Obstructive sleep apnea /certified fixed orthodontic courses by Indian dental academy

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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.

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Obstructive sleep apnea /certified fixed orthodontic courses by Indian dental academy

  1. 1. INDIAN DENTAL ACADEMY Leader in continuing dental education www.indiandentalacademy.com www.indiandentalacademy.com
  2. 2. Contents Introduction  Epidemiology  Normal upper airway anatomy  Etiology & pathogenesis  Clinical features  Diagnostic aids  Treatment modalities  Conclusion  www.indiandentalacademy.com
  3. 3. Introduction  Obstructive Sleep Apnea (OSA) was first described by Charles Dickens in The Pickwick papers in 1836  In 1906 William Osler said “ an extraordinary phenomenon in excessively fat young persons with an uncontrolled tendency to sleep www.indiandentalacademy.com
  4. 4.  In 1950’s the research in sleep disorders gained momentum after the works of Aserinsky, Klutman and Demat who also termed the REM and non – REM sleep  In 1956 Burwell first described the features of Obesity, hypersomnolesence, decreased alveolar ventilation and cor pulmonale, now termed OSA, termed it as Pickwickan syndrome  In 1980’s research showed high incidence of mortality and also oral appliances came into being www.indiandentalacademy.com
  5. 5.  Obstructive sleep apnea syndrome-  Characterized by constellation of s/s related to arterial oxygen desaturation & sleep fragmentation caused by pharyngeal obstruction during sleep.  Potentially life threatening condition  Periodic cessation of breathing during sleep inspite of inspiratory effort.  Significant morbidity www.indiandentalacademy.com
  6. 6.  It was 1st described by Gastaut- disorder associated with repetitive cessation of breathing during sleep.  Sleep apnea defined as 30 or more apneic episodes (cessation of airflow for more than 10 sec) occurring during 7hrs of nocturnal sleep.  Most common is obstructive type. www.indiandentalacademy.com
  7. 7.  Reduced blood oxygen saturation leads to Hypertension  Cardiac arrhythmias  Nocturnal angina  Myocardial ischemia  Impaired sleep quality leads to-  Reduced concentration  Risk of falling asleep during day  Behavioral changes www.indiandentalacademy.com
  8. 8.  Related to orthodontics-  Peculiar cranio-facial & soft tissue morphology  Non-invasive modes of therapy i.e dental appliances used in treatment of syndrome. www.indiandentalacademy.com
  9. 9.  Snoring- produced by vibration of soft palate or oropharyngeal tissues. Various factors related Sleep related loss of m. tone  Large tonsils  Large tongue  Retrognathia  Obesity  Alcohol  Sedative medication  Certain medical condition www.indiandentalacademy.com
  10. 10.  Classification:  Mild: 5 to 15 involuntary sleep episodes occurring during activities that require little attention  Moderate: 15 to 30 sleep episodes during activities that require some attention  Severe: > than 30 episodes of sleep during conversation, walking, eating www.indiandentalacademy.com
  11. 11. Epidemiology of obstructive apnea syndrome  Mc Namara found 1-9% prevalence of OSAS  Recent study by Young et al suggested prevalence of OSAS to be at least 9% in males & 4% in females  Lugaresi reported incidence of snoring to be 19% in adult population & increased significantly with age  Katsantonics reported snoring 53% in men, 38% in women. www.indiandentalacademy.com
  12. 12. Normal upper airway anatomy  Nose- extends from external nares to posterior nasal apertures & subdivided into by nasal septum.  Nasal septum osteocartilagenous  Bony partition. part-  Vomer  Perpendicular plate of ethmoid  Nasal spine of frontal  Rostrum of sphenoid  Nasal crests of palatine bone  Maxillary bones www.indiandentalacademy.com
  13. 13.  Cartilaginous part-  Septal cartilage  Septal process of interior nasal cartilage  Cuticular part- fibro fatty tissue covered with skin lower margin of septum called columella. www.indiandentalacademy.com
  14. 14. www.indiandentalacademy.com
  15. 15. Lateral wall Bony part Cartilaginous part Frontal process of maxilla nasal cartilages Nasal bone 3-4 cartilages of ala Lacrimal bone Labyrinth of Ethmoid (superior & middle concha) Inferior nasal concha Perpendicular plate of palatine Medial pterygoid plated www.indiandentalacademy.com
  16. 16. www.indiandentalacademy.com
  17. 17. Decreased nasal patency may contribute to OSAS in many ways Nasal obstruction with closed mouth may result in obstructed airway, resulting in arousal.  Nasal congestion may induce mouth breathing which in turn leads to posterior positioning of mandible causing hypo pharyngeal narrowing.  With nasal congestion there is large inspiratory pressure drop across nose leading to sub-atmospheric pressure within potentially collapsible pharynx. www.indiandentalacademy.com
  18. 18. Soft palate  Movable muscular fold suspended from posterior aspect of hard palate. Separates nasopharynx from oro-pharynx.  Muscles Tensor palati  Levator palati  Musculus uvulae  Palatopharyngeas  Palatoglossus  Enlarged soft palate- Might be contributing factor in OSAS www.indiandentalacademy.com
  19. 19. Pharynx 3 parts-  Nasopharynx- posterior aspect of nasal turbinates to soft palate  Oro-pharynx- from soft palate to base of tongue  Laryngopharynx- from base of tongue to larynx www.indiandentalacademy.com
  20. 20. www.indiandentalacademy.com
  21. 21. Muscles of pharynx Superior Constrictor Middle constrictor Inferior constrictor Stylopharyngeus Palatopharyngeus Salpinopharyngeus www.indiandentalacademy.com
  22. 22. www.indiandentalacademy.com
  23. 23.  Nasopharyngeal patency can be compromised by Local mass lesions  Scarring secondary to surgery  Under development of local bony structures  Palatal uvular hypertrophy or edema  Adenoids www.indiandentalacademy.com
  24. 24.  Oropharyngeal patency can be compromised by Palatine tonsil hypertrophy or inflammation  Palatal or uvular enlargements  Macroglossia www.indiandentalacademy.com
  25. 25.  Hypo pharyngeal patency can be compromised Macroglossia  Posterior & superior displacements of hyoid bone www.indiandentalacademy.com
  26. 26. Tongue  Muscular mouth.  Muscles- gland situated at floor of Intrinsic Superior longitudinal Inferior longitudinal Transverse Vertical www.indiandentalacademy.com Extrinsic Genioglossus Hyoglossus Styloglossus Palatoglossus
  27. 27. www.indiandentalacademy.com
  28. 28. Hyoid bone  Semi circular bone found in midline b/w mandible & thyroid cartilage.  MusclesSuprahyoid Digastric Geniohyiod Stylohyoid Mylohyoid www.indiandentalacademy.com Infrahyoid Omohyoid Sternohyoid Sternothyroid Thyrohyoid
  29. 29. www.indiandentalacademy.com
  30. 30. Etiology & pathophysiology of OSAS  Predisposing factors still debated  Syndrome can be Central  Obstructive (most common)  Sub-obstructive  mixed www.indiandentalacademy.com
  31. 31.  Obstruction prevented by action of pharyngeal dilator & abductor muscles- sleep reduces activityairway resistance increases.  Genioglossus largest & best studied upper airway m. Conditions that retract mandible lead to posterior movement of tongue & narrowing of airway- can be overcome by moving jaw forward. www.indiandentalacademy.com
  32. 32.  Balance b/w pharyngeal musculature & negative intrapharyngeal pressure of inspiration determines patency of upper airway. Structural narrowing of airway- hinders muscular component of balance even at rest.  Most pts with OSAS have narrowed airway- confirmed by CT scan. www.indiandentalacademy.com
  33. 33.  Alterations in facial morphology may also be responsible for airway abnormality as pharyngeal musculature intimately related to bony structure. Eg- positive correlation b/w OSAS & short or posteriorly displaced mandible in many pts. www.indiandentalacademy.com
  34. 34.  Most of obstruction in OSAS pts seen in oropharynx & associated with large tongue volumes & also mainly in obese persons (excess peripharyngeal & subcutaneous fat)  Sleep with their jaws open- passive or active jaw opening- triggers afferents in TMJreflexly inhibit Genioglossus m.  Anatomic aberration of pharyngeal airway &/or neurogenic failure to preserve patency of pharyngeal airway- 2 most common theories. www.indiandentalacademy.com
  35. 35. Table 1 www.indiandentalacademy.com
  36. 36.  Many hereditary or acquired variables have also been described that precipitate OSASAdenoid & tonsillar hypertrophy in children & adults Glottic webs Vocal cord paralysis Acromegaly Lymphoma or hodgkins ds Micrognathia Ectopic thyroid Upper airway radiation edema or fibrosis Retrognathia Severe kyposcoliosis Correlation of velopharyngeal incompetence in infants Cushings ds www.indiandentalacademy.com
  37. 37.  Physiologic abnormalities predisposing to OSASPoliomyelitis, muscular dystrophies, amyotrophic lateral sclerosis & other ds with bulbar incordination sec. to brain stem abnormalities. Acquired dysautonomia Hypothyroidism Flurazepam & other sedative hypnotic agents Alcohol ingestion Testosterone administration Epilepsy Encephalitis www.indiandentalacademy.com
  38. 38. Mouth breathing and OSA  The tongue is no more in contact with the anterior palate hence producing a dorsal motion of the belly of the genioglossus that falls back into the pharynx.  Diminishes the axis of action of the genioglossus hence decreasing the efficiency of pulling the genioglossus out of the airway.  Also the pressure is now exerted across the palate hence further narrowing the soft palate. www.indiandentalacademy.com
  39. 39.  Opening of the mouth by 1.5cm pushes back the gonial angle by 1cm, which decreases the distance between the ventral attachment of the genioglossus and the posterior pharyngeal wall hence decreasing the lumen by 1cm  Decrease in nasal airflow decreases the neuroregulatory mechanism of respiration -bringing about depression of respiration predisposing to apnea www.indiandentalacademy.com
  40. 40. Clinical & demographic features of OSAS 2 cardinal symptoms-  Nocturnal symptom- snoring  Diurnal symptom- excessive day-time sleepiness  Other symptoms of sleep deprivation-  Excessive fatigue  Lethargy  Early morning headaches  Impaired concentration & impotence www.indiandentalacademy.com
  41. 41.  Clinical spectrum of sleep apneaHeavy habitual snoring Excessive day-time sleepiness Short term memory deficits Intellectual deterioration Personality changes Abnormal motor behavior Impotence nocturnal enuresis www.indiandentalacademy.com
  42. 42.  Other features includes               Nocturnal choking & coughing Orthopnea Ankle edema Right sided heart failure Pulmonary hypertension Central cyanosis Systemic arterial hypertension Cardiac arrhythmias Polycythemia Obesity Hypothyroidism Acromegaly Short thick neck Retrognathia Nasal obstruction www.indiandentalacademy.com
  43. 43. www.indiandentalacademy.com
  44. 44. Diagnostic Aids in OSA www.indiandentalacademy.com
  45. 45. Diagnostic aids in OSAS  History –  Snoring- 4-5 loud snores followed by silence, followed again by series of loud snores  Excessive day-time sleepiness  Clinical examinationExamination of the entire upper aerodigestive tract. www.indiandentalacademy.com
  46. 46.  Nasal examination:  Nose : nasal valve examination, alar collapse  Nasal speculum examination for mucosa changes, turbinates, DNS, pathology like cysts and polyps.  Oral cavity and the oropharynx:  Tongue : size , shape and the position.  High arched palate  Tonsils  Relation of tongue to oropharynx www.indiandentalacademy.com
  47. 47.  Evaluate presence of disproportionate anatomy: Long soft palate, uvula, base of the tongue, and retrognathic mandible and maxilla  Evaluate hypo pharynx and larynx for presence of tumors, large epiglottal folds, lingual tonsils, vocal cords usually done with fibroptic endoscope www.indiandentalacademy.com
  48. 48.  Sleep monitoring (polysomnography)-  Simultaneous recording of no. of physiological variables during sleep. Electroencephalogram- brain activity Electromyogram- muscle activity Electro ophthalmogram- eye movements Electro cardiogram- cardiac activity Ear oximeter- oxygen saturation Nasal & oral sensors- nasal & oral airflow Plethysmograph- thoracic & abdominal movements www.indiandentalacademy.com
  49. 49. www.indiandentalacademy.com
  50. 50. www.indiandentalacademy.com
  51. 51.  It is best done at night with atleast 4hrs of sleep time recorded. Most sleep studies are conducted for atleast 2 consecutive nights.  Extreme sleep apnea includes oxygen saturations level below 60%, an apneic index greater than 50, prolonged apnea lasting more than 45 sec. & concurrent cardiac arrhythmias. www.indiandentalacademy.com
  52. 52.  Abdominal or thoracic strain gauges provide movement tracings during respiratory efforts.  When there is simultaneous pause of airflow & thoracic or abdominal movement, a central type of apnea has occurred.  If airflow ceases but respiratory effort continues, obstructive type of apnea. www.indiandentalacademy.com
  53. 53.  Data then scrutinized. Duration & total no. of apnoeic periods, oxygen saturation, time during which oxygen saturation level below 90%, no. of arousals, quantity of REM sleep seen. www.indiandentalacademy.com
  54. 54.  Obstructive apnea- upper airway obstruction causes cessation of airflow with concomitant continuation of thoracic breathing movements.  Central apnea- simultaneous cessation of both airflow & thoracic breathing movements.  Mixed apnea- episodes of central apnea lasts 10 sec or longer followed by obstructive apnea.  Apnea – cessation of airflow for more than 10 sec.  Hypoapnea – reduction in tidal volume accompanied by fall in blood oxygen saturation, lasting more than 10 sec. www.indiandentalacademy.com
  55. 55. To diagnose OSA  30 or more apnoeic episodes within a course of 7hrs of sleep, resulting in excessive sleepiness during waking hrs. 5 episodes of apnea or hypo apnea must occur per hr  To make diagnosis & access severity of ds  To determine need & urgency of treatment. www.indiandentalacademy.com
  56. 56. Epworth sleepiness scale A questionnaire designed to assess how likely person would doze off in 8 specific situations Sitting & reading  Watching TV  As a passenger sitting in car for an hr  Sitting inactive in public place  Lying down to rest in afternoon  Sitting & talking to someone  Sitting quietly after lunch, without having consumed alcohol.  As a driver of a car, stopped for a few min in traffic. www.indiandentalacademy.com
  57. 57.  Scores0 – no chance  1 – low likelihood  2 – moderately possible  3 – high chance A score above 12 indicates subject is more sleepy than normal individual. www.indiandentalacademy.com
  58. 58.  Computerized tomography-  Non invasive scanning technique  Confines radiation to plane of interest  Minimizes blurring  Permits visualization of small variations in tissue density.  3 dimensional description of airway, tongue & other associated structures.  But it is time consuming procedure & expensive. www.indiandentalacademy.com
  59. 59. Study in AJO 1986 www.indiandentalacademy.com
  60. 60.  Many studies shown-  Lowe et al- large tongue , soft palate & reduced airway volumes. Majority of constriction occurred in oropharynx  Hapnik et al- reduced cross sectional areas of nasopharynx, oropharynx & hypopharynx.  Subjects with severe OSA- larger tongue & smaller airway surface volume.  More obese subjects- large tongue surface areas & smaller airway surface areas. www.indiandentalacademy.com
  61. 61.  Magnetic resonance imaging-  Produces high resolution images without use of ionizing radiation & yields both transverse & sagittal sections of pharynx.  Ideally suited in assessing conditions with increased tissue water content.  Horner et al – used MRI to assess upper airway in obese pts showed an excess on fat deposition in soft palate, tongue & surrounding collapsible segment of the pharynx. www.indiandentalacademy.com
  62. 62.  Fibre optic endoscopy-  Of value in location site of obstruction in upper airway  Particular emphasis is on the base of tongue, its position & its forward movement on protrusion pf jaws. www.indiandentalacademy.com
  63. 63.  Electromyography Genioglossus m. activity in OSA  Timing relationship b/w genioglossus inspiratory effort is of physiologic importance in pathogenesis in OSA www.indiandentalacademy.com
  64. 64.  Cephalometry –  Lowe et al showed following hard & soft tissue morphological characteristics in pts. with OSA Hard tissue featuresSmall mandible which is retropositioned Increase in anterior facial ht Enlarged occlusal & mandibular plane angle Over erupted maxillary & mandibular molars Steep occlusal plane Posteriorly positioned maxillae & mandible Proclined incisors Decreased overbite Inferior position of hyoid bone www.indiandentalacademy.com
  65. 65.  Soft tissue features-  Elongated tongue, soft palate & pharyngeal lt  Thickened soft palate  Decreased A-P pharyngeal space at superior, middle & inferior levels  Enlarged cross-sectional areas of tongue & soft palate  Decreased cross-sectional areas of oropharynx & hypopharynx www.indiandentalacademy.com
  66. 66.  Lyberg and Kronstad also documented similar craniofacial features. Also noticed that in all their patients the hyoid bone was inferiorly positioned (usually at junction of C3 and C4) had shifted much lower to C4, C5, C6 suggesting it could be pushed down by the tongue.  Large deposits of submental and submandibular fat. www.indiandentalacademy.com
  67. 67. www.indiandentalacademy.com
  68. 68. www.indiandentalacademy.com
  69. 69. www.indiandentalacademy.com
  70. 70. Study in angle 1996 www.indiandentalacademy.com
  71. 71. www.indiandentalacademy.com
  72. 72. www.indiandentalacademy.com
  73. 73.  Nasopharyngoscopy: Widely available easily performed, no radiation, performed sitting or supine, Muller’s maneuver can be performed possibility of predicting the outcome of UPPP depending on the site of obstruction Invasive and requires nasal anesthesia, evaluate only the airway lumen and not surrounding soft tissue and patient is usually awake. www.indiandentalacademy.com
  74. 74. Management of OSA  Since etiology not precisely understood so diversity of treatment options.  Treatment of OSA depend on –  Severity of symptoms  Magnitude of clinical complications  Etiology of upper airway obstruction www.indiandentalacademy.com
  75. 75.  Normally accepted options as outlined by J.M Battagel Wt reduction  Elimination of aggravating factors  ENT assessment plus any necessary treatment  CPAP  Mandibular advancement  Surgical options www.indiandentalacademy.com
  76. 76. Elimination of aggravating factors  Chronic obstructive airway ds  Asthma  Hypothyroidism  Other such medical conditions that may 1 st be eliminated  Alcohol intake  Sedative medication www.indiandentalacademy.com
  77. 77. Weight loss  Dramatic loss in wt. can result in significant decrease in apneic episodes in obese pts suffering from OSA.  Recommended as 1st form of therapy in mild to moderate cases. www.indiandentalacademy.com
  78. 78. Sleep posture  Cartwright suggested that change in sleep posture from supine posture to a lateral decubital position can reduce tendency for airway collapse.  In supine position especially during REM sleep, gravity & reduced tone of genioglossus m. increase the possibility of obstruction. www.indiandentalacademy.com
  79. 79. Drug therapy  Progesterone has been used in an effort to diminish obstructive apneas during sleep by acting as respiratory stimulant to airway, diaphragm & intercostals. www.indiandentalacademy.com
  80. 80. Nasopharyngeal airway  Placed beyond clinical obstruction site can have positive effect in OSA pts. www.indiandentalacademy.com
  81. 81. Continuous positive airway pressure (CPAP)  Discovered by Collin Sullivan in Sydney  Continuous stream of air under pressure is filtered & delivered to pharynx via a nasal mask.  Act as pneumatic splint.  This constant flow enough to prevent airway from collapsing but yet not enough to prevent periodic expiration. So to be secured firmly in place.  Should be worn 6hrs at night, 7 days a week. www.indiandentalacademy.com
  82. 82.  Advantages –  Most common & successful treatment for OSA  Subject no longer dozes off  Sleeps well & feel less irritable  Disadvantages –  Studies by Clark et al found 10-20% of subjects found it extremely uncomfortable & discontinued it.  Overall long term compliance with this device60-70% www.indiandentalacademy.com
  83. 83. www.indiandentalacademy.com
  84. 84. Dental appliances  Inexpensive  Non-invasive  Easy to fabricate  Quite well tolerated by pt. www.indiandentalacademy.com
  85. 85. 3 rationales  Reposition tongue in a more forward position (TRD)  Reposition mandible forward (nocturnal airway potency appliance NAPA, snore guard, herbst, mandibular positioner)  To lift soft palate or reposition the uvula (equalizer) www.indiandentalacademy.com
  86. 86. Approach to patient     Evaluate for periodontal health, dental restorations, occlusion, TMJ function, mandibular movement and craniofacial skeletal type Enough teeth must be present – at least 6 teeth in each arch and one good posterior teeth in each quadrant. patient should be able to protrude the mandible at least 5 mm without discomfort A patient with deep palate, long soft palate and steep mandibular plane may not be a good candidate, though there is no set criteria. After insertion and final adjustment a PSG must be done to evaluate the efficiency and a base line Ceph, must have been obtained. www.indiandentalacademy.com
  87. 87. Appliances  Almost 32 commercial appliances available:  Basically two types: Mandibular advancement devices (MAD) and Tongue repositioning devices. www.indiandentalacademy.com
  88. 88. TRD  Described by Cartwright & Samelson in 1982.  To keep tongue in forward position- places it into cup or bubble positioned in the anterior region with surface adhesion holding tongue in position.  Jaws to be kept in partly open position. www.indiandentalacademy.com
  89. 89. Disadvantages  Tongue not always held in forward position- surface adhesion lost  Esthetically intolerable  Forces nasal breathing- may be troublesome in some pts.  Tongue may get irritated becoz of lack of blood supply. www.indiandentalacademy.com
  90. 90.  Advantages:  Can be used in edentulous patients,  Will not loosen restoration as they do not require retention,  Minimal or no adjustment and no sensitivity to teeth  Offset fluctuation of the genioglossus muscle. www.indiandentalacademy.com
  91. 91. Anterior tongue repositioner www.indiandentalacademy.com
  92. 92.  Ferguson et al 1996- TRD most successful in pts who are less than 50% above ideal wt & in whom OSA is worse when they sleep in supine position.  Clark et al 1989- TRD effective in 75% of mild to moderate cases compared to CPAP, more easily tolerated. www.indiandentalacademy.com
  93. 93. TRD & genioglossus m. activity  Cartwright et al 1982- altered genioglossus m. activity significantly improved with TRD.  Ono et al 19962 tongue retaining devices made for each subjects- TRD A & TRD B  TRD A- no anterior bulb  TRD B- has bulb www.indiandentalacademy.com
  94. 94.  Both TRD A & B- reduced apnea-hypoapnea index (AH index)  TRD A- activation of genioglossus m. activity by creating passive jaw opening- TMJ receptors send information to CNS regarding jaw rotation which affects tongue protrusion by genioglossus m. activity.  TRD B- normalized time lag b/w peak inspiratory genioglossus m. EMG activity & max. inspiratory effort. Also normalized amplitude of peak genioglossus m. EMG activity that fluctuated during AH episodes while used TRD A. www.indiandentalacademy.com
  95. 95.  Anterior tongue position with TRD alleviates narrowing of upper airway that produces more positive pressure during inspiration. OSA pts otherwise will suffer from scarcity of negative pressure-driven reflex during sleep. www.indiandentalacademy.com
  96. 96. Anterior mandibular positioning devices  Many designs there  2 consistent features Moves mandible forward several mms  Maintains jaw in forward position even though pt is asleep  Could be 1 piece appliance or 2 piece appliance with tube & rod attachment (herbst appliance) www.indiandentalacademy.com
  97. 97. 2 piece appliance  Advantages Maintains constant forward position of tongue  Can be designed to allow continued oral breathing  More esthetically pleasing  Disadvantages Deleterious effect such as TMJ remodeling & subsequent dysfunction  Occlusal change- proclination or crowding of lower anteriors www.indiandentalacademy.com
  98. 98. Nocturnal airway patency appliance  Designed by George 1987  Designed to keep airway open during sleep by Posturing tongue more anteriorly  Inhibiting wide jaw opening  Assuring adequate air intake through mouth whenever nasal obstruction occurs. www.indiandentalacademy.com
  99. 99. Nocturnal airway patency appliance www.indiandentalacademy.com
  100. 100.  Results showed-  Improvement in sleep  Snoring decreased or completely disappeared.  Daytime somnolence diminished markedly.  Does produce some discomfort at night but pts get used to it. www.indiandentalacademy.com
  101. 101. Mandibular advancement splints     Like CPAP, mandibular advancement splints are a nonInvasive and therefore reversible form of treatment, and are worn only during sleep. Many designs have been described, but essentially these resemble a functional appliance: full coverage upper and lower splints are constructed to a protrusive working bite. To be effective, the appliance must have good retention to both upper and lower teeth, sufficient protrusion to prevent pharyngeal collapse in the supine position and as little vertical opening as possible. An anterior space between upper and lower segments of the splint is helpful for those who are mouth breathers. www.indiandentalacademy.com
  102. 102.  Seventy-five per cent of maximal protrusion has been advised.  Furthermore, the amount of protrusion must be tolerated by the individual. Since tolerance increases with time, splints which are capable of incremental advancement would seem to have clear advantages.  Suitable designs include cribbed activator, vacuum formed devices & removable herbst. www.indiandentalacademy.com
  103. 103. Mandibular advancement splint www.indiandentalacademy.com
  104. 104. Magnetic appliance  Maximal attractive force b/w magnets was 8.5N.  Intermagnetic distance 0.6-1mm, which reduce force magnitude for mandibular advancement to 5-6.5N.  Clasps for additional retention provided.  It is seen decrease in day time sleepiness & nocturnal snoring. Blood saturation level improved in some pts. No effect on TMJ. www.indiandentalacademy.com
  105. 105. Magnetic appliance www.indiandentalacademy.com
  106. 106. Karwetzky activator  Acc. To Marklund et al therapeutic efficacy of activator is optimal when pts had A-H index less than 10 events/hr.  Results showed- respiratory parameters significantly improved, decrease snoring & day time sleepiness. A-H index increased. www.indiandentalacademy.com
  107. 107. Karwetzky activator www.indiandentalacademy.com
  108. 108. Herbst appliance  Introduced by Emil Herbst in 1905 & reintroduced in 1970’s by Hans Pancherz.  Clark et al in 1993 evaluated the effect of herbst type of anterior mandibular positioning device in 24 OSA pts. Results were satisfactory & follow up investigation 3 yrs later showed appliance to have been used successfully & continually used in 52% of the sample. www.indiandentalacademy.com
  109. 109.  Potential complications include-  TMJ remodeling & dysfunction  Jaw pain  Occlusal changes like lower incisor crowding  If not protruded by 75% it did not work. www.indiandentalacademy.com
  110. 110. www.indiandentalacademy.com
  111. 111. The Equalizer  Constructed of vinyl and repositions the mandible in a “neuromuscular balanced position” determined by “myomonitor (TENS)”, incorporating “equalizing tubes” which are believed to “decrease the negative pressure in oropharynx” during inspiration. www.indiandentalacademy.com
  112. 112. www.indiandentalacademy.com
  113. 113. www.indiandentalacademy.com
  114. 114. Adjustment  Initially 70 – 75% of maximum forward positioning of the mandible  Kept so for a week and if symptoms do not subside then further advancement at a rate of .25mm per week till symptoms subside or TMJ limitations start to show  Recalls at every 2 weeks; 1 month; 6 months www.indiandentalacademy.com
  115. 115. Problems  Disocclussion of the posterior teeth  Forward movement of the lower teeth  Excessive salivation  Feeling of fullness  TMJ sensitivity and sensitivity of teeth www.indiandentalacademy.com
  116. 116. Efficiency Shows good prognosis in mild to moderate cases.  Many showed immediate symptomatic improvement.  Base of the tongue was advanced and dorsal surface appeared more superior  Hyoid bone positioned anteriorly and cross section of oropharynx increased from 41.6 mm to 92.3 mm  Airway volume increased by 27.6% and tongue volume decreased by 17.6% due to the forward and superior tongue posture.  www.indiandentalacademy.com
  117. 117. Antisnoring devices  Clark & Nakano 1989 described 2 devices to have an effect at reducing snoringLabial shieldPrevent mouth breathing & forces nasal breathing Maintains patency b/w soft palate & pharynx Palatal liftStop soft palate vibration so reduces snoring. www.indiandentalacademy.com
  118. 118. Surgical management of OSA  Current surgical techniques used-  Tracheostomy  Uvulopalatopharyngoplasty (UPPP)  Osteomy (anterior sagittal) with hyoid myotomy & suspension.  Maxillary, mandibular & hyoid advancement.  Genioglossus advancement  Partial glossectomy  Radiofrequency volumetric shrinkage of soft palate & tongue base  Tongue base suspension sutures www.indiandentalacademy.com
  119. 119. Tracheostomy  1st reported as treatment of OSA in 1969 by Guilleminault et al.  Indications –  Disabling sleepiness with severe familial & socioeconomic impact  Severe cardiac arrhythmias with sleep apnea.  A high apneic index (>60)  Notable oxygen desaturation level during sleep i.e below 40%  No improvement of clinical symptoms or polysomnographic findings after medical trials. www.indiandentalacademy.com
  120. 120.  Results showed-  Surgery may result in sec. local & general acute & subacute complications.  But on long term basis pts were completely relieved of clinical symptoms. www.indiandentalacademy.com
  121. 121. Uvulopalatopharyngoplasty  Proposed by Ikematsu in 1964 & introduced by Fujita et al in 1981.  Resect posterior margin of the soft palate & redundant lateral pharyngeal wall mucosa.  Soft palate resection ranges from 8-15mm stopping short of thick muscular part of the palate.  Lateral pharyngeal wall treated by resecting redundant mucosa & developing a flap along the posterior wall. www.indiandentalacademy.com
  122. 122.  Flap is advanced & sutured to anterior tonsillar pillar.  When sites of obstruction included excessive pharyngeal tissues combined with low-arched palates response rate is increased.  Complications of UPPP Pharyngeal dryness  Loss of taste  Nasopharyngeal stenosis www.indiandentalacademy.com
  123. 123. www.indiandentalacademy.com
  124. 124. Kamami technic  Proposed laser assisted uvulo palatoplasty.  Carbon dioxide laser at 20 watts (continuous mode)  Reports success rates comparable or better than convectional UPPP. www.indiandentalacademy.com
  125. 125. Inferior sagittal osteotomy of the mandible with hyoid myotomy & suspension  1st reported by Riley et al 1984  He treated 55 pts 67% good response  33% non responders www.indiandentalacademy.com
  126. 126. Supra hyoid myotomy: to elevate the redundant lateral pharyngeal tissues sometimes accomplished with genioglossal advancement www.indiandentalacademy.com
  127. 127. Genioglossus suspension sutures www.indiandentalacademy.com
  128. 128. Maxillary, mandibular & hyoid advancement  Lefort I osteotomy & sagittal split osteotomy  Gives more predictable results  Best alternative to Tracheostomy.  Indications –  Pts with normal skeletal development & severe OSA  Morbidly obese pts  Severe skeletal deficiency  Other modes of treatment failed. www.indiandentalacademy.com
  129. 129. www.indiandentalacademy.com
  130. 130. Conclusion  High prevalence of OSA has only been recently appreciated in part becoz s/s of chronic sleep disruption are often overlooked inspite of debilitating consequences.  Challenge to clinician is to routinely consider the diagnosis & to incorporate several basic questions in the historical review of symptoms regarding daytime or inappropriate sleepiness. www.indiandentalacademy.com
  131. 131.  Clinician s/b aware of the role of orthodontists in prevention & treatment of sleep disorders by various orthodontic appliances.  Team approach for management of such pts with OSA currently includes support of pulmonologist, neurologist, sleep lab technician, oral surgeon & otolaryngologist. www.indiandentalacademy.com
  132. 132.  Most recently consistent use of ceph analysis has been recommended to aid in diagnosis & treatment planning for OSA pts.  This coupled with new & promising treatment alternative of the orthodontic appliances, would suggest that the orthodontist could contribute to team management of these pts. www.indiandentalacademy.com
  133. 133. Thank you For more details please visit www.indiandentalacademy.com www.indiandentalacademy.com

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