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Obstructive sleep apnea (OSA) is a potentially serious sleep disorder that causes breathing to repeatedly stop and start during sleep. There are several types of sleep apnea, of which OSA is the most common. OSA occurs when the throat muscles intermittently relax and block the airway during sleep. Patients with normal upper-airway anatomy typically do not have sleep apnea.1 OSA is a common chronic disorder that often requires lifelong care and multidisciplinary management.
During routine dental evaluations, patients should be asked questions to aid in detection of OSA. Before treatment is initiated, the presence or absence and severity of OSA must be determined through a comprehensive sleep analysis. After the diagnosis is established, the patient should be consulted on the decision for an appropriate treatment strategy, which may include positive airway pressure devices, oral appliances, behavioral treatments, surgery, and/or adjunctive treatments.2
OSA has profound effects on the health and well-being of those who have the condition. Typical nocturnal signs and symptoms of OSA include snoring, observed apnea, waking with a sensation of choking or gasping, unexplained tachycardia, restless sleep, sweating during sleep, nocturia, bruxism, nocturnal gastroesophageal reflux, insomnia, disrupted sleep, sleep walking, and sleep terrors. Symptoms of OSA can also occur during the day and may include excessive daytime sleepiness, forgetfulness, impaired concentration and attention, personality changes, and morning headaches.3
OSA is thought to be more prevalent in men than in women; it occurs in 2% of female and 4% of male adults, with a considerable number of affected individuals remaining undiagnosed.4 Some studies show prevalence as high as 20% in men aged 40 to 59 years and postmenopausal women.5-7 OSA prevalence is positively correlated with age and obesity.8 In epidemiologic studies, the prevalence of OSA has increased over time. This increase has been likely due to changes in diagnostic equipment, definitions, study design, and characteristics of subjects, including effects of the obesity epidemic.8 Although most symptoms are mild, OSA is related to cardiovascular disease and stroke and is correlated with an increased risk of early death in patients younger than 70 years.8,9
Continuous Positive Airway Pressure
Medical, behavioral, and surgical options are available for the treatment of OSA. The current standard of care for patients with OSA is nasal continuous positive airway pressure (CPAP). However, poor adherence to CPAP limits its clinical effectiveness, leading to a need for additional therapeutic options. A strong demand for new OSA therapies exists, and several are emerging. Oral appliances, which include mandibular advancement devices, have variable success rates in the treatment of sleep apnea.
Positive airway pressure provides pneumatic splintering of the upper airway and is effective in reducing the apnea-hypopnea index (AHI).10 It can be delivered in continuous (CPAP), bilevel (BPAP), or autotitrating (APAP) modes. CPAP is a common treatment that has been shown to eliminate respiratory disturbances, thereby reducing the AHI compared with placebo, conservative management, and positional therapy.10
Efficient CPAP treatment requires regular CPAP use, and adherence is often not ideal. A major clinical trial found relatively low long-term adherence to nasal CPAP, from 40% to 80% depending on the usage metric employed.11 Adherence is often higher in older individuals and women.12 Studies find nasal resistance is a reason for noncompliance in CPAP usage (also for noncompliance to mandibular advancement therapy).13,14
Oral Appliance Alternatives
Various oral appliances have emerged as alternatives to CPAP for OSA treatment, such as SomnoDent® (SomnoMed, somnomed.com), Respire (Whole You™, respiremedical.com, and the O2Vent™ with Oventus™ Airway Technology (Oventus, oventusmedical.com). CPAP and Oventus Airway Technology both focus on air flow; the former pumps air through, whereas the latter allows air to flow through the oropharynx with an almost identical effect on airway collapsibility. Airway phenotype is an important predictor of CPAP alternative therapy success.15,16
Mandibular advancement devices bring the jaw forward to improve the position of the tongue base. These devices have an impact on sleep apnea caused by the tongue base, as well as some effect on obstruction or resistance in the soft palate and epiglottis. Another anatomic factor may be nasal obstruction (Figure 1). In the case of nasal obstruction, inhalation leads to large negative pressure swings developing in the oropharynx. Negative pressure swings in the oropharynx can cause fragmented sleep and soft-palate collapse. This in turn may lead to a very unstable airway and mouth breathing, which can be highly problematic, potentially resulting in poor oxygen concentration in the bloodstream. Low oxygen concentration in the blood has been associated with high blood pressure and cardiac failures.17-19 When mouth breathing occurs as a response to increased nasal resistance or negative pressure swings, the base of the tongue collapses (hypoglossal collapse) and the lack of oral seal leads to dry mouth and other dental issues. Furthermore, soft-palate collapse and nasal obstruction can negatively affect current treatment options for sleep apnea.20 There are also situations in which nasal congestion or obstruction and multiple levels of collapse, such as soft-palate and lateral-wall collapse, cannot be addressed effectively by simply bringing the jaw forward.
In addition to addressing soft palate, tongue base, and epiglottal challenges, Oventus Airway Technology addresses nasal obstructions and lateral-wall collapses in a way that mandibular advancement devices do not. When an Oventus Airway is incorporated into an oral appliance, there may still be cases of nasal resistance and soft-palate collapse (Figure 2). In this situation, instead of switching to mouth breathing with unstable ventilation, the switch is to device breathing, which provides stable ventilation and stable oxygen saturations. When the switch to device breathing occurs, the oral seal is maintained, as well as a stable jaw position and normal ventilation (Figure 3). Importantly, nose breathing remains possible.
The goal of Oventus Airway and similar technology is to make oral appliance therapy more effective, particularly for patients with increased nasal obstruction or multiple levels of collapse. As described, the method of prevention varies across technologies. The materials these technologies are composed of may also impact their effectiveness; therefore, it is important to research devices based on their materials in addition to method. Oventus Airway, for example, is printed in titanium with extremely thin sectional walls and is often less bulky than standard dorsal devices.
In addition to the aforementioned anatomic factors, there are non-anatomic factors involved in sleep apnea; these factors relate to muscle control, reduced arousal threshold, and ventilatory instability.3 Between 30% and 50% of all patients with OSA have a low respiratory-arousal threshold.3 A low threshold for arousal to airway narrowing is thought to cause OSA through the destabilizing effects of repeated arousals. These destabilizing effects include decreased sleep continuity and the prevention of a deeper, more stable sleep; excessive reductions in partial pressure of carbon dioxide, promoting dynamic ventilatory instability; and decreased respiratory drive to the upper-airway muscles.21
Behavioral Strategies
Behavioral strategies for treatment of OSA may include weight loss, exercise, positional therapy, and the avoidance of alcohol and sedatives before bed.22 For obese patients, even modest reductions in body weight are associated with changes in OSA, with a 10% reduction in body weight predicting an approximate change of 26% to 32% in the AHI.23 Other individuals may experience sleep apnea primarily when sleeping in the supine position. Positional therapy may involve wearing a special device around one's waist or back, which renders compliance as a major factor in treatment effectiveness.24Alcohol intake reduces motor output to the upper airways, with hypotonia of the oropharyngeal muscles as a result.25 In studies performed in the laboratory, alcohol increases both the number of apneas and the duration of apnea.26,27
Surgery
Surgery is another treatment option for OSA. Not everyone is a good candidate for surgery. Surgical procedures address blockage of breathing in the throat, either in the area behind the soft palate (roof of the mouth), behind the tongue and epiglottis, or both. Palate procedures for sleep apnea generally involve tonsil removal or repositioning of the soft palate, uvula, and soft tissues next to the palate and tonsils on the side of the throat.28 Hypopharyngeal procedures treat the area of the throat behind the tongue and epiglottis. Inspire® Upper Airway Stimulation (Inspire Medical Systems, inspiresleep.com) involves surgery to place a medical device inside the body that will function somewhat like a pacemaker for the tongue during sleep.29 Jaw advancement surgery treats sleep apnea by moving the upper and lower jaws forward, thereby enlarging the space for breathing in the throat.30
Conclusion
Sleep medicine is a relatively new and highly multidisciplinary field. Understanding of the nature and consequences of upper-airway obstruction during sleep continues to evolve, as do treatment options. A variety of devices that serve as treatment options are on the market or will be soon. Treatment should be specialized for the individual, depending on specific circumstances. Treatment often requires the cooperation of professionals with different areas of expertise, such as dentists and physicians with various specialties; everyone involved in OSA therapy must understand it well.
About the Author
Chris Hart, BSc, BDSc (Hons), MPhil (Cantab)
Chris Hart invented the O2Vent in 2012 and founded Oventus in 2014. Oventus is an Australian medical device company with a proprietary technology for the treatment of obstructive sleep apnea. Hart is currently clinical director at Oventus Medical, overseeing the clinical trial program of sponsored and independent trials and managing the clinical rollout of the O2Vent range of products in Australasia, North America, and Europe.
References
1. Schwab RJ, Gupta KB, Gefter WB, et al. Upper airway soft tissue anatomy in normal subjects and patients with sleep-disordered breathing. Significance of the lateral pharyngeal walls. Am J Respir Crit Care Med. 1995;152(5 pt 1):1673-1689.
2. Epstein LJ, Kristo D, Strollo PJ Jr, et al; Adult Obstructive Sleep Apnea Task Force of the American Academy of Sleep Medicine. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. J Clin Sleep Med. 2009;5(3):263-276.
3. Eckert DJ, White DP, Jordan AS, et al. Defining phenotypic causes of obstructive sleep apnea. Identification of novel therapeutic targets. Am J Respir Crit Care Med. 2013;188(8):996-1004.
4. Stierer T, Punjabi NM. Demographics and diagnosis of obstructive sleep apnea. Anesthesiol Clin North America.2005;23(3):405-420.
5. Kryger MH, Roth T, Dement WC, et al. Epidemiology of sleep disorders. In: Kryger MH, Roth T, Dement WC, eds. Principles and Practice of Sleep Medicine. 4th ed. Philadelphia: Elsevier; 2005:626-647.
6. Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-1235.
7. Phillips BA, Berry DT, Schmitt FA, et al. Sleep-disordered breathing in healthy aged persons: two- and three-year follow-up. Sleep. 1994;17(5):411-415.
8. Franklin KA, Lindberg E. Obstructive sleep apnea is a common disorder in the population-a review on the epidemiology of sleep apnea. J Thorac Dis. 2015;
7(8):1311-1322.
9. Costanzo MR, Khayat R, Ponikowski P, et al. Mechanisms and clinical consequences of untreated central sleep apnea in heart failure. J Am Coll Cardiol. 2015;65(1)72-84.
10. Gay P, Weaver T, Loube D, Iber C; Positive Airway Pressure Task Force, Standards of Practice Committee, American Academy of Sleep Medicine. Evaluation of positive airway pressure treatment for sleep related breathing disorders in adults. Sleep. 2006;29(3):381-401.
11. Kushida CA, Littner MR, Hirshkowitz M, et al; American Academy of Sleep Medicine. Sleep. 2006;29(3):375-380.
12. Sin DD, Mayers I, Man GC, Pawluk L. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest. 2002;121(2):430-435.
13. Sugiura T, Nora A, Nakata S, et al. Influence of nasal resistance on initial acceptance of continuous positive airway pressure in treatment for obstructive sleep apnea syndrome. Respiration. 2007;74(1):56-60.
14. Zeng B, Ng AT, Qian J, et al. Influence of nasal resistance on oral appliance treatment outcome in obstructive sleep apnea. Sleep. 2008;31(4):543-547.
15. Milano F, Billi MC, Marra F, et al. Factors associated with the efficacy of mandibular advancing device treatment in adult OSA patients. Int Orthod. 2013;11(3):278-289.
16. Friedman M, Ibrahim H, Bass L. Clinical staging for sleep-disordered breathing. Otolaryngol Head Neck Surg. 2002;127(1):13-21.
17. Andreas S, von zur Mühlen F, Stevens J, Kreuzer H. Nocturnal oxygen and hypercapnic ventilatory response in patients with congestive heart failure. Respir Med.1998;92(3):426-431.
18. Agostoni P, Bussotti M, Cattadori G, et al. Gas diffusion and alveolar-capillary unit in chronic heart failure. Eur Heart J. 2006;27(21):2538-2543.
19. Naughton MT, Lorenzi-Filho G. Sleep in heart failure. Prog Cardiovasc Dis. 2009;51(4):339-349.
20. Prescinotto R, Haddad FL, Fukuchi I, et al. Impact of upper airway abnormalities on the success and adherence to mandibular advancement device treatment in patients with Obstructive Sleep Apnea Syndrome. Braz J Otorhinolaryngol.2015;81(6):663-670.
21. Eckert DJ, Younes MK. Arousal from sleep: implications for obstructive sleep apnea pathogenesis and treatment. J Appl Physiol.2014;116(3):302-313.
22. Morgenthaler TI, Kapen S, Lee-Chiong T, et al. Practice parameters for the medical therapy of obstructive sleep apnea. Sleep. 2006;29(8):1031-1035.
23. Peppard PE, Young T, Palta M, et al. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA. 2000;284(23):3015-3021.
24. Heinzer RC, Pellaton C, Rey V, et al. Positional therapy for obstructive sleep apnea: an objective measurement of patients' usage and efficacy at home. Sleep Med. 2012;13(4):425-428.
25. Krol RC, Knuth SL, Bartlett D, Jr. Selective reduction of genioglossal muscle activity by alcohol in normal human subjects. Am Rev Respir Dis.1984;129(2):
247-250.
26. Issa FG, Sullivan CE. Alcohol, snoring and sleep apnea. J Neurol Neurosurg Psychiatry. 1982;45(4):353-359.
27. Dolly FR, Block AJ. Increased ventricular ectopy and sleep apnea following ethanol ingestion in COPD patients. Chest. 1983;83(3):469-472.
28. 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):923-934.
29. Van de Heyning PH, Badr MS, Baskin JZ, et al. Implanted upper airway stimulation device for obstructive sleep apnea. Laryngoscope. 2012;122(7):1626-1633.
30. Sher A, Schechtman KB, Piccirillo JF. The efficacy of surgical modification of the upper airway in adults with obstructive sleep apnea syndrome. Sleep. 1996;19(2):156-177.
