by Marc Ackerman
Much heat and very little light has been shed on the topic of airway orthodontics. The treatment of sleep disordered breathing in the pediatric population differs significantly than that in the adult population. It’s pretty obvious. One population is growing and the other is not. Even more specifically in the growing population, there are differential rates of growth between lymphoid, neural, general and genital tissues (Scammon, Ring a bell?). Lymphoid tissue (tonsils, adenoids) size obtained as a percentage of total postnatal growth reaches 190% by roughly age 11 and then regresses back to 100% by age 20. However, this doesn’t tell you where the tissue is located nor does it tell you how much tissue is present in any given patient. To date, the airway orthodontists among us, utilize conventional cephalometric radiology and cone-beam CT scans for assessing the location and quantity of lymphoid tissues in their patient’s. The really cool software will subtract out the soft-tissue airway (kind looks like pre-cooked chitlins). Though not useful, this probably gives the patient the illusion that you might know what you’re actually looking at.
Not really. Breathing is a dynamic process. Radiographic techniques save CineMRI are a static view of a dynamic space. Although dynamic, a sleep study (polysomnogram) only tells the clinician the amount of rem/nonrem sleep, types of apneas and hypopneas and oxygen/carbon dioxide levels during the various sleep stages. So, the first line evaluation of dynamic movements of the airway is ambulatory nasal endoscopy. However, this too falls short in its ability to evaluate the airway during sleep. Competent multi-disciplinary sleep teams (I serve on one, so don’t call bullsh$t off the bat) will employ drug-induced sleep endoscopy (DISE) for children with persistent OSA after tonsillectomy, those with OSA without tonsillar hypertrophy, children with risk factors predisposing then to multiple sites of obstruction, or when sleep‐state dependent laryngomalacia (congenital softening of the tissues of the larynx above the vocal cords) is suspected. After assessing the soft-tissues of the airway (far more causal in pediatric sleep-disordered breathing) via DISE, a more honed differential diagnosis and evidence-based treatment plan can be initiated.
As far as I can tell, pediatric airway orthodontic practitioners assume that the teeth and jaws are the primary cause of sleep disordered breathing or in few cases assume that if residual sleep-disordered breathing exists post adenotonsillectomy, then it must be dental in nature. Aside from the micrognathic, severely retrognathic and syndromic mandibles out there, I’d have to say the assumptions above are misguided.
Is there a role for orthodontics in sleep-disordered breathing? Maybe. But the onus of proof is on those airway-friendly orthodontists who say it is. You’re entitled to your own opinion but not your own evidence. So ladies and gentleman, let’s see some peer-reviewed data.
So, if you’ve just attended the AAO Consensus Conference on pediatric airway orthodontics and you’re about to jump head first in this type of treatment, good luck rolling the dice. As Ben Burris and I wrote in a previous blog about orthodontic consensus conferences, there are three drivers of these meetings:
CON– to trick
non-SENS-to present untested theories
US-to expand orthodontist’s scope of practice with the hope of generating revenue…
PS-I’M SORRY TO NERD OUT ON THE ANATOMIC AND CLINICAL TERMINOLOGY BUT SOMEBODY’S GOT TO DO IT.