Obstructive Sleep Apnea Syndrome: Diagnosis and Management

• Reginald H.B. Goodday, DDS, MSc, FRCD(C) •
• David S. Precious, DDS, MSc, FRCD(C ) •
• Archibald D. Morrison, DDS, MSc, FRCD(C) •
• Chad G. Robertson, DDS •


Increased awareness that changes in sleeping habits and daytime behaviour may be attributable to obstructive sleep apnea syndrome (OSAS) has led many patients to seek both information and definitive treatment. The purpose of this article is to provide information to dentists that will enable them to identify patients who may have OSAS and to assist these patients in making informed decisions regarding treatment options. In patients who have identifiable anatomic abnormalities of the maxilla and mandible resulting in a narrow pharyngeal airway, orthognathic surgery appears to be an excellent treatment option.

MeSH Key Words: sleep apnea, obstructive/diagnosis; sleep apnea, obstructive/surgery

© J Can Dent Assoc 2001; 67(11):652-8
This article has been peer reviewed.

An increasing number of people are realizing that changes in their sleeping habits and daytime behaviour may be attributable to obstructive sleep apnea syndrome (OSAS). This new awareness has led many patients to seek both information and definitive treatment. Because the jaws and related structures influence the development of this syndrome, dentists play an important role in both identifying patients who should be assessed by sleep specialists and instituting treatment in selected cases. The purpose of this article is to provide information to dentists that will enable them to identify patients who may have OSAS and to assist these patients in making informed decisions regarding treatment options.


OSAS is characterized by repetitive episodes of upper airway obstruction that occur during sleep usually in association with a reduction in blood oxygen saturation.1 The prevalence of OSAS in the middle-aged population (30 to 60 years) is 4% in men and 2% in women.2 However, prevalence rises dramatically with age, to an estimated 28% to 67% for elderly men and 20% to 54% for elderly women.3

Clinical Manifestations

The clinical manifestations of OSAS are related to obstruction of the upper airway, fragmented sleep, and the respiratory and cardiovascular consequences of disordered breathing. Excessive daytime somnolence is a key feature of OSAS resulting from disrupted sleep. Patients may report that they frequently fall asleep during the day while driving, working, reading and watching television.4 Thus, performing activities related to transportation or the use of machinery and heavy equipment can put both the patient and others at significant risk of injury.5,6 Chronic daytime sleepiness also leads to poor work performance and decreased productivity. Snoring, ranging in severity from mild to extremely loud, is invariably present. The partners of people with OSAS may witness gasping, choking or periods of apnea, with repeated arousals through the night. In many cases these symptoms are significant enough that the partner sleeps in another room. When questioned in the morning the patient is usually unaware of the frequency of arousals. Other complaints include a feeling of not being rested despite a full night of sleep, dry mouth, morning headaches, absence of dreams, fatigue, decreased libido and symptoms of depression.

The respiratory consequences of OSAS are related to the extent of hypoxemia and hypercapnia that develop as a result of the disordered breathing. Advanced cases of OSAS are associated with pulmonary hypertension, corpulmonale, chronic carbon dioxide retention and polycythemia.7 The cardiovascular consequences of OSAS may include systemic hypertension, cardiac arrhythmias, myocardial infarction, and cerebral vascular accidents, all of which lead to a higher mortality rate than in the general population.8,9

Clearly, OSAS can be a debilitating and potentially life-threatening condition. Thus, both proper diagnosis and appropriate treatment are important.

Diagnostic Tools

The dental office can play an important role in screening patients who may have OSAS by including 2 questions on the medical questionnaire: Do you snore loudly? Do you have difficulty staying awake when you are inactive (e.g., while reading, watching television or driving)? A positive response to these 2 questions should lead the dentist to suspect OSAS. Additional questions should then be asked to help identify the extent of the problem: Has your partner witnessed pauses in your breathing while you are asleep? Have you fallen asleep in a potentially dangerous situation? Has your work performance suffered? Has your concentration, memory or mood been affected?

If the history supports the diagnosis of OSAS, the patient should be referred to a sleep disorders laboratory for overnight polysomnography, the objective method of establishing the diagnosis and assessing the potential success of treatment. The most important variables used in determining the presence and severity of OSAS are the apnea index, the hypopnea index, the respiratory disturbance index (RDI) and the lowest oxyhemoglobin saturation.10 Apnea is defined as cessation in air flow for 10 seconds or more, and the apnea index is the number of apneic episodes occurring in a 1-hour period.11 Hypopnea has been defined as a 50% reduction in tidal volume for more than 10 seconds, and the hypopnea index is the number of hypopneic episodes in a 1-hour period.11 The RDI is defined as the number of apneic and hypopneic episodes per hour of sleep.11 The lowest oxyhemoglobin saturation is simply the lowest oxygen saturation measured by pulse oximetry during the study. OSAS is diagnosed if the RDI reaches a certain threshold level, typically 5 or 10.3,11 OSAS becomes clinically significant when the RDI is greater than 20 and oxygen desaturation events fall to a level below 80% to 85%.12


Obstructive sleep apnea can be caused by an anatomic abnormality that narrows or obstructs the airway. Investigations to localize the site of functional obstruction in the upper airway have shown that there is rarely a single site of occlusion. Obstruction more commonly occurs at multiple levels of the upper airway during episodes of hypopnea and apnea13 (Figs. 1a, 1b).

In any patient, upper airway patency is maintained through many interrelated anatomic and physiologic factors.14 Normally, negative intrapharyngeal pressure develops during inspiration. Collapse of the airway is prevented by the action of the pharyngeal abductor and dilator muscles. The pharynx consists of 3 segments: the nasopharynx, the oropharynx and the hypopharynx. The muscles become hypotonic during sleep, and airway stability becomes dependent on pharyngeal size and pharyngeal tissue compliance in these 3 segments.14,15 If the compliance of the soft tissues in the narrowed segments of the passive airway is inadequate to offset the negative intraluminal pressure created during inspiration, airway obstruction occurs. As a result, the central nervous system adjusts to a lighter level of sleep by increasing muscle tone to allow opening of the airway and resumption of the breathing cycle.

Once the diagnosis of OSAS has been confirmed but before treatment is instituted, upper airway imaging is often performed to obtain additional information regarding the anatomy of the airway. For example, clinical examination does not always reveal a gross facial deformity (Fig. 2), but cephalometric radiography can help in determining the anatomic factors contributing to OSAS. This information can then be used to direct treatment, particularly surgery, and may lead to more predictable treatment outcomes. Studies involving cephalometric radiography in patients with OSAS have demonstrated that these patients have smaller retropositioned mandibles, narrower posterior airway spaces, and larger tongues and soft palates than control patients, as well as inferiorly positioned hyoid bones and retropositioned maxillae.16


OSAS can be managed nonsurgically or surgically. The treatment should target the potential contributing factors identified by the history, the physical examination and upper airway imaging. The severity of the patient’s condition must also be considered in developing a treatment plan.

Nonsurgical Management

Because obesity is a risk factor for OSAS, a reduction in body weight can reduce sleep apnea.17,18 However, the patient may have difficulty losing weight, particularly in more severe cases, because excessive daytime somnolence and fatigue may discourage the patient from exercising. The severity of the OSAS may have to be reduced through some other form of treatment before an exercise program can be started. It is important to note, however, that many patients with OSAS are not obese (Fig. 2).

The most successful nonsurgical treatment is continuous positive airway pressure (CPAP). The use of CPAP in the treatment of OSAS was first described in 1981.19 Since then it has become the gold standard in the treatment of this condition.10 However, because of physical discomfort associated with wearing the unit, drying of the nasal and oral mucosal membranes, dislodgement during sleep, noise and the social consequences of using the unit, compliance may be as low as 46%.20

Oral appliances can also be used in the treatment of OSAS.21 A review of 20 studies, involving a total of 304 patients, revealed that oral appliances were effective in 51% of cases, as defined by achievement of an RDI of less than 10.22 In 2 studies that compared oral appliances for mandibular advancement with CPAP, the oral appliances were effective in mild to moderate cases but were less effective than nasal CPAP in more severe cases.23,24 In both these studies the patients strongly preferred the oral appliance over nasal CPAP for reasons of comfort. The most significant negative long-term effects of oral appliances are temporomandibular joint problems and movement of teeth.25-27 Tooth movements may result in a posterior open bite and decreased anterior overjet.21

Other nonsurgical treatments for OSAS include medications such as protriptyline and medroxyprogesterone. Protriptyline, a tricyclic antidepressant, has shown reasonable symptomatic improvement of OSAS and may reduce the degree of oxygen desaturation, but anticholinergic side effects and incomplete efficacy limit its use.7 Medroxyprogesterone has limited value in the treatment of OSAS but it may be effective in cases of obesity hypoventilation syndrome with chronic hypercapnia.7

Surgical Management

Tracheostomy was the first successful surgical treatment for OSAS. It was introduced for this purpose in the 1970s.28 This procedure, which bypasses the upper airway, is successful in virtually 100% of cases.29 Complications associated with tracheostomy include hemorrhage, recurrent infections, airway granulations, and tracheal or stomal stenosis.29 The medical and obvious social problems associated with tracheostomy have stimulated the search for alternatives.7

Fujita and others30 first described the use of the uvulopalatopharyngoplasty (UPPP) for the treatment of OSAS in 1981. This procedure involves shortening the soft palate, amputating the uvula, and removing redundant lateral and posterior pharyngeal wall mucosa from the oral pharynx. Despite the popularity of this procedure, reviews have reported improvement in less than 50% of patients and complete control of OSAS in 25% or less.31,32 Postoperative lateral cephalometric radiographs of patients who have undergone UPPP and whose symptoms persist reveal that the soft palate has been shortened but is much thicker, which results in a narrow nasopharyngeal airway (Fig. 3). The unsatisfactory results obtained with UPPP have contributed to the realization that there are usually multiple sites of obstruction in the upper airway. When patients are selected on the basis of retropalatal obstruction demonstrated by computed tomography during wakefulness or by catheter measurements of nasal pharyngeal pressure, the success rate of UPPP is only 50%.16

UPPP also carries a risk of significant hemorrhage, and patients report substantial postoperative pain, which may last for an extended period. Velopharyngeal insufficiency and nasophyaryngeal stenosis may also complicate UPPP.10

Use of orthognathic surgery to treat OSAS began toward the end of the 1970s, when mandibular advancement was reported to have reversed the symptoms of OSAS.33,34 Since then, this procedure has become widely accepted.11,35-42 Orthognathic treatment for OSAS may involve advancement of the maxilla, mandible or chin (Fig. 4). These 3 procedures can be performed in any combination, but advancement of the maxilla and the mandible, with or without advancement genioplasty, is the most common procedure. The treatment plan is based on craniofacial cephalometric analysis, which determines whether the position of the maxilla, mandible and chin are normal or abnormal. The architectural and structural craniofacial analysis of Delaire43 allows precise planning of the surgical advancement to maximize the increase in pharyngeal dimensions while maintaining normal facial balance.

Hochban and others35 reported a series of 38 consecutive patients with OSAS treated by 10 mm maxillomandibular advancement. Patients were selected on the basis of the results of lateral cephalometric radiography; those who had pharyngeal narrowing, with or without retrognathic mandibles, were offered the procedure. Polysomnographic sleep studies were performed preoperatively and 2 months after surgery. In 37 of the 38 patients, postoperative RDI was reduced to below 10.

Waite and others44 performed maxillomandibular advancement in 23 patients with obstructive sleep apnea. All of the patients had preoperative RDI of greater than 20 and some form of craniofacial deformity. Adjunctive procedures such as partial turbinectomy, septal reconstruction and advancement genioplasty were also performed, depending on individual variation. Sleep studies were performed and lateral cephalometric measurements obtained 1 and 6 weeks after surgery. Surgical success, defined as RDI of less than 10, was 65%, although 96% of the patients showed both subjective and objective improvement.

Goodday and others45 compared preoperative and postoperative cephalometric radiographs in 25 consecutive patients who had undergone orthognathic surgery for the treatment of OSAS. The median increase in the distance between the posterior pharyngeal wall and the soft palate was 100%. Similarly, the median increase in the distance between the posterior pharyngeal wall and the base of tongue was 81%. These findings help explain why selected patients experience improvement after orthognathic surgery.

Robertson and others46 studied subjective outcomes after maxillomandibular advancement for the treatment of OSAS. Twenty-four patients completed a questionnaire a mean of 24 months after surgery. They reported an improvement in daytime sleepiness from the levels seen in patients with severe OSAS to levels similar to those seen in normal controls. Statistically significant reductions were observed in the number of patients reporting problems with memory, concentration and stress. Of patients who snored preoperatively, 45% stopped snoring and 45% reported a reduction in snoring severity.

Compliance is not a factor in the success of orthognathic surgery as it is for CPAP and oral appliances. Relative to tracheostomy and CPAP, orthognathic surgery is more socially accepted. It is also more successful in treating severe OSAS than UPPP and oral appliances. Recent studies have demonstrated significant improvements in OSAS symptoms in patients who have undergone orthognathic surgery, and this procedure is associated with a high level of patient satisfaction and low risk.47


OSAS is a common condition associated with significant morbidity and mortality. It is therefore important that dental professionals be aware of the signs and symptoms of OSAS, so that the diagnosis can be confirmed and treatment initiated as soon as possible. As knowledge about the pathophysiology of OSAS improves, treatments may be designed to address the specific causes of the condition. In patients with identifiable anatomic abnormalities of the maxilla and mandible resulting in a narrow pharyngeal airway, orthognathic surgery appears to be an excellent treatment option. 

Dr. Goodday is associate professor and head, division of oral and maxillofacial surgery, Dalhousie University.

Dr. Precious is professor and chair, department of oral and maxillofacial sciences, Dalhousie University; head, department of maxillofacial surgery, Queen Elizabeth II Health Sciences Centre (Victoria General Hospital) and director of the 6-year MD/MSc graduate oral and maxillofacial surgery programme, Dalhousie University.

Dr. Morrison is an assistant professor of oral and maxillofacial surgery, Dalhousie University.

Dr. Robertson is a resident in oral and maxillofacial surgery, Dalhousie University.

Correspondence to: Dr. Reginald H.B. Goodday, Division of Oral and Maxillofacial Surgery, Dalhousie University, Halifax, NS B3H 3J5. E-mail: reginald.goodday@dal.ca

The authors have no declared financial interest.


1. Diagnostic Classifications Steering Committee: The international classification system of sleep disorders diagnostic and coding manual. Rochester, MN: American Sleep Disorders Association, 1990.

2. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing in middle-aged adults. N Engl J Med 1993; 328(17):1230-5.

3. Goodday RH. Nasal respiration, nasal airway resistance, and obstructive sleep apnea syndrome. Oral Maxillofac Surg Clin North Am 1997; 9(2):167-77.

4. Bahammam A, Kryger M. Decision making in obstructive sleep-disordered breathing: putting it all together. Otolaryngol Clin North Am 1999; 32(2):333-48.

5. Findley LJ, Fabrizio MM, Knight H, Norcross BB, LaForte AJ, Surratt PM. Driving simulated performance in patients with sleep apnea. Am Rev Respir Dis 1989; 140(2):529-30.

6. George CF, Boudreau AC, Smiley A. Simulated driving performance in patients with obstructive sleep apnea. Am J Respir Crit Care Med 1996; 154(1):175-81.

7. Wiggins RV, Schmidt-Nowara WW. Treatment of the obstructive sleep apnea syndrome. West J Med 1987; 147(5):561-8.

8. He J, Kryger MH, Zorick FJ, Conway W, Roth T. Mortality and apnea index in obstructive sleep apnea. Experience in 385 male patients. Chest 1988; 94(1):9-14.

9. Shepard JW Jr. Hypertension, cardiac arrhythmias, myocardial infarction, and stroke in relation to obstructive sleep apnea. Clin Chest Med 1992; 13(3):437-58.

10. Troell RJ, Riley RW, Powell NB, Li K. Surgical management of the hypopharyngeal airway in sleep disordered breathing. Otolaryngol Clin North Am 1998; 31(6):979-1012.

11. Riley RW, Powell NB, Guilleminault C. Maxillary, mandibular, and hyoid advancement for treatment of obstructive sleep apnea: a review of 40 patients. J Oral Maxillofac Surg 1990; 48(1):20-6.

12. Riley RW, Powell N, Guilleminault C. Current surgical concepts for treating obstructive sleep apnea syndrome. J Oral Maxillofac Surg 1987; 45(2):149-57.

13. Guilleminault C, Hill MW, Simmons FB, Dewent WC. Obstructive sleep apnea: electromyographic and fiberoptic studies. Exp Neurol 1978; 62(1):48-67.

14. Remmers JE, DeGroot WJ, Sauerland EK, Anch AM. Pathogenesis of upper airway occlusion during sleep. J Appl Physiol 1978; 44(8):931-8.

15. Lowe AA, Santamaria JD, Fleetham JA, Price C. Facial morphology and obstructive sleep apnea. Am J Orthod Dentofacial Orthop 1986; 90(6):484-91.

16. Schwab RJ, Goldbert AN. Upper airway assessment: radiographic and other imaging techniques. Otolaryngol Clin North Am 1998; 31(6):931-68.

17. Loube DI, Loube AA, Mitler MM. Weight loss for obstructive sleep apnea: the optimal therapy for obese patients. J Am Diet Assoc 1994; 94(11):1291-5.

18. Strobel RJ, Rosen RC. Obesity and weight loss in obstructive sleep apnea: a critical review. Sleep 1996; 19(2):104-15.

19. Sullivan CE, Issa FG, Berthon-Jones M, Eves L. Reversal of obstructive sleep apnea by continuous positive airway pressure applied through the nares. Lancet 1981; 1(8225):862-5.

20. Sanders MH, Gruendl CA, Rogers RM. Patient compliance with nasal CPAP therapy for sleep apnea. Chest 1986; 90(3):330-3.

21. Millman RP, Rosenberg Cl, Kramer NR. Oral appliances in the treatment of snoring and sleep apnea. Otolaryngol Clin North Am 1998; 31(6):1039-48.

22. 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(6):501-10.

23. Clark GT, Blumenfeld I, Yoffe N, Peled E, Lavie P. A crossover study comparing the efficacy of continuous positive airway pressure with anterior mandibular positioning devices on patients with obstructive sleep apnea. Chest 1996; 109(6):1477-83.

24. Ferguson KA, Ono T, Lowe AA, Keenan SP, Fleetham JA. A randomized crossover study of an oral appliance vs nasal-continuous positive airway pressure in the treatment of mild-moderate obstructive sleep apnea. Chest 1996; 10(5)9:1269-75.

25. Panula K, Keski-Nisula, K. Irreversible alteration in occlusion caused by a mandibular advancement appliance: an unexpected complication of sleep apnea treatment. Int J Adult Orthodon Orthognath Surg 2000; 15(3):192-6.

26. Clark GT, Sohn JW, Hong CN. Treating obstructive sleep apnea and snoring: assessment of an anterior mandibular positioning device. J Am Dent Assoc 2000; 131(6):765-71.

27. Bloch KE, Iseli A, Zhang JN, Xie X, Kaplan V, Stoeckli PW, and other. A randomized, controlled crossover trial of two oral appliances for sleep apnea treatment. Am J Respir Crit Care Med 2000; 162(1):246-51.

28. Fee WE Jr, Ward PH. Permanent tracheostomy: a new surgical technique. Ann Otol Rhinol Laryngol 1977; 86(5 Pt 1):635-8.

29. Mickelson SA. Upper airway bypass surgery for obstructive sleep apnea syndrome. Otolaryngol Clin North Am 1998; 31(6):1013-23.

30. Fujita S, Conway W, Zorick F, Roth T. Surgical correction of anatomic abnormalities of obstructive sleep apnea syndrome: uvulopalatopharyngoplasty. Otolaryngol Head Neck Surg 1981; 89(6):923-34.

31. Guilleminault C, Hayes B, Smith L, Simmons FB. Palatopharyngoplasty and obstructive sleep apnea: a review of 35 cases. Bull Eur Physiopathol Respir 1983; 19(6):595-9.

32. Conway W, Fujita S, Zorick F, Sicklesteel J, Roehrs T, Wittig R, and other. Uvulopalatopharyngoplasty: one year follow-up. Chest 1985; 88(3):385-7.

33. Bear SE, Priest JH. Sleep apnea syndrome: correction with surgical advancement of the mandible. J Oral Surg 1980; 38(7):543-9.

34. Kuo PC, West RA, Bloomquist DS, McNeil RW. The effect of mandibular osteotomy in three patients with hypersomnia sleep apnea. Oral Surg Oral Med Oral Pathol 1979; 48(5):385-92.

35. Hochban W, Conradt R, Brandenburg U, Heitmann J, Peter JH. Surgical maxillofacial treatment of obstructive sleep apnea. Plast Reconstr Surg 1997; 99(3):619-26.

36. Riley RW, Powell NB, Builleminault C. Obstructive sleep apnea syndrome: a review of 306 consecutively treated surgical patients. Otolaryngol Head Neck Surg 1993; 108:117-25.

37. Powell NB, Riley RW. Obstructive sleep apnea: orthognathic surgery perspectives, past, present, and future. Oral Maxillofac Surg Clin North Am 1990; 2(4):843-56.

38. Powell NB, Riley RW, Guilleminault C. Maxillofacial surgery for obstructive sleep apnea. In: Partinan M, Guilleminault C, editors. obstructive sleep apnea syndrome: clinical research and treatment. New York: Raven Press; 1989. p. 153-82.

39. Riley RW, Powell NB, Guilleminault C. Obstructive sleep apnea syndrome: a surgical protocol for dynamic upper airway reconstruction. J Oral Maxillofac Surg 1993; 51(7):742-7.

40. Riley RW, Powell NB, Guilleminault C. Maxillofacial surgery and nasal CPAP. A comparison of treatment for obstructive sleep apnea syndrome. Chest 1990; 98(6):1421-5.

41. Riley RW, Powell NB, Guilleminault C, Nino-Murcia G. Maxillary, mandibular, and hyoid advancement: An alternative to tracheostomy in obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg 1986; 94(5):584-8.

42. Waite PD, Wooten V, Lachner J, Guyette RF. Maxillomandibular advancement surgery in 23 patients with obstructive sleep apnea syndrome. J Oral Maxillofac Surg 1989; 47(12):1256-61.

43. Delaire J, Schendel SA, Tulasne JF. An architectural and structural craniofacial analysis: a new lateral cephalometric analysis. Oral Surg Oral Med Oral Pathol 1981; 52(3):226-38.

44. Waite PD, Wooten V, Lachner J, Guyette RF. Maxillomandibular advancement surgery in 23 patients with obstructive sleep apnea syndrome. J Oral Maxillofacial Surg 1989; 47(12):1256-61.

45. Goodday RH, Precious DS, Morrison A, Robertson C. Post-surgical pharyngeal airway changes following orthognathic surgery in OSAS patients. J Oral Maxillofac Surg 1999; 57(8)Suppl. 1:80.

46. Robertson CG, Goodday R, Precious D, Morrison A, Shukla S. Subjective evaluation of orthognathic surgical outcomes in OSAS patients. J Oral Maxillofac Surg 2000; 58(8)Suppl. 1:57.

47. Precious DS, Lanigan DT, editors. Oral and Maxillofacial Surgery Clinics of North America: Risks and Benefits of Orthognathic Surgery. Philadelphia: WB Saunders; 1997. 9(2):133-278.

CDA Resource Centre

The Resource Centre has compiled an Information Package on Sleep Apnea. CDA members can order the package by contacting the Resource Centre at tel.: 1-800-267-6354 or (613) 523-1770, ext. 2223; fax: (613) 523-6574; e-mail: info@cda-adc.ca  There is a charge of $10 (plus tax) for the package.