OSA is characterized by the reduction of airflow during sleep. Slight reduction of airflow can cause disturbances un-noticeable to the person asleep, but significantly disrupts the quality of sleep.

This results in excessive sleepiness during the daytime and can be dangerous in activities such as driving and operating machinery.

Persistent reduction of airflow can lead to loss of oxygenation. In the short term, this leads to disruptive waking during sleep.

In the long-term, this worsens conditions such as arrhythmia, hypertension, and diabetes.

There are also significant implications for mental health, as OSA is associated with depression and anxiety.

There are anatomic and non-anatomic cases of OSA. Generally, anatomic causes relate to obstruction or collapsibility of the upper airway that worsens during sleep. Obstruction anywhere along the upper airway can contribute to OSA.

Starting with the nasal passages, obstruction can be caused by nasal allergy. Structural causes include deviated septum, enlarged inferior turbinates, and collapsible upper lateral cartilage.

For children, the adenoids (lymphoid tissue at the back of the nasopharynx) is an important site of obstruction. Palatine tonsil enlargement is also frequently associated with OSA.

In adults, this can be associated with redundancy of the soft palate.

The tongue is a complex cause of obstruction.

1) It can have excessive fat.

2) It can have enlarged lingual tonsils.

3) It can also feel “too large for the mouth.” Although, this usually means that the intraoral cavity, confined by the upper and lower jaws, is too small for the tongue.

4) There are muscles attached to the tongue that propel it forward during sleep. One major muscle is the genioglossus muscle. When this muscle does not function well, the tongue obstructs the airway during sleep.

Two less described but important anatomic contributors to OSA are 1) the size and positions of upper and lower jaws, and 2) floppy (collapsible) side walls of the airway (lateral pharyngeal walls).

Jaws that are too small to accommodate properly functioning of the soft palate and the tongue can be a problem. Their orientation can also be a concern. For example, if they are too posterior, or present with an unfavorable angle.

The lateral pharyngeal wall (floppy side walls of the airway) is an important contributor to severity of adult OSA.

Finally, the epiglottis, a flap that closes when we eat so that food does not enter the airway, can also be an anatomic site of obstruction.

Non-anatomic causes of OSA are neurological in nature. You may hear terms such as arousal index, loop-gain, or muscle tone. These are complex neurologic interactions between the brain to the airway muscles.

OSA diagnosis begins with an assessment of symptoms, best captured by “patient reported outcome measures” such as the Epworth Sleepiness Scale (ESS). This is then followed by a “sleep study” called “polysomnography.” This can be done either in a lab setting (attended), or at home. Your doctor can help determine the type of study that is most appropriate. It is frequent that a home study is performed, prior to an in-lab study (if needed).

For children, the risk factors include nasal allergies, enlarged adenoid, palatine, and lingual tonsils, and mal or under-development of the upper and lower jaws.

While obesity is often described in relation to OSA, it is important to know that in younger children, they can actually be underweight.

For adults, obesity becomes a bigger problem with fat accumulation in the airway. Obesity can also lead to hypoventilation, where the lungs do not inflate as readily due to body weight.

As the airway increases in length with age, there is more redundancy and/or collapsibility of the soft palate and side walls of the airway.

Fat accumulation in the tongue, as well as poor functioning of the dilator muscles during sleep, further worsens the condition.

As the jaws stop growing, there is no other way to modify its size or position with the exception of surgery.