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

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Contents
Introduction
 Epidemiology
 Normal upper airway anatomy
 Etiology & pathogenesis
 Clinical features
 Diagnostic aids
 Treatment modalities
 Conclusion



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

 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

 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

 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.

 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

 Related

to orthodontics-

 Peculiar

cranio-facial & soft tissue
morphology
 Non-invasive modes of therapy i.e dental
appliances used in treatment of syndrome.


 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

 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


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.

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

 Cartilaginous

part-

 Septal

cartilage
 Septal process of interior nasal cartilage
 Cuticular

part- fibro fatty tissue
covered with skin lower margin of
septum called columella.


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

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.


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

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


Muscles of pharynx

Superior Constrictor
Middle constrictor
Inferior constrictor

Stylopharyngeus
Palatopharyngeus
Salpinopharyngeus


 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


 Oropharyngeal

patency can be
compromised by Palatine

tonsil hypertrophy or
inflammation
 Palatal or uvular enlargements
 Macroglossia


 Hypo

pharyngeal patency can be
compromised Macroglossia
 Posterior

& superior displacements of hyoid

bone


Tongue
 Muscular

mouth.
 Muscles-

gland situated at floor of

Intrinsic
Superior longitudinal
Inferior longitudinal
Transverse
Vertical

Extrinsic
Genioglossus
Hyoglossus
Styloglossus
Palatoglossus

Hyoid bone
 Semi

circular bone found in midline
b/w mandible & thyroid cartilage.
 MusclesSuprahyoid
Digastric
Geniohyiod
Stylohyoid
Mylohyoid

Infrahyoid
Omohyoid
Sternohyoid
Sternothyroid
Thyrohyoid

Etiology & pathophysiology of OSAS
 Predisposing

factors still debated
 Syndrome can be Central
 Obstructive

(most common)
 Sub-obstructive
 mixed


 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.

 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.

 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.


 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.

Table 1



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



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


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.

 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

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


 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



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

Diagnostic Aids in OSA


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.


 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

 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


 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


 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.

 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.

 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.




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.

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.

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.

 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.

 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.

Study in AJO 1986

 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.

 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.

 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.


 Electromyography Genioglossus

m. activity in OSA
 Timing relationship b/w genioglossus
inspiratory effort is of physiologic importance
in pathogenesis in OSA


 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

 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

 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.


Study in angle 1996


 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.


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


 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


Elimination of aggravating factors
 Chronic

obstructive airway ds

 Asthma
 Hypothyroidism
 Other

such medical conditions that may 1 st
be eliminated
 Alcohol intake
 Sedative medication


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.


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.

Drug therapy
 Progesterone

has been used in an effort
to diminish obstructive apneas during
sleep by acting as respiratory stimulant to
airway, diaphragm & intercostals.


Nasopharyngeal airway
 Placed

beyond clinical obstruction site can
have positive effect in OSA pts.


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.

 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%

Dental appliances
 Inexpensive
 Non-invasive
 Easy

to fabricate
 Quite well tolerated by pt.


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)


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.

Appliances
 Almost

32 commercial appliances
available:
 Basically

two types:

Mandibular

advancement devices (MAD) and
Tongue repositioning devices.


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.


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.

 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.


Anterior tongue repositioner


 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.


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

 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.

 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.


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)

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


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.


Nocturnal airway patency appliance


 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.


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.

 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.

Mandibular advancement splint


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.

Magnetic appliance


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.


Karwetzky activator


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.

 Potential

complications include-

 TMJ

remodeling & dysfunction
 Jaw pain
 Occlusal changes like lower incisor crowding
 If not protruded by 75% it did not work.


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.


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

Problems
 Disocclussion

of the posterior teeth
 Forward movement of the lower teeth
 Excessive salivation
 Feeling of fullness
 TMJ sensitivity and sensitivity of teeth


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.



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.

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

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.

 Results

showed-

 Surgery

may result in sec. local & general
acute & subacute complications.
 But on long term basis pts were completely
relieved of clinical symptoms.


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.

 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

Kamami technic
 Proposed

laser assisted uvulo
palatoplasty.
 Carbon

dioxide laser at 20 watts (continuous

mode)
 Reports success rates comparable or better
than convectional UPPP.


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


Supra hyoid myotomy: to elevate the redundant lateral
pharyngeal tissues sometimes accomplished with
genioglossal advancement

Genioglossus suspension sutures


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.


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.


 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.

 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.

Thank you
For more details please visit


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

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