13:437-58.
Hung J, Whitford EG, Parsons RW, Hillman DR. Association of sleep apnoea with myocardial infarction in men. Lancet 1990;336:261-4.
Findley LJ, Levinson MP, Bonnie RJ. Driving performance and automobile accidents in patients with sleep apnea. Clin Chest Med 1992;13:427-35.
Jureyda S, David W. Shucard obstructive sleep apnea - An overview of the disorder and its consequences. Semin Orthod 2004;10:63-72.
Udwadia ZF, Doshi AV, Lonkar SG, Singh CI. Prevalence of sleep-disordered breathing and sleep apnea in middle-aged urban Indian men. Am J Respir Crit Care Med 2004;169:168-73.
Partinen M, McNicholas WT. Epidemiology, morbidity and mortality of the sleep apnoea syndrome. In: McNicholas WT, editor. Respiratory Disorders during Sleep. European Respiratory Monographs. Vol. 3. Copenhagen, Denmark: Munksgard Press; 1998. p. 63-74.
García-Río F, Racionero MA, Pino JM, Martínez I, Ortuño F, Villasante C, et al.
Sleep apnea and hypertension. Chest 2000;117:1417-25.
Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 2000;342:1378-84.
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. Sleep Heart Health Study. JAMA 2000;283:1829-36.
Lavie P, Herer P, Hoffstein V. Obstructive sleep apnoea syndrome as a risk factor for hypertension: Population study. BMJ 2000;320:479-82.
Brooks D, Horner RL, Kozar LF, Render-Teixeira CL, Phillipson EA. Obstructive sleep apnea as a cause of systemic hypertension. Evidence from a canine model. J Clin Invest 1997;99:106-9.
Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Nieto FJ, et al.
Sleep-disordered breathing and cardiovascular disease: Cross-sectional results of the Sleep Heart Health Study. Am J Respir Crit Care Med 2001;163:19-25.
Bassetti C, Aldrich MS. Sleep apnea in acute cerebrovascular diseases: Final report on 128 patients. Sleep 1999;22:217-23.
Kiely JL, McNicholas WT. Cardiovascular risk factors in patients with obstructive sleep apnoea syndrome. Eur Respir J 2000;16:128-33.
Remmers JE, De Groot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978;44:931-8.
Deegan PC, McNicholas WT. Pathophysiology of obstructive sleep apnoea. Eur Respir J 1995;8:1161-78.
Mezzanotte WS, Tangel DJ, White DP. Waking genioglossal electromyogram in sleep apnea patients versus normal controls (a neuromuscular compensatory mechanism). J Clin Invest 1992;89:1571-9.
Mezzanotte WS, Tangel DJ, White DP. Influence of sleep onset on upper-airway muscle activity in apnea patients versus normal controls. Am J Respir Crit Care Med 1996;153:1880-7.
Hers V, Liistro G, Dury M, Collard P, Aubert G, Rodenstein DO. Residual effect of nCPAP applied for part of the night in patients with obstructive sleep apnoea. Eur Respir J 1997;10:973-6.
Lowe AA. Neural control of tongue posture. In: Neurophysiology of the Jaws and Teeth. London: McMillan Press Ltd.; 1990. p. 322-68.
Strohl KP, Hensley MJ, Hallett M, Saunders NA, Ingram RH Jr. Activation of upper airway muscles before onset of inspiration in normal humans. J Appl Physiol Respir Environ Exerc Physiol 1980;49:638-42.
Kryger M. What data do we need to diagnose and treat obstructive sleep apnoea syndrome? Sleep Med Rev 2002;6:3-6.
Meoli AL, Casey KR, Clark RW, Coleman JA Jr, Fayle RW, Troell RJ, et al.
Hypopnea in sleep-disordered breathing in adults. Sleep 2001;24:469-70.
Deegan PC, McNicholas WT. Predictive value of clinical features for the obstructive sleep apnoea syndrome. Eur Respir J 1996;9:117-24.
Ward Flemons W, McNicholas WT. Clinical prediction of the sleep apnea syndrome. Sleep Med Rev 1997;1:19-32.
Haponik EF, Smith PL, Bohlman ME, Allen RP, Goldman SM, Bleecker ER. Computerized tomography in obstructive sleep apnea. Correlation of airway size with physiology during sleep and wakefulness. Am Rev Respir Dis 1983;127:221-6.
Suratt PM, Dee P, Atkinson RL, Armstrong P, Wilhoit SC. Fluoroscopic and computed tomographic features of the pharyngeal airway in obstructive sleep apnea. Am Rev Respir Dis 1983;127:487-92.
Riley R, Guilleminault C, Herran J, Powell N. Cephalometric analyses and flow-volume loops in obstructive sleep apnea patients. Sleep 1983;6:303-11.
Rivlin J, Hoffstein V, Kalbfleisch J, McNicholas W, Zamel N, Bryan AC. Upper airway morphology in patients with idiopathic obstructive sleep apnea. Am Rev Respir Dis 1984;129:355-60.
Burstone CJ, James RB, Legan H, Murphy GA, Norton LA. Cephalometrics for orthognathic surgery. J Oral Surg 1978;36:269-77.
Guilleminault C, Riley R, Powell N. Obstructive sleep apnea and abnormal cephalometric measurements. Implications for treatment. Chest 1984;86:793-4.
Lowe AA, Santamaria JD, Fleetham JA, Price C. Facial morphology and obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986;90:484-91.
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.
Wiggins RV, Schmidt-Nowara WW. Treatment of the obstructive sleep apnea syndrome. West J Med 1987;147:561-8.
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.
Riley RW, Powell N, Guilleminault C. Current surgical concepts for treating obstructive sleep apnea syndrome. J Oral Maxillofac Surg 1987;45:149-57.
Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1981;1:862-5.
Sanders MH, Moore SE, Eveslage J. CPAP via nasal mask: A treatment for occlusive sleep apnea. Chest 1983;83:144-5.
Abbey NC, Cooper KR, Kwentus JA. Benefit of nasal CPAP in obstructive sleep apnea is due to positive pharyngeal pressure. Sleep 1989;12:420-2.
Pépin JL, Leger P, Veale D, Langevin B, Robert D, Lévy P. Side effects of nasal continuous positive airway pressure in sleep apnea syndrome. Study of 193 patients in two French sleep centers. Chest 1995;107:375-81.
Cartwright RD, Samelson CF. The effects of a nonsurgical treatment for obstructive sleep apnea. The tongue-retaining device. JAMA 1982;248:705-9.
Clark GT, Nakano M. Dental appliances for the treatment of obstructive sleep apnea. J Am Dent Assoc 1989;118:611-5, 617-9.
Liu Y, Zeng X, Fu M, Huang X, Lowe AA. Effects of a mandibular repositioner on obstructive sleep apnea. Am J Orthod Dentofacial Orthop 2000;118:248-56.
Tiner BD, Waite PD. Surgical and nonsurgical management of obstructive sleep apnea. Petersons Principles of Oral and Maxillofacial Surgery. 2 nd
ed., Vol. II, Ch. 63. 2004, p. 1297-30.
Lowe AA, Sjöholm TT, Ryan CF, Fleetham JA, Ferguson KA, Remmers JE. Treatment, airway and compliance effects of a titratable oral appliance. Sleep 2000;23 Suppl 4:S172-8.
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.
Thornton WK, Roberts DH. Nonsurgical management of the obstructive sleep apnea patient. J Oral Maxillofac Surg 1996;54:1103-8.
Bernhold M, Bondemark L. A magnetic appliance for treatment of snoring patients with and without obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1998;113:144-55.
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]