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Oral Appliance Therapy for Snoring and/or Obstructive Sleep Apnea PowerPoint Presentation
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Oral Appliance Therapy for Snoring and/or Obstructive Sleep Apnea

Oral Appliance Therapy for Snoring and/or Obstructive Sleep Apnea

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Oral Appliance Therapy for Snoring and/or Obstructive Sleep Apnea

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  1. Oral Appliance Therapy for Snoring and/or Obstructive Sleep Apnea Yuehua Liu, DDS, PhD, M.Ortho.RCS(Ed) Faculty of Dentistry, Tongji University Shanghai, China

  2. INTRODUCTION

  3. DEFINITIONS • Apnea • Sleep Apnea Syndrome • Obstructive Apnea • Central Apnea • Mixed Apnea • Hypopnea • Apnea-Hypopnea Index (AHI)

  4. EPIDEMIOLOGY OF SLEEP APNEA 2% women, 4% men (middle-aged) (AHI>5 with a history of daytime sleepiness) 9% women, 24% men (AHI>5 without regard to daytime sleepiness) Young T et al. New Engl J Med 1993;328:1230-5. 57% women, 78% men (AHI>5, 35-69 yrs, community-based) Olson LG et al. Am J Respir Crit Care Med 1995;152:707-10.

  5. Table. Prevalence of Sleep Apnea by Age and AHI Age(yr) AHI>5 AHI>15 Females Males Females Males <15 11% 16% 0 1% 25-60 21% 50% 4% 22% >60 58% 88% 32% 47%

  6. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  7. A Male to Female Ratio 10 : 1 (sleep clinic) 3 : 1 (community) Young T. et al. New Engl J Med 1993;328:1230-5 Redline et al. Am J Respir Crit Care Med 1994;149:723

  8. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  9. 1. Obesity is present in 60-90% of SAS patients (sleep clinic). Lugarsi et al. Reven Press, New York, 1990;25-36. 2. Obesity appears to increase the risk of SAS 10-14-fold. Bloom et al. Chest 1988;93:678. Wilhoit SC. Chest 1987;91:654-8. 3. Central body fat distribution may be particularly important. Millman RP et al. Chest 1995;107:362-6.

  10. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  11. 1. Data from the family study of the elderly demonstrated higher levels of RDIs in African Americans as compared with Caucasians. Redline S et al. Am J Respir Crit Care Med 1997;155:186-96. Ancoli-Israels et al. Am J Respir Crit Care Med 1995;152:1946-9. 2. Liu YH et al revealed more severe underlying cranifacial skeletal discrepancies in the Chinese group as compared with the Caucasian group by matching for age, gender, skeletal pattern, BMI, and AHI. Liu YH et al. Am J Orthod Dentofac Orthop 1999: in press.

  12. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  13. 1. Craniofacial features in OSA patients include facial elongation, posterior facial compression, reduced posterior and superior airway spaces, retrognathia, and inferior displacement of hyoid. Guilleminault C et al. Chest 1984;86:793-4. Lowe AA et al. Am J Orthod Dentofac Orthop 1986;90:481-91 Prackarktam N.Angle Orthod 1994;64:63-73 2. A brachycephalic head form is associated with reduced airway dimensions in Caucasians. Tishler PV et al. AM J Respir Crit Care Med 1996;153:1857-63). 3. Studies have incorporated cephalometric data to improve OSA prediction. A family study has shown that anatomic factors may interact with physiological risk to increase the expression of OSA. El-Bayadi S et al. Chest 1990;98:554-9.

  14. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  15. 1. Airway patency is influenced dynamically by a variety of complex processes associated with the control of both chest wall and upper airway neuromuscular function. Some of those processes may be closely related to the responses to respiratory chemical and mechanical loading. Dempsey IS. Am Rev Respir Dis 1986;133:1163-70 2. Blunted chemosensitivity could contribute to prolonging the duration of apneas or lead to the propagation of apneas during sleep , or both. Kunitomo F et al. Am Rev Respir Dis 1989;139:164-9.

  16. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  17. 1. A low vital capacity has been identified as a risk factor for SAS in at least two community studies. Bliwise DL et al. Chest 1991;99:600-8. 2. SAS has also been reported to be more frequent in children with asthma. Linder-Aronson S et al. 1983;71:149-66.

  18. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  19. 1. Family studies have suggested that the risk of SAS may be twofold to fourfold greater in relatives of patients with SAS as compared with controls and that nearly 40% of the variance in the AHI may be explained by familial factors. Redline S et al. AM J Respir Crit Care Med 1995;155:682-7. 2. There may be physiological factors or unmeasured anatomic factors that are both inherited and predispose to SAS. 3. In addition, there are relatively rare genetic syndromes that are associated with SAS, such as Marfan’s disease, Down syndrome, and Pirre Robin syndrome.

  20. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  21. 1. It has been speculated that hypertension may alter neurogenic reflexes or brain stem integration of neural signals, predisposing to breathing instability and apneas. 2. Vascular disease, through their effects on cardiac and cerebral function, may alter respiratory stability, also increasing SAS risk. 3. Diabetes and insulin resistances are associated with central obesity, which in turn is related to SAS. Thus, these conditions, through general effects on cardiopulmonary function, metabolism, and fat distribution, may predispose to SAS.

  22. RISK FACTORS • Male Gender • Obesity and Body Fat Distribution • Race • Craniofacial Morphology • Ventilation Control Pattern • Underlying Pulmonary Dysfunction • Family and Genetic Risk • Metabolic and Vascular Disease • Environmental Exposure

  23. 1. Tobacco smoke and various irritants or allergens present in the work or home environment could increase upper airway mucosal congestion. Wetter D et al. Arch Intern Med 1994;154:2219-24 2. Alcohol intake and hypnotic and sedative medications are exposures that may reduce upper airway neuromuscular drive, increasing the propensity for apneas.

  24. CLINICAL CONSEQUENCES OF OSA Obstructive Sleep Apnea Sleep fragmentation Hypoxia/hypercapia Excessive daytime sleepiness Cardiovascular dysfunction Morbidity Mortality

  25. SLEEPINESS AND PERFORMANCE 1. EXCESSIVE DAYTIME SLEEPINESS Excessive sleepiness is the presenting complaint of the majority of patients evaluated in sleep disorders centers and is present in up to 90% of patients with OSA Roth T et al. Semin Repir Med 1988;554-9. 2. PERFORMANCE AND NEUROCOGNITIVE EFFECTS Hypersomnolence caused by sleep deprivation or sleep fragmentation has been shown to cause significant impairment of daytime functioning in normal subjects, with decrement in memory, intellectual capacity, motor coordination, and mood. Roehrs T. Sleep 1990;13:395-402.

  26. SLEEPINESS AND PERFORMANCE 3. QUALITY OF LIFE The combination of sleepiness, performance and cognitive decrements, and mood alterations adversely affects OSA patients’ perception of their quality of life. OSA patients report greater sickness-related behavioral limitations, lower social functioning, and poorer psychological adjustment to illness, even with mild OSA. 4. MOTOR VEHICLE ACCIDENTS Sleepiness has been identified as a contributing factor to driving accidents. OSA patients have as seven times greater rate of MVAs than do controls with normal sleep studies and an eight times greater rate of fault MVAs. Am Thoratic Society. Am J Respir Crit Care Med 1994;150:1463-73. Findley et al.Clin Chest Med 1992;13:427-35.

  27. CARDIOVASCULAR DYSFUNCTION 1. A causal link between OSA and hypertension pulmonary and systemic is better substantiated. Patients with systemic hypertension should be questioned for clinical features of OSA and evaluated with sleep studies if the symptoms are severe, particularly if the hypertension is difficult to control. 2. Several line of evidence suggest that OSA can reduce lifespan. First, OSA can lead to disorders known to increase mortality such as systemic and pulmonary hypertension. Second, published reports so suggest that OSA may result in early death if untreated, and clinical anecdotes suggest that severe OSA may contribute to sudden death, particularly during sleep.

  28. PATHOPHYSIOLOGY FOR OSA

  29. LOCATION OF COLLAPSE Studies have characterized the location of collapse at either retropalatal or retroglossal sites. Slightly more than half of the patients showed retropalatal collapse and the rest had collapse in the oropharynx. The site of upper airway collapse differs among patients and may not stay constant even within the same patient during all stages of sleep. Therefore, it appears that collapse may occur along with the entire length of the upper airway in OSA. Shepard JW et al. Am Rev Respir Dis 1990;141:1350-5. Hudgel DW et al. J Appli Physiol 1986;61:1403-9

  30. NEUROMUSCULAR FACTORS Reflexes: chemical, pressure, postural. CNS Depressants: anesthetics, alcohol, sedatives. Neuromodulators: protrityline, serotonin.

  31. STRUCTURAL FACTORS Elongation: tracheal traction, neck extension. Dilation/compression: adiposity, adenotonsillar hypertrophy, retrognathia, and macroglossia.

  32. DIAGNOSTIC STRATEGIES

  33. PRETEST PROBABILITIES

  34. POLYSOMNOGRAPHY (PSG)

  35. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  36. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  37. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  38. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  39. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  40. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  41. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  42. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  43. BEHAVIOR MANAGEMENT OF OSA • Sleep and driving • Weight loss as treatment for OSA • Nasal sprays • Smoking cessation as treatment for OSA • Body position and sleep • Medical treatment • Avoidance of fatigue • Avoidance of alcohol and other muscular relaxants

  44. CONTINUOUS POSITIVE AIRWAY PRESSURE (CPAP)

  45. MECHANISM OF CPAP

  46. EFFICACY AND SIDE EFFECTS OF CPAP

  47. SURGERY FOR OSA I. Soft-tissue surgery II. Hypopharyngeal airway surgery

  48. SURGICAL INDICATIONS The American Sleep Disorders Association (ASDA) made recommendations that include. 1. patients who have an underlying specific abnormality that is causing the sleep apnea. 2. patients for whom noninvasive medical therapies have been unsuccessful or have been rejected, who desire therapy, and who are medically stable enough to undergo the procedure. 3. patients with mild OSA (RDI<20) who have refused or rejected medical therapy, who desire therapy, and who are medically stable enough to undergo the procedure. Sleep 1996:19(2):152-5.

  49. SOFT-TISSUE SURGERY FOR OSA • Uvulopalatopharyngoplasty (UPPP) • Uvulopalatopharyngoglossoplasty (UPPGP) • Laser-assisted uvulopalatoplasty (LAUP) • Laser midline glossectomy (LMG) • Linguoplasty