This presentation gives some basic information regarding the definition , etiology and pathophysiology of " obstructive sleep apnea" which is a serious sleep disorder .Treatment methods are briefly reviewed with special emphasis on the role of the oral surgeon and orthodontist in the management of this medical condition .

1. Obstructive Sleep Apnea
‫االنسدادي‬ ‫الليلي‬ ‫المؤقت‬ ‫النفس‬ ‫انقطاع‬ ‫أو‬ ‫ٌهر‬‫ب‬‫ال‬
Dr. Marwan Mouakeh
Consultant Orthodontist, Scientific Adviser of Al-Hokail
Polyclinic Academy - Khobar , KSA

2. • Good sleep hygiene is critical for one’s overall
physical and mental health.
• Normally it should take about 10 - 15 minutes to
fall asleep after going to bed.
• If you are asleep in less than 5 minutes, that could
be a sign of excessive sleepiness .
Introduction

3. •There are 2 forms of sleep: REM sleep and non-REM sleep.
REM stands for rapid eye movement and is associated with
dreaming. It accounts for 25% of normal sleep, coming in
longer periods toward morning. The rest of our sleep time is
spent in NREM, which consists of four stages from light sleep
(stage 1) to deep sleep (stage 4).
The Sleep Cycle

4. • Repeated episodes of partial or complete
upper airway obstruction during sleep .
 A Sleep disorder characterized by recurrent
episodes of narrowing or collapse of pharyngeal
airway during sleep despite ongoing breathing
efforts.
What Is Obstructive Sleep Apnea (OSA) ?

5. • 1st description of the disorder in the
medical literature was in 1965 .
Gastaut H, Tassinari CA, Duron B. Polygraphic study of diurnal and nocturnal
(hypnic and respiratory) episodal manifestations of Pickwick syndrome [in
French]. Rev Neurol (Paris) 1965; 112:568–579
 Obstructive sleep apnea (OSA) is a public health
problem and a potentially life-threatening condition .
What Is Obstructive Sleep Apnea (OSA) ?

6. Patent Vs Collapsed Airway
Cardinal Symptoms of OSA
 Snoring
 Sleepiness
 Sleep Apnea Episodes

7.  Terminology
– Apnea = Cessation of airflow > 10 seconds
– Hypopnea = Decreased airflow > 10 seconds
( transient reduction of breathing )

8. Terminology
 AHI (Apnea - Hypopnea Index)
– apnea + hypopnea / hour of sleep
 RDI (Respiratory Disturbance Index)
– apnea + hypopnea + arousal / hour of sleep
Apnea Hypopnea
↓ in airflow > 80% ↓ in airflow 50 % - 30%
↓ O2 sat ↓ O2 sat > 4%
> 10 sec ≥ 10 sec
Ending in arousal Ending w/ arousal

9. •Defining Severity of OSA
 Length of time in apnea event
 % ↓ O2 Desaturation
 Apnea- Hypopnea Index (AHI):
– Mild 5-15 events / hour
– Moderate 15-30 events / hour
– Severe > 30 events / hour

10. •Defining Severity of OSA

11. • Clinical features of Obstructive Sleep Apnea:
Excessive daytime sleepiness
Morning headache
Cardiopulmonary dysfunction
– hypertension
– cardiac arrhythmias
– heart failure
Impaired memory and concentration
Reduced intellectual ability
Disturbed personality and mood .
•The dominant symptoms of OSA are excessive sleepiness,
impaired concentration and snoring.

12. •Incidence of OSA
 Approximately 40% of adults over 40 years old
snore (about 100 million Americans) .
 Middle age (30 – 60 yo) American
– 4% of men and 2% of women (18 million)
 Geriatrics
– 24 - 42% have RDI > 5
 Two thirds are obese

13. •Incidence of OSA
 National Commission on Sleep Disorders Research (1993)
– 95% of pts w/ OSA may be undiagnosed
 More prevalent than asthma
 Equally prevalent as diabetes

14. Pathophysiology of OSA

15. Sleeping
Decreased pharyngeal
muscles tonicity
Upper Airway
collapse
Apnea
Hypoxia
Hypercapnia
Respiratory efforts
Increase in tonicity
Clearance of upper
airways
Micro reveille
Hyperventilation:
correction of O2 & CO2
Mechanisms of OSA

16. Pathophysiology of OSA
 Tissue laxity and redundant mucosa
 Anatomic abnormalities
 Decreased muscle tone with REM sleep
 Airway collapse
 Desaturation ( O2 )
 Arousal with restoration of airway
 Sleep Fragmentation leading to
Hypersomnolence

17.  Etiology of OSA
 Multifactorial :
- Anatomic factors
- Neuromuscular factors

18. – Anatomic factors resulting in narrowing of pharynx :
•Skeletal anatomy (micrognathia, retrognathia)
•Soft tissue (macroglossia, tonsillar hypertrophy,
fatty infiltration of pharyngeal tissue assoc w/
obesity)
 Etiology of OSA

19.  Skeletal anatomy ( micrognathia, retrognathia)
 Etiology of OSA

20. •Skeletal anatomy
•Inferiorly positioned hyoid
bone .
• Constricted osseous
airways .
 Etiology of OSA

21. •Tonsillar hypertrophy
•Enlarged Adenoids
•Skeletal Abnormalities
 Etiology of OSA

22. •Long soft palate
•Skeletal Abnormalities
 Etiology of OSA

23. •Macroglossia
•Skeletal Abnormalities
 Etiology of OSA

24. – Neuromuscular factors
•Decreased activity of pharyngeal dilator muscles
•Increased compliance of pharyngeal airway
•Active inhibition of muscle activity during REM
sleep
•Alcohol, sedatives, and muscle relaxants
 Etiology of OSA

25.  Complications
• Desaturation ( O2 )with compensatory
polycythemia
• Hypercapnia ( CO2)with pulmonary
hypertension
• Systemic hypertension
• Arrhythmias

26. •Risk Factors
 Obesity, body mass index > 28 kg/m2
 Increased age
 Male sex
 Hypertension
 Hypothyroidism / Acromegaly
 Use of sedatives/narcotics/alcohol
 Smoking

27.  Obesity
 Strongest risk factor for OSA
– Present in > 60% of patients referred for
a diagnostic sleep evaluation
– Wisconsin Sleep Cohort Study
• A one standard deviation difference in BMI was
associated with a 4-fold increase in disease
prevalence
Risk Factors

28. • Obesity
 Alters upper airway mechanics during sleep
1. Increased parapharyngeal fat deposition:
neck circumference: > 17” males
> 16” females
With subsequent:
 smaller upper airway
 increase the collapsibility of the pharyngeal
airway

29. • Obesity
2. Changes in neural compensatory
mechanisms that maintain airway
patency:
 diminished protective reflexes
which otherwise would increase upper
airway dilator muscle activity to
maintain airway patency

30. Risk Factor: Age
Adapted from Young T et al. N Engl J Med 1993;328.

31. Risk Factor: Smoking
Adapted from Wetter DW et al. Arch Intern Med 1994:154
©1994 American Medical Association.

32. Diagnosis
Of
Obstructive Sleep Apnea

33.  Diagnosis
 History
 Physical examination
 Radiographs
 Polysomnography

34. History
 Snoring
 Restless sleep
 Morning Headache
 Insomnia

35. History
 Excessive daytime sleepiness
 Personality changes
 Insomnia

36.  Symptoms
• Loud snoring
• Excessive daytime sleepiness
• Choking/gasping during sleep
• Unrefreshing sleep
• Daytime fatigue
• Impaired concentration
Symptoms and Signs of OSA

37. •Diagnosis: Clinical Features
 Nocturnal symptoms
1. Snoring :
– reflects the critical narrowing
- population survey: habitual snorers
25% of men, 15% of women

38. •Diagnosis: Clinical Features
 Nocturnal symptoms
1. Snoring :
- prevalence increases with age (60%, 40%)
- the most frequent symptom of OSA
- absence makes OSA unlikely
(only 6% of patients with OSA did not report)

39.  Nocturnal Symptoms
2. Witnessed Apneas
3. Nocturnal Choking or Gasping
4- Restless Sleep
5. Insomnia
•Diagnosis: Clinical Features

40. • Clinical features
 Daytime symptoms
1. Excessive daytime sleepiness
- severity can be assessed
 subjectively = questionnaires
(Epworth Sleepiness Scale)
 objectively
MSLT = Multiple Sleep Latency Test

41. The most common symptom of OSA is
excessive daytime sleepiness, which can be
assessed using the Epworth Sleepiness Scale.

42. •Epworth Sleepiness Scale
0 = would never doze
1 = slight chance of dozing
2 = moderate chance of dozing
3 = high chance of dozing
•A score of more than 10 suggests clinically
significant daytime sleepiness, although a lower
score does not exclude it.

43. •Clinical features
 (Daytime symptoms)
2. Fatigue
3. Memory impairment
4. Personality changes
5. Morning headaches or nausea
6. Depression

44.  Signs of OSA
•Obesity (particularly upper body)
•Mandibular/maxillary hypoplasia
(receding chin)
• Crowding of the oropharynx
•Large tonsils or tongue
•Nasal and nasopharyngeal
obstruction

45.  Evaluation
 Thyroid function tests
 Arterial blood gas
 Complete blood count
 ECG
 Echocardiography
 Radiological studies
 Polysomnography

46. •Radiography
 Cephalometrics
 Computed tomography
 Magnetic resonance imaging
 Evaluation

47. • Cephalometrics
Airway evaluation
Adenoids
Tongue

48. •Computed tomography
 Volumetric reconstruction
- Disadvantages :
– Cost
– Weight limitations
– Ionizing radiation
 Evaluation

49. •Magnetic Resonance Imaging
 Excellent soft tissue anatomy
 Multiple planes
 No ionizing radiation
- Disadvantages :
– Cost
– Weight limitations
– Noisy
– Claustrophobia
 Evaluation

50. Polysomnography
 Simultaneous recordings of multiple physiological
signals during sleep.

51.  Electroencephalogram
(EEG)
 Electrooculogram (EOG)
 Electromyogram (EMG)
 Electrocardiogram (ECG)
 Oronasal airflow
 Chest wall effort
 Snore microphone
 Oxyhemoglobin saturation
 The gold standard: Overnight Polysomnogram
 Evaluation

52. Obstructive sleep apnea. Note the absence of flow (red arrow)
despite paradoxical respiratory effort (green arrow ).
Polysomnogram

53. Apnea Patterns
There are 3 characteristic patterns of apnea.
An obstructive apnea is defined by the absence of airflow despite
persistent ventilatory efforts,.
A central apnea, in contrast, is the absence of airflow due to the lack
of ventilatory effort.
A mixed apnea includes both central and obstructive components,
usually with an initial central component followed by the obstructive
component.

54. • Diagnosis of OSA
 American Academy of Sleep Medicine criterias:
A. Excessive daytime sleepiness that is not better
explained by other factors
B. Two or more of the following that are not better
explained by other factors:
choking during sleep; recurrent awakenings;
unrefreshing sleep; daytime fatigue; impaired
concentration.
C. AHI (five or more obstructed breathing
events per hour during sleep).

55. Medical Consequences
 The narrowing and closure of the airway
during sleep causes fragmented sleep and
patho-physiologic conditions:
– Neurobehavioral Derangement
– Cardiopulmonary Derangement

56. Medical Consequences
Neurobehavioral Derangement
 Excessive daytime sleepiness
 Depression
 Impotence
 Personality change, Irritability
 Learning and memory difficulties
 Morning headache
 Lack of energy
 Loss of employment, Uninsurability, Marital
Discord
 Traffic accident, 7x higher

57. The accident incidence was seven-fold greater in patients with
sleep apnea than in matched controls without the disorder
• MVA ( motor-vehicles accidents )
Adapted from Findley LJ et al. Am Rev Respir Dis 1988;138.

58.  Hypertension
– Occur in 50% OSA patients
– About 30% of HTN have OSA
– Repetitive hypoxia and hypercapnia at night may contribute
to inc in sympathetic tone resulting in HTN
Medical Consequences
Cardiopulmonary Derangement

59.  RV hypertrophy and failure
– Resulting from pulmonary HTN due to hypoxemia
 Cardiac arrythmias
– Most common being nocturnal bradycardia, which occurs
during apneic episode followed by tachycardia at resolution
of apnea
 MI, angina
Medical Consequences
Cardiopulmonary Derangement

60. Treatment of OSA

61.  Indication for Treatment
 AHI 15 or more (moderate-severe)
 AHI 5-14 (mild) and with documented
symptoms of :
– Excessive daytime sleepiness, or
– Impaired cognition, mood disorders or insomnia, or
– Documented hypertension, ischemic heart disease
or history of stroke .

62.  Treatment of OSA
Behavioral Modifications
Nonsurgical modalities
Surgical modalities

63.  Behavioral Modifications
– Weight reduction
– Avoid CNS depressants (alcohol, sedatives)
– Sleep on side w/ tennis ball on back
– Stop smoking
– External nasal dilators/steroid spray
 Treatment of OSA

64.  Weight Reduction
– Exercise
– Diet
– Bariatric Surgery
 Treatment of OSA

65. •Weight Loss
 Remains a highly effective method
 10 – 15 % reduction in weight can lead to
an approximately 50 % reduction in sleep
apnea severity in moderately obese male
patients.
Stop / Reduce Smoking
 Treatment of OSA

66. • Sleep Position Training
 Avoid sleeping in the supine position
 Treatment of OSA

67. • Sleep Position Training
Use of a tennis ball sewn into the back of a night shirt as
a means of training the patient to avoid the supine
position and sleep in the lateral recumbent position.
 Treatment of OSA

68. •Pharmacotherapy
 Protriptyline – decreases REM sleep
 Thyroxine or Medroxyprogestrone : in
Hypothyroidism patients
 Progestrone : in postmenopausal women
 Decongestants : nasal congestion , pharyngeal
odema .
 Antibiotics
Non-Surgical Treatment:

69. •Non-Surgical Treatment
CPAP
Continuous Positive Airway Pressure

70. • CPAP
•Sullivan introduced CPAP in 1981
Non-Surgical Treatment

71. • Continuous Positive Airway Pressure
Act as a pneumatic splint to maintain patency of the pharyngeal
airway by preventing collapse of the pharyngeal tissues .
Non-Surgical Treatment

72. • Nasal & Facial Masks
Non-Surgical Treatment

73. NASAL
NASAL
PILLOWS
NASAL
FULL FACE NASAL PILLOWS
CPAP &
humidification

74.  CPAP
 Titrate the airway pressure needed to overcome
airway obstruction
 Average CPAP setting is about 5-15 cm H2O
 May be delivered via a nasal
or face mask
 Effective in > 90%
Non-Surgical Treatment

75. • CPAP
 Has been shown to objectively:
– Decrease MVA
– Decrease blood pressure
– Decrease day time sleepiness
 Problems:
– Mask discomfort
– Patient acceptance
– Claustrophobia
Non-Surgical Treatment

76. Polysomnogram : Before CPAP

77. Polysomnogram : After CPAP

78. •Non-Surgical Treatment - CPAP
 Physical issues :
– Facial skin abrasions/discomfort
– Air leaks leading to drying of eye
– Difficulty with expiration
– Nasal dryness and congestion
– Sore throat
– Loud noise

79.  Tongue retaining devices
– Keep tongue in forward position by creating negative
pressure in a plastic bulb, fit between the lips
 Mandibular advancing devices
– Cause forward/downward movement of mandible when
attached to dental arches
 Soft palate lifter
– Effective only for treatment of snoring
•Non-Surgical Treatment:
Oral Devices

80. • Tongue Retaining Devices ( TRD)
• TRDs use suction pressure to maintain the tongue
in a protruded position during sleep .

81. Mandibular Advancement Devices

82. Mandibular Advancement Devices
•The aim of all of these devices is to improve the patency of the
upper airway during sleep by increasing its dimensions and
reducing its collapsibility .

83. • Mandibular Advancement Devices
 Advance Base of the
tongue to ↑ airway
 Advance and raise hyoid
bone, tightening the
pharyngeal musculature
which reduces airway
collapsibility.
 Stretch the masseter
muscles which
stimulates the
genioglossus muscle

84. • Oral Devices
• Activator, Herbst, Twin
block …
• Tongue Retaining
appliances

85.  Reposition and stabilize
the mandible & tongue
(sometimes soft palate)
 Increase size of airway in
lateral dimension
 Mandibular Advancement Devices

86. • Fabrication of Mandibular Protruding Appliance
•Good Impressions of upper & lower dental arches

87. • Assessment of the amount of maximum mandibular
protrusion

88. • Recording the Protruded position of the mandible
• Progressive mandibular
protrusion to ensure treatment
efficiency .
• Start by 50-60% of the
maximum active protrusion .
•
•Titration

89. • Recording the Protruded position of the mandible
•Positive relationships between
amount of mandibular protrusion
and :
- Increased airways patency
- Decreased airways resistance
- Decreased episodes of OSA
•Titration

90. • Oral appliances
 Most effective in non-obese patients with
retro or micrognathia
 Better for mild to moderate cases
 51% achieve normal sleep, 61% improved
RDI < 20
 Consider TMJ dysfunction and occlusal
changes

91. • Oral Devices : Contra-indications
•Insufficient tooth support
•Periodontal problems
•Poor oral hygiene ( multiple caries )
•Temporomandibular disorders
• Mandibular protrusion < 5 mm
• Bruxism ??
- Articular
- Dental ???

93. Oral appliance treatment for obstructive sleep
apnea in a partly edentulous patient

94. Oral appliance treatment for obstructive sleep
apnea in a partly edentulous patient

95. • Oral Devices : Contra-indications
•Class III malocclusion
•Severe malocclusion
- Orthodontic

96. Dental Appliance Treatment for Obstructive Sleep Apnea
DOI 10.1378/chest.06-2038 Chest 2007;132;693-699
Andrew S. L. Chan, Richard W. W. Lee and Peter A. Cistulli

97. Nightly use of an MPD for 2 years
by OSA patients and snorers was
found to increase their airway
passages because of an increase in
pharyngeal area, which to a large
extent was caused by a reduction
in velum area.
Franson et al . Am J Orthod Dentofacial
Orthop 2002;122:371-9)
Influence of mandibular protruding device on
airway passages and dentofacial characteristics
in obstructive sleep apnea and snoring

98. • American Sleep Disorders Association
Standards of Practice Committee
– Primary snoring
– Pts w/ mild OSA who do not respond to general
treatment
– Pts w/ moderate to severe OSA who cannot
tolerate nasal CPAP and who refuse or are not
candidate for surgical treatment .
• Non-Surgical Treatment:
Oral Devices

99.  Summary of the Key Adverse Effects of Oral Appliances
Short-term adverse effects
Excessive salivation
Mouth dryness
Tooth pain
Gum irritation
Headaches
Temporomandibular joint discomfort.
•Long-term adverse effects
Reduction in overjet
Increase in facial height
Increase in degree of mouth opening
Changes in inclination of incisors
Increase in mandibular plane angle

100.  Surgical Methods- Soft tissues
 Reconstruct upper airway
Uvulopalatopharyngoplasty (UPPP)
Laser-assisted uvulopalatopharyngoplasty
(LAUP)
Genioglossal advancement
Nasal reconstruction
 Adenotonsillectomy :
preferred treatment in children
 Partial Glossectomy
 Bypass upper airway
Tracheostomy

101. •Uvulopalatopharyngoplasty (UPPP)
•Fujita (1981)
•Most common procedure
•1st line tx for retropalatal collapse
•10-50% success
 OSA : Surgical Treatment

102. •Uvulopalatopharyngoplasty (UPPP)
Devised to surgically excise the tonsils
(if present) and portions of the soft
palate, and reorientate the tonsillar
pillars in order to enlarge the
oropharyngeal space .
 OSA : Surgical Treatment

103. •Tongue reduction
 Lingual tonsillectomy
 Laser midline glossectomy
 Lingual plasty
 Radiofrequency volumetric tissue
reduction
 OSA : Surgical Treatment

104. •Partial Glossectomy
 An enlarged tongue (macroglossia)
may call for tongue reduction surgery
extending from the midline of the
posterior tongue down to the free
margin of the epiglottis.
 Since speech and swallowing may be
significantly compromised by this
procedure, it is limited to few cases
where there is true macroglossia
present.
 OSA : Surgical Treatment

105.  Adenotonsillectomy - preferred treatment in
children .
 Tracheostomy - cure for OSAS
– used for failure of more conservative treatment
– life threatening cardiopulmonary complications
– alternative techniques to lessen complications
 Surgical Methods - Soft tissues

106.  Surgical Methods - Maxillofacial elements
 Mandibular advancement
 Maxillomandibular advancement ± advancement
genioplasty
 Geniotubercle advancement ± hyoid suspension
 Advancement genioplasty .

107.  Geniotubercle advancement
For advancing the tongue forwards
without changing lower facial
aesthetics or the dental occlusion .
 The advancement of the central
block of bone below the mandibular
incisor effectively advances the
attachment of the genioglossus and
geniohyoid muscles which brings
forward both the tongue and hyoid
bone.
 OSA : Surgical Treatment

108. – Advances hyoid bone
anteriorly and inferiorly.
– Advances epiglottis and base
of tongue .
– Performed in conjunction
with other procedures .
– Dysphagia may result .
 Hyoid Myotomy and Suspension
 OSA : Surgical Treatment

109.  Adult female patient
 OSA
Severe skeletal open bite
•Surgical-Orthodontic Treatment

111. Assessment and Management of Obstructive
Sleep Apnea in Adults

112. Otherwise snore
and this will
happen to you….
Or sleep alone….