OSA Physiology

The critical abnormality in Obstructive Sleep Apnea (OSA) is the repetitive complete or partial collapse of the upper airway during sleep. This tends to occur with an anatomically compromised upper airway, resulting from skeletal abnormalities, soft tissue abnormalities, or combination of these factors. Also, other factors such as upper airway neuromuscular reflexes, ventilatory control stability, lung volume and surface tension may also play a role.

Because OSA has been associated with serious long-term adverse health consequences (including hypertension, metabolic dysfunction, cardiovascular disease, stroke, neurocognitive deficits, and motor vehicle accidents), it is a major public problem.  Dentist are encouraged to screen their patients for sleep and airway issues. Treatment of OSA should target the specific pathophysiologic processes that contribute to the collapse of the upper airway, in an attempt to alleviate symptoms and modify the long-term health consequences.

Pathophysiology of obstructive sleep apnea

Obstructive sleep apnea (OSA) is the most prevalent sleep related breathing disorder. The dangerous irregularity in OSA is the repetitive partial or complete collapse of the upper airway during sleep.

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Upper airway structure and function

The upper airway is made up of bony structures (mandible, maxilla, and hyoid bone) and soft tissues. The upper airway can be divided into four sections the nasopharynx, velopharynx, oropharynx, and the hypopharynx.

The routine functions of the upper airway (such as swallowing, breathing, and speech) require the capacity for both opening and closing. The upper airway has a collapsible segment, spanning form the hard palate to the vocal cords. This segment accommodates these functions (opening and closing) but also allow the occurrence of OSA in susceptible individuals.

Anatomic Factors on OSA

Given the relationship between structure and function, upper airway anatomy is an important consideration in the pathophysiology of OSA. Physical principles suggest that a smaller upper airway is more susceptible to collapse. Hence, the size and probably the shape of the upper airway influence the likelihood of upper airway collapse. Imaging studies have shown that the volume of the upper airway is smaller in OSA patients than in control subjects. This has been demonstrated using a number of imaging modalities, including computed tomography (CT), and magnetic resonance (MRI).

The degree of patency of the upper airway can be viewed as a function of circumstances that collapse the airway and those that promote airway patency. This is the “balance of pressure” concept. Factors that collapse the airway include the negative intraluminal pressure generated by the diaphragm during inspiration and the pressure of the promote airway patency include the elastic properties of the pharyngeal wall and the contraction of pharyngeal dilator muscles. The specific pathophysiologic mechanism causing OSA are likely to vary among individuals.

The airway pressure required to collapse the upper airway is known as the critical closing pressure. The upper airway generally remains patent in normal individuals. Thus, in normal individuals, the extraluminal tissue pressure (the force that will tend to collapse the airway) is lower than the elastic properties of the pharyngeal wall. The extraluminal tissue pressure is the result of the pressure from surrounding soft tissue and bony structures. The magnitude of the extraluminal tissue pressure is determined by the interaction of the volume of soft within the upper airway and the size of the bony compartment. In OSA patients, an excess of soft tissue (such as in obesity), restriction in size of the bony compartment (such as that caused by retrognathia), or a combination of these factors can cause an increase in extraluminal tissue pressure, thereby reducing the caliber of the upper airway.

Non-anatomic Factors in OSA

Accompanying the anatomical factors, the activity of the pharyngeal dilator muscles and the central control of ventilation are important in the pathophysiology of OSA. The pharyngeal dilator muscles can be divided into the following groups:

  • influencing hyoid bone position
  • muscles of the tongue
  • muscles of the palate
  • muscles that protrude the mandible

Negative intraluminal pressure is the major stimulus of an upper airway reflex that activates pharyngeal dilator muscles during wakefulness. While a person is awake, the activity of pharyngeal dilator muscles compensates for the anatomic deficiency in the upper airway. This is demonstrated by the greater activity of the genioglossus muscle in patients with OSA compared to normal patients. Yet, this compensatory effect is considerably diminished when the action of upper airway reflexes and pharyngeal dilator muscles decreases during sleep, and, in particular, during rapid eye movement sleep.

In the brainstem there is a respiratory control pattern generator. It is responsible for the automatic control of ventilation. Respiratory rhythm is regulated by chemoreceptors and by neural input from the upper airway and lungs to the brainstem. The peripheral and central sensory systems are sensitive to levels of carbon dioxide (PaCO2) and oxygen (PaO2). Several neurotransmitters, including acetylcholine, histamine, norepinephrine, serotonin, and dopamine have meaningful functions in the control and maintenance of respiration and ventilation. Instability of ventilatory control may be a contributing factor in the pathophysiology of OSA.

Factors predisposing to collapse of the upper airway and the development of OSA

  • Restriction in size of bony compartment
  • Maxillary hypoplasia or retrodisplacement
  • Mandibular hypoplasia or retrodisplacement
  • Increase in soft tissue volume
  • Deposition of fat around upper airway (obesity)
  • Enlargement of tongue (macroglossia)
  • Enlargement of soft palate
  • Thickening of lateral pharyngeal walls
  • Adenotonsillar enlargement
  • Pharyngeal inflammation and edema
  • Increase in pharyngeal compliance
  • Decrease in pharyngeal dilator muscle activity
  • Impairment of mechanoreceptor sensitivity
  • Impairment of upper airway neuromuscular reflexes
  • Impairment of strength and endurance of pharyngeal dilator muscles
  • Instability of ventilatory control
  • Decrease in lung volume
  • Increase in surface tension
  • Hormonal factors
  • Presence of testosterone (male gender or testosterone replacement)
  • Absence of progesterone (, menopause)
  • Endocrine disorders (hypothyroidism or acromegaly)

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