Airway Dentistry: Why We Start With the Small Wins

Here’s a question we put to patients, and it sounds blunt because it is. Is it better to start with myofunctional therapy, or with breaking a jaw?

Almost everyone answers that the same way once it’s put plainly. Start with what’s reversible. Then see what’s left.

We’re not against the big interventions, and this isn’t the skeptical case against them. We look for airway problems, and we’ve looked for them for years, before it became a marketing category. We work closely with an orthodontist who performs palatal expansion and facilitates jaw advancement surgery, and we refer for both when they’re warranted. But airway has become a busy corner of dentistry, a lot of what gets said about it is louder than the evidence behind it, and we’ve grown more careful about what we claim can be fixed by changing anatomy alone.

If you’ve already been told your palate needs expanding or your jaw needs advancing, and you’re not quite sure how a dental exam arrived there, this article is the second opinion.

What we actually look for

These are structural findings, and a dental exam is a good place to catch them:

• A narrow or high palate. The roof of your mouth is the floor of your nose. A narrow upper arch usually means a narrower nasal floor above it.
• A tongue that can’t reach the palate, whether from a tie or from years of resting low.
• Tongue posture. Where the tongue lives at rest shapes the arch during growth, and holds space at the back of the throat at every age.
• The downstream signs. Gum inflammation confined to the upper front teeth, scalloped tongue edges, lips apart at rest, wear that doesn’t match the diet. Mouth breathing leaves a signature.

Finding those things is genuinely useful. It’s the next step where the field goes wrong.

The part we got wrong, and corrected

For a while our instinct was straightforward: find the anatomical restriction, fix the anatomy, problem solved.

We don’t think that anymore, and the honest reason is that the data doesn’t support it as cleanly as it’s usually presented. Fixing the anatomy is often part of the answer. It’s rarely the whole answer.

Sleep apnea is a hard problem with a lot of inputs. It isn’t as simple as changing the shape of the skeleton, and we’d rather say that plainly than imply we have a tidier answer than we do.

The container and the contents

This is the clearest way we’ve found to explain it.

Your airway is a space, and two things determine how open it stays: the size of the skeletal container around it, and the volume and behavior of the soft tissue inside it. Surgery and expansion work on the container. On their own they do nothing to the contents.

That distinction isn’t theoretical. When researchers looked at why weight loss improves sleep apnea, the improvement in the apnea-hypopnea index was mediated specifically by reductions in tongue fat. The soft tissue volume was doing the work. The same literature notes plainly that most current therapies don’t target tongue fat at all, which is offered as one reason some patients remain difficult to treat.

Wang SH et al. Effect of weight loss on upper airway anatomy and the apnea-hypopnea index: the importance of tongue fat. Am J Respir Crit Care Med. 2020;201(6):718-727.

So if you enlarge the container and leave whatever is driving the contents untouched, you should expect the benefit to erode over time. The long-term surgical data is consistent with that: improvements hold up over the medium term, then the apnea-hypopnea index drifts back toward moderate over many years.

Camacho M, Noller MW, Del Do M, et al. Long-term results for maxillomandibular advancement to treat obstructive sleep apnea: a meta-analysis. Otolaryngol Head Neck Surg. 2019;160(4):580-593. The apnea-hypopnea index fell from a mean 48.3 to 8.4 events per hour at one to four years, and from 65.8 to 7.7 at four to eight years, then rose to a mean 23.1 at eight years and beyond, which is the moderate range. Of 445 studies screened, 6 met criteria, covering 120 patients, with only 35 of those in the very-long-term group. The authors state that definitive generalizations cannot be made.

A colleague of ours in Philadelphia is a dentist who makes sleep appliances for a living, and he had MARPE for his own apnea. His apnea-hypopnea index came back worse afterward, in the thirties, which is the severe range.

What eventually moved his numbers was three things, none of them skeletal: managing his light exposure and circadian rhythm, changing his diet, and working on tongue function. He puts most of it down to the light environment. That’s his own read on his own case rather than a finding, and we pass it on as that.

The container had been enlarged and nothing else had changed. It was everything else that finally registered on a sleep study. He tells that story openly, which is to his credit, because it isn’t the story the field usually tells.

That isn’t an argument against surgery. It’s an argument for treating the function as well as the structure, which is exactly how we sequence it.

Being fair about MARPE and MMA

We’re not going to undersell these. They’re serious tools and the evidence behind them is better than the skeptical version of this article would suggest.

• Maxillomandibular advancement is among the most effective surgical treatments for obstructive sleep apnea. Meta-analysis reports the apnea-hypopnea index falling from roughly 64 to roughly 10 events per hour, with surgical success around 86% and cure in about 43%.
• Miniscrew-assisted palatal expansion in adults with a genuinely narrow maxilla has produced meaningful improvement, including substantial reductions in the apnea-hypopnea index in a multi-center controlled trial.

Advancement figures: Holty JE, Guilleminault C. Maxillomandibular advancement for the treatment of obstructive sleep apnea: a systematic review and meta-analysis. Sleep Med Rev. 2010;14(5):287-297. Apnea-hypopnea index 63.9 to 9.5 events per hour across 627 adults, with pooled surgical success of 86.0% and cure of 43.2%. Expansion figures: Brunetto DP, Moschik CE, Dominguez-Mompell R, et al. Mini-implant assisted rapid palatal expansion (MARPE) effects on adult obstructive sleep apnea (OSA) and quality of life: a multi-center prospective controlled trial. Prog Orthod. 2022;23:3. Apnea-hypopnea index 28.75 to 11.45 events per hour, a 65.3% reduction, against no significant change in the control group. Fourteen patients received the intervention and ten served as controls, so this is a small trial.

For malocclusion in adults, both are excellent, and that’s often the clearest reason to do them.

Here’s the care we think the numbers deserve. Those studies were done in patients with severe, diagnosed apnea. A mean starting index around 64 events an hour is profound disease. That’s a very different person from someone with a narrow palate, a low tongue, mild symptoms and no sleep study. Applying one group’s success rate to the other is where the overclaiming happens.

Myofunctional therapy before and after, every time

This is the part of our approach we’d defend hardest, and it applies to the surgical cases just as much as the conservative ones.

Before, because nothing about it is permanent, and because it tells you how much of the problem was functional rather than structural. That’s information you want in hand before anyone operates, and occasionally it’s enough on its own.

None of which makes myofunctional therapy easy, and it isn’t free. It asks for daily practice and your own consistency, and that’s a genuine commitment. What it doesn’t ask for is a surgeon, an anesthetic, or a decision you can’t take back.

After, for the reason this whole article has been building toward. Surgery gives you a larger container. It doesn’t teach the tongue to rest in it, or the lips to seal, or the swallow to behave. Retraining that afterward is the piece that works on the contents, and it’s the most direct answer we have to the drift the long-term data shows.

We’ve seen what happens without it. Patients in our own practice have had expansion or advancement for reasons that genuinely warranted it, usually a bite that needed correcting, with better breathing as the hoped-for bonus. The breathing benefit didn’t hold, and neither of them did the functional work afterward, though we’d recommended it.

That’s two cases and it settles nothing on its own. It’s the reason that when a patient of ours is going to go through expansion, we evaluate tongue function first, and myofunctional therapy before and after is generally what we recommend.

Dr. Lee-Mirzayan is certified in myofunctional therapy and handles that side here. A typical program runs about 8 weeks, with a check-in every other week.

So where do we start

With what’s reversible, for the reason at the top of this article. Specifically:

• Make the nose work. Saline rinses, treating allergy properly rather than seasonally, and a real ENT opinion when the obstruction is structural. A nose that works is the precondition for everything else.
• Retrain the pattern. Myofunctional therapy. No appliance, no surgery, nothing to wear.
• Release a genuine tether first. No amount of therapy helps a tongue that physically can’t reach the palate. Tongue-tie release is sometimes the precondition, not the treatment.
• Fix the timing, and the light. Light at night suppresses melatonin, and short-wavelength blue light does it more effectively than any other part of the spectrum. Sleep timing and evening light exposure are unglamorous levers and they move the needle. So does avoiding late meals.
• Address the soft tissue burden where weight is part of the picture, because that’s the one intervention shown to work on the contents rather than the container.
• Get a diagnosis. If apnea is a real possibility, that means a sleep study, from a physician. We can’t diagnose it from a dental chair and we’ll say so.

On light and melatonin: Brainard GC, Hanifin JP, Greeson JM, et al. Action spectrum for melatonin regulation in humans: evidence for a novel circadian photoreceptor. J Neurosci. 2001;21(16):6405-6412. Thapan K, Arendt J, Skene DJ. An action spectrum for melatonin suppression: evidence for a novel non-rod, non-cone photoreceptor system in humans. J Physiol. 2001;535(Pt 1):261-267. Two independent studies, published weeks apart, both found peak sensitivity for melatonin suppression in the short-wavelength range around 460 to 480 nm, and both concluded that a photoreceptor other than the rods and cones was responsible.

Every item on that list is low risk, and every one of them can be undone. Between them they also tell you something you can’t learn any other way: how much of the problem was behavioral, and how much is genuinely structural.

And when the answer is structural, we say so

Sometimes the simple measures get a fair run and the problem is plainly skeletal. Then expansion or advancement is the right conversation, and we’ll have it without hedging.

We work closely with an orthodontist who performs MARPE and facilitates maxillomandibular advancement. Referring for either is a normal part of what we do, not a last resort we avoid discussing. The surgery happens with surgeons, not here. The therapy on both sides of it happens with us.

What we’re not

We’re not a sleep clinic and we don’t diagnose sleep apnea. We’re a dental practice that pays attention to the airway, catches the anatomy that contributes to it, treats the parts a dentist can treat, refers the parts we shouldn’t, and is honest about which is which.

That second opinion costs you very little. We’ll tell you what we see, what we’d try first, and what the evidence does and doesn’t support.

Worth a conversation

Call us at 702-734-0776 or tell us what’s going on.

Common Questions