Pacific Coast Society of Orthodontists Bulletin Winter 2021 - 48

Presentation Summary

Doctors

Sleep Disordered Breathing and
Orthodontics:
Separating Fact from Fiction
Dr. Amanda Tompkins
PCSO Bulletin Contributor

Dr. Benjamin Pliska
University of British Columbia

Presented by Dr. Benjamin Pliska at the PCSO/
RMSO/MSO/SWSO Annual Session, Oct. 3, 2020
Dr. Pliska discusses the shifting trend in orthodontics toward airway-focused treatment and the
orthodontist's role, including screening for sleep
apnea in orthodontic patients, diagnosing and
managing airway problems, and using orthodontics to help treat obstructive sleep apnea (OSA).
He begins his discussion by defining OSA and
then goes on to discuss OSA symptoms in adults
and children and associated comorbidities, the
pathophysiology of OSA, the reliability and validity of cone-beam computed tomography (CBCT)
in diagnosing OSA, and the orthodontic interventions of maxillary expansion and orthognathic
surgery and their impact on OSA.
OSA is defined as recurrent episodes of partial or
complete obstruction of the upper airway during
sleep that results in oxygen desaturation, sleep
fragmentation, and activation of the sympathetic
nervous system. Chronic poor sleep that results
from OSA has a multitude of associated systemic morbidities including high blood pressure,
poor glucose control, obesity, mood disorders,
poor alertness, excessive sleepiness, and cancer,
among others. OSA in children can be associated with similar cardiovascular issues, mood
disorders, and cognitive impairment, but rather
than excessive sleepiness or sluggishness seen in
adults with OSA, OSA in children often results in
hyperactivity, poor attention, and poor learning.
The pathophysiology of OSA is complex and
multifactorial and is classified by four principal
components that reduce the caliber of the airway,
promote airway collapsibility, increase sleep instability, and leads to the disease: collapsibility of the
airway, arousal threshold, altered neuromuscular
tone, and altered ventilatory control. Determining
from which category the OSA is originating can
help lead to targeted treatment strategies.
Collapsibility of the airway corresponds to the
size and shape of the airway, is influenced by

muscular tonicity, and is measured in Pcrit (critical
closing pressure). Sleep alters the function of
airway musculature, and the tight integration of
the airway muscles is necessary to prevent apneic
events. The velopharynx valve, which is located
in the adenoidal tissue area, controls airflow to
the oropharynx. The required integrated control
is altered in patients with OSA. In addition, not all
soft tissue associated with the airway is the same,
as adipose tissue varies in its deposition and location from patient to patient and affects airway
function. The elasticity of the airway also plays a
role in OSA. Patients without OSA tend to have
stiffer airways than those with OSA. Pcrit in normal
patients can fall into the −10 to −15 cm H20 range
before the airway collapses, but patients with
OSA can have airways collapse while in positive
Pcrit value ranges because of the increased collapsibility of the airway. However, some patients with
OSA do not display alterations associated with
Pcrit values and would therefore not benefit from
anatomical changes to the airway that would
increase the overall airway size and volume.
Alterations in arousal threshold are often observed in patients with OSA. A decrease in airflow
pressure during sleep will generally cause stimulation/activation of the muscles of the airway
first and ultimately a cortical arousal that will
awaken a patient from sleep. Patients with low
arousal thresholds will reach an arousal threshold
before muscle activation occurs in response to a
decrease in airflow pressure and oxygen desaturation. Nonobese patients with OSA generally
have low arousal thresholds. Zopiclone, which is
a hypnotic medication, may be useful in treating such patients, as it depresses the arousal
threshold, which will allow muscle activation to
occur before the arousal threshold is reached and
maintain a patent airway during sleep.
As previously mentioned, when the airway
pressure decreases, the muscles of the airway
should activate before the arousal threshold is
reached to maintain sleep. However, the lack
of muscle responsiveness when the airway

PCSO Bulletin Winter 2021

Pacific Coast Society of Orthodontists Bulletin Winter 2021

Table of Contents for the Digital Edition of Pacific Coast Society of Orthodontists Bulletin Winter 2021