How common is OSA?

Recent studies suggest that the prevalence of OSA is 1-4% in children of normal weight but those numbers climb to over 50% in children who are obese. 10% of the men and 3% of the women between the ages of 30 and 50 have OSA. Those numbers rise to 17% in men and 9% in women over the age of 50 as their overall muscular tonicity decreases. The prevalence of OSA in obese men and women rises to over 75% as body mass increases.

What are the causes of OSA?

Decreased or altered neuromuscular tone in the upper airway, increased volumes of soft tissue around the airway (obesity), old age (general loss of muscle tonicity throughout body), neuromuscular conditions, and the presence of abnormal adjacent structures that narrow the airway (like enlarged tonsils, adenoids, pharyngeal pillars, and the uvula). There has been no evidence linking the position of the teeth, the width of the arches, the size of the nasal cavity, or the length of the lingual frenum to the occurrence of OSA. Neither has there been any evidence linking any orthodontic procedure (headgear, extractions, or so-called “backwards pulling mechanics,” etc.) to the development of OSA. Additionally, there has been “no direct causal relationship between craniofacial structure and pediatric SDB.” OSA is not simply an anatomical disease.

Whare are the risk factors for OSA?

Decreased muscle tonicity of the upper airway which allows its collapse is the cause of OSA, and anything that causes, reduces, or contributes that condition can be a factor. Obesity is the #1 risk factor as decreased muscle tonicity in combination with a reduction in the lumen of the airway due to fat deposits makes obturation much more likely. Aging, injury, neuromuscular disorders, being male, having a larger neck circumference, smoking, and genetics are also known risk factors. In children, tonsil and adenoid hypertrophy is an important factor. It is important to note that there has been no direct causal relationship identified between craniofacial structure and pediatric SDB (i.e., arch constriction, dental extractions, headgear therapy, or retraction of the anterior teeth).

How is OSA diagnosed?

As of right now, the only accepted diagnosis of OSA is made via a formal laboratory sleep study using a technique called polysomnography (PSG). Although home study kits and smartphone apps are available and gaining popularity, it was the consensus of the experts who spoke that to date none of them have all of the necessary features to provide an accurate diagnosis (i.e. none currently measure brainwaves). Orthodontists cannot order, nor are they qualified to interpret the results of a PSG. The current standard for measuring the severity of OSA is the Apnea Hypopnea Index (AHI) which represents the number of sleep disturbance “events” per hour. For adults, less than 5 is normal, 5 to 15 is mild, 15 to 30 is moderate, and over 30 is considered severe. For children, less than 1 is normal (in other words, children should have no apnea or hypopnea events during sleep).

Can OSA be diagnosed in radiographs?

Interesting and instructive 3D images can be constructed from CBCT scans that can produce measurements like Minimum Cross-sectional Area (MCA). Although some correlations have been found between MCA values and the “risk of OSA,” OSA cannot be diagnosed from radiographs. Only a formal sleep study provides a definitive diagnosis. Tonsils and adenoids seen in lateral cephalograms may be a factor in pediatric OSA, but again their presence alone does not yield a diagnosis. ENT’s confirm airway obstruction using endoscopy, not radiographs. Because OSA is not simply a structural problem, identification of “predisposing morphologies” can be misleading. Many patients who have these predisposing morphologies do not suffer from OSA. Conversely, other patients who have absolutely “normal” appearing anatomy may suffer from it. In summary, “2D and 3D images do not provide a proper risk assessment technique or screening method.”

What treatments help treat OSA in adults?

The “gold standard” for the treatment of sleep apnea in adults is continuous positive air pressure (CPAP). CPAP has a success rate of over 90%. For patients who cannot wear a CPAP, oral appliance therapy (OAT) has been shown to be 65% successful. Other approaches to treating OSA in adults include dieting and exercise (low success rate due to low compliance), gastric surgery (better than dieting alone because it is more permanent), myofunctional therapy, oxygen therapy, oral pressure therapy, tongue stabilization therapy, cervicomandibular collars and oral surgery. Of these approaches, only surgery and permanent weight loss appear to offer possible “cures” for the condition.

What kinds of oral surgery are used to treat OSA?

Oral surgery involving the oropharynx, nasal cavity, tongue, hyoid bone, throat, and jaws have all been used to treat OSA. Surgeries involving the uvula, tonsillar pillars, and septum are all aimed at increasing the flow of air through the oropharynx. Tongue surgeries attempt to pull the tongue forward, pull the back of the tongue down, make the tongue smaller, or stimulate the tongue to increase the tonicity of its muscles. These surgeries are only successful if these structures are actually a factor in the collapse of the oropharynx. There is no evidence that a SARME helps prevent this collapse and is not typically indicated for the treatment of OSA. The most aggressive, and most successful surgical procedure used to treat OSA is the two-jaw maxillomandibular advancement (MMA).

Why would a patient need Maxillomandibular advancement?

The maxillomandibular advancement provides a “cure” for OSA in 86% of patients. Patients may choose this option if they can’t tolerate CPAP, oral appliances, are young and don’t want to spend the rest of their lives wearing CPAP or appliances, or if other craniofacial issues exist that justify the movement of the jaws. The biggest challenge for these patients is the change in the occlusion after both jaws are moved, which is why MMA is always performed in conjunction with orthodontic treatment. Although highly successful, there are still 14% of patients who still have problems with their oropharynx collapsing after surgery (not surprising since OSA in not merely an anatomical condition).

What treatments help children with OSA?

Weight loss alone eliminates OSA in over 50% of young patients who are able to comply (obesity being the #1 risk factor). Hypertrophic adenoids and tonsils are the second most common cause of breathing disorders in children and adenotonsillectomies (T&A) are still the treatment of choice. If there is a concomitant maxillary constriction, RME therapy AFTER a T&A may be prescribed by the attending physician. Otherwise, for non-OSA orthodontic patients, there is no reason to expand “in the name of airway” if there is no maxillary transverse deficiency or crossbite. Hoxha et al reported that although palatal expansion for OSA children may result in increased dental arch width, nasal width, and pharyngeal area, there are no differences in OSA parameters between expanded versus control patients. Additional therapies include treating allergies, myofunctional therapy, oral appliances, oral surgery, and CPAP.

Can we prevent or cure OSA with orthodontics?

Maxillary expansion (with or without TAD support) has not been definitely shown to prevent nor cure OSA. “The benefit of RME for children with OSA is mostly supported by low-quality studies (no control groups to compare patients against normal growth) … ranodomized trials [have] found no grounds for its use.” There is no evidence that merely expanding the palate (including the nasal cavity) reduces “OSA parameters.” The size of the nasal cavity is not linked to the collapsibility of the oropharynx. In other words, increasing the size of the underlying skeletal structures does not insure that the overlying “soft structures” will follow suit or respond differently. Dr. Charles Guilleminault, a pioneer in the field of sleep medicine, suggests that frenectomies performed in the first year of life may help prevent OSA. Although there may be other reasons to perform them after the age of 1, OSA is not one of them.

What is the appropriate role of the orthodontist in OSA?

The most important thing orthodontists can do is understand the disease, screen for it among their patient population (where the prevalence of OSA is higher than in the general population), refer to the appropriate specialist when it is suspected, and under the direction of the physician provide dental or orthodontic procedures as requested. In young patients, that treatment may include orthopedic expansion after a T&A. In both young and old, it may be providing oral appliances that hold the mandible forward during sleep. It is recommended that any orthodontist desiring to provide oral appliances for the treatment of OSA receive additional training to do so properly and be highly vigilant of the likely dental changes that will take place by the long-term use of these devices.

How can orthodontists screen for OSA in their practice?

There are two important tools that we use with all of our new patients. First, the Pediatric Sleep Questionnaire (PSQ) is currently the best way to identify OSA in children. It is a simple one-page form that is easy for parents to fill out and for us to interpret. The STOP-BANG survey is currently the best screening tool we can use to identify adults who have, or are at risk of having, OSA. When a patient is suspected of having OSA or at high risk, we make a referral to an appropriate ENT or sleep medicine physician in our medical community.

What can't or shouldn't orthodontists do relative to OSA?

Orthodontists cannot predict, prevent, diagnose, or cure sleep apnea. As mentioned previously, neither lateral cephalograms nor CBCT scans allow us to diagnose OSA. There are no orthodontic procedures that prevent or cure OSA. An exhaustive review of the currently accepted scientific literature does not support the routine use of expanders or frenectomies for the prevention of OSA. “Airway” should not be used as an excuse for advocating specific approaches to treatment (i.e. early palatal expansion, non-extraction treatment, non-retraction treatment, etc.) Simply put, there is no evidence in the literature that any orthodontic procedure helps prevent nor predisposes patients to OSA. “When one considers the complex multifactorial nature of the disease, assigning the cause of OSA to any on minor dental factor or change in dentofacial morphology is not logical. In spite of this, misinformation is created and disseminated widely.”