Comprehensive Oral Appliance Treatment for Obstructive Sleep Apnea
SUMMARY -
SUMMARY - Obstructive sleep apnea (OSA) occurs when the pharyngeal airway gets plugged by the tongue base; sometimes with soft tissues such as the distal end of the soft palate filling in the space between the tongue base and the pharyngeal wall to complete the seal in the nasopharynx; and sometimes with the epiglottis just beneath the tongue base closing the glottis like a trap door in the hypopharynx. Because the obstruction usually occurs at multiple levels of the pharynx, surgery is only predictably effective if it is multi-level. CPAP is usually effective, because ballooning out the pharynx makes it too large to be obstructed at any level above the epiglottis; but people find it difficult to tolerate, and the continuous positive pressure reduces the intermittent negative pressure needed for glymphatic drainage. Mandibular advancement appliances are well tolerated, but they are only effective in about half of OSA patients, because the mandible is only loosely attached to the tongue base, and not at all to the soft palate. For OSA patients who have failed to improve from wearing a mandibular advancement appliance, the appliance can now be made effective by adding devices to also control the soft tissues at each level of the pharynx, one at a time, until the problem is solved. First, a low-force silicone rubber soft palate elevator is added to "tent" the soft palate in order to draw its untouchable distal end antero-superiorly away from the pharyngeal wall in the nasopharynx. Second, the tongue body and lateral borders of the tongue base are “pinned” against the advanced mandible, between tongue gripping plates covered with thousands of tiny forward slanted bristles (tongue velcro), which prevent it from dropping back against the pharyngeal wall in the oropharynx. Third, small adjustment mechanisms can be added to the back of the upper tongue gripping plate to gradually and progressively pry its tail segments and thereby also the lateral borders of the tongue base antero-inferiorly away from the epiglottis in the hypopharynx. For edentulous patients, the soft tissue controls can be attached to denture base plates (dentures without teeth); where the tongue holding is especially effective, because the tongue gripping plates can extend all the way out to the cheeks; and the base plates require little retention, because they are constantly cushioned by the tongue.
RATIONALE - Current OSA treatment is inadequate. Some people benefit from pharyngeal soft tissue surgeries such as cutting out hypertrophic soft tissue from the tonsils or distal end of the soft palate (UPPP), advancing the genioglossus muscle, suspending the tongue base along with the hyoid bone from the lingual plate of the symphysis,1-2 implanting an electrical stimulator to protrude the tongue base during inhalation,3 and radiofrequency ablation or surgical reduction of the tongue base; but it's hard to know which treatments will benefit whom. Predictable success surgically requires multi-level structural rebuild, usually maxillo-mandibular advancement that advances both upper and lower jaws by 8-10 mm.4
CPAP is usually effective, but many find it difficult to tolerate; and the positive air pressure that it employs to keep the pharynx open also extends into the chest, where it reduces the negative intrathoracic pressure that is needed to drain the waste products of neural metabolism as part of the glymphatic circulation process. During sleep, especially slow wave sleep, the neurons stop producing new waste products, and the brain removes the old waste products in a nightly cleansing (brainwashing) in which the interstitial spaces increase about 60% to become a mixing chamber. The interstitial fluids and neurologic waste products are sucked out by the negative intrathoracic pressure during each inbreath along perivenous channels, 1-2 drops per inbreath. Then, during each exhalation, fresh CSF is pumped in by articular pressure along periarterial channels. However, CPAP supplies positive pressure in the same tubes that require negative pressure to suck CSF out of the cranium. Arterial pressure can still drive the system; but the loss of negative intrathoracic pressure must interfere with the drainage. Glymphatic circulation diminishes with age and in proportion to amyloid burden increases, and the biomarkers of Alzheimer's and other neurodegenerative diseases are first detected in the CSF, suggesting that loss of glymphatic drainage could be an important etiologic factor.
PATHOPHYSIOLOGY - Some researchers blame OSA on an inadequate neuromuscular arousal mechanism - commonly described as the muscles relaxing too much during sleep. The pharyngeal dilator muscles can certainly open the airway. In monkeys, airway obstruction triggers firing of the genioglossus in synchrony with inspiration.15 In humans, it triggers a rapid increase in tonus of the pharyngeal dilator muscles (loop gain) until the arousal threshold is reached and breathing is restored. In younger people, the autonomic system is more efficient, and this arousal mechanism is strong enough to open the airway with each breath (the model for Inspire), or to be able to pull the air through a narrow vibrating tunnel. It may allow hypopneas but not apneas (upper airway resistance syndrome), because loop gain restores breathing before the airway is obstructed for long enough to produce hypoxia. In some people with high loop gain, obstruction events can cause an over-reaction, destabilize the ventilatory system, and prevent return of normal breathing. Some people with low arousal thresholds have their sleep repeatedly disturbed by minor obstructions (respiratory effort related arousals) or even by events that are not associated with desaturation, such as snoring or a CPAP mask. Precision medicine can use medications that change arousal threshold and loop gain to improve sleep by altering the response to airway obstruction; but an inadequate response to the obstruction should not be considered the cause of the obstruction; and the goal of treatment should be to provide a resting airway passage that does not become obstructed, trigger sympathetic arousals, or require a protective neuromuscular response.
Other researchers blame OSA on collapse of the pharyngeal walls; and they cite the model of a Starling resistor, in which the rate of flow through a tube within a pressurized chamber depends on the pressure in the chamber, and the flow through the tube stops if the pressure in the chamber is greater than the pressure in the tube. Rapid airway flow through a narrow tunnel pulls the pharyngeal walls into the tunnel (Bernoulli forces), however that pull stops as soon as the airway flow stops, leaving only the weight of the soft tissues and the cohesion (stickiness) between the mucous membranes lining the pharyngeal walls to resist the much greater pressure produced inside the tube by a diaphragm desperately trying to inhale. Maintaining the obstruction requires a stopper; and the only structure inside the tube with enough physical integrity to function as a stopper is the tongue base. People don't choke on noodles. They choke on a piece of meat. The piece of meat in OSA is the 6 cm thick slab of muscle at the base of the tongue. Floppy pharyngeal tissues can fill in around the tongue base to complete the stopper like a gasket in the nasopharynx, but they can't obstruct the airway without the support of the tongue base.12-14
The tongue base is thus the basis for obstructive sleep apnea. It can obstruct the oropharynx by directly contacting the pharyngeal wall; the nasopharynx by incorporating a wedge of soft tissues in the narrow gap between it and the pharyngeal wall; and the hypopharynx by pushing on the epiglottis just beneath it. Imaging has found the location of the obstruction too variable to provide a basis for targeted treatment. It can even seesaw back and forth between different locations. During drug induced sleep endoscopy, the obstruction occurs most frequently in the nasopharynx; but it also occurs frequently in the oropharynx, behind the tongue, and at the epiglottis.11
Multi-level oral appliance treatment can treat the pharynx at all levels, by adding one modality at a time, until the problem is solved. The suggested protocol for dentate patients begins with a mandibular advancement appliance, followed by adding a soft palate elevator, then a tongue holding device, then tongue base titraters. The protocol in four stages is described below.
STAGE ONE - ADVANCING THE MANDIBLE - reduces the Pcrit - the amount of positive pressure needed to push air through the obstruction. It enlarges the airway passage tunnel by stiffening the pharyngeal walls and pulling the lateral pharyngeal walls further laterally. It also enlarges the space in front of the tongue base; however it can't advance the tongue base into the space created, because the mandible is only attached to the tongue base by muscles, which lose their tonus during sleep. As a result, even extreme mandibular advancement cannot prevent the tongue base from falling back into the pharynx - it just has further to fall; and mandibular advancement is only effective when it shifts the tongue base anteriorly far enough to enlarge the oropharynx.16
HERBST APPLIANCES – are the mandibular advancement appliances with the longest history of effective treatment for OSA and the best control of mandibular position; but the hardware they employ was designed more than a century ago for bite jumping in children, and it is unnecessarily bulky and restrictive for use in adults. The bolted connectors bind in a manner that prevents wide lateral mandibular movements, which leads to frequent breakage; the downward vector of force on the mandible can force the mouth open leading to habitual mouth breathing; and adjustments require a special tool and have limited range. To solve these problems, Dr. Summer's has redesigned the Herbst appliance for adults (FDA # K243752); with a lower profile, virtually unbreakable components, freely moveable connectors that cannot bind or restrict lateral movements, a more upwardly directed force on the mandible, and an unlimited range of adjustment without tools just by sliding the rod out of the tube, rotating the tubing assembly on the externally threaded connector arm, and re-inserting the rod into the tube to lock in the adjustment. Palate expansion can be included by using detachable telescopic components so the upper member with the expansion screw and embedded anchors can be used all day, and the lower member with the telescopic components can be hooked onto the upper anchors every night for sleep.
TITRATION - Advancing the mandible to a position of maximal tolerable benefit improves effectiveness; but extreme advancement can damage the dentition, and its beneficial effects on airway dimensions diminish over time due to regressive osseous remodeling at sites of large forces.
TESTING - After titrating a mandibular advancement appliance, its effectiveness should be tested; because partial reductions of OSA can feel like success, but they usually fade over time as the remaining incidents continue to stretch out the pharyngeal soft tissues. Multi-night testing eliminates the first night effect, in which some patients do not spend enough time in deep sleep to demonstrate their apnea. If sleep testing shows that OSA persists despite mandibular advancement, more effective treatment requires also clearing the soft tissues from the nasopharynx and hypopharynx, as described below.
STAGE TWO - "TENTING" THE SOFT PALATE
In the nasopharynx, loose pharyngeal soft tissues get sucked into the narrow gap between the tongue base and the posterior pharyngeal wall like a wedge to form a seal that plugs the airway like a gasket. In children, the loose soft tissues often come from the lateral pharyngeal walls, such as swollen tonsillar tissues. In adults, they usually come from the distal end of the soft palate, sometimes in combination with the lateral pharyngeal walls (so-called concentric collapse).
The distal end of the soft palate is full of gag reflexes, so it can't be contacted directly; but it can be drawn antero-superiorly away from the obstruction by elevating the center of the soft palate, where there are no gag reflexes. The soft palate is a thin sheet of muscles suspended from a tendinous keel-like aponeurosis running along its midline from the hard palate to the uvula. During sleep, its muscles lose their tonus, leaving its distal end hanging in the airway passage and swinging back and forth due to airway flow.17 In this relaxed state, the midportion of the aponeurosis can be easily elevated 1/4" or more by a silicone rubber bulb on the end of a thin flat stainless steel arm without any negative consequences. The light pressure there is easily tolerated, and the arm is flexible enough to accommodate the functional movements of the soft palate during swallowing, when breathing stops anyway. Most patients don’t even know it’s there. The soft palate elevator is FDA cleared # K222127.
The anatomical effect of a soft palate elevator can be seen in the X-rays below, where the black arrows mark the top of the soft palate and the thin white line in the right side X-ray is the metal arm of the soft palate elevator. A tongue holding device is also used in the right side X-ray.
BEFORE INSERTING THE SOFT PALATE ELEVATOR AFTER INSERTING THE SOFT PALATE ELEVATOR
Tenting the soft palate also tightens the nearby pharyngeal wall by stretching it, as was demonstrated above, after horizontal lines were stamped on the pharyngeal wall with gentian violet. Inserting the device caused the straight lines on the left side photo below to become curved on the right-side photo. Tightening the pharyngeal wall makes it less easily sucked into obstructive contact with the tongue base and less prone to vibrate during snoring, as was shown by ability of inserted palatal stiffeners (Pillar procedure) to successfully treat some people.
Soft palate elevation is often combined with mandibular advancement, because the two modalities work better together than either one alone. Simply removing the gasket (the distal end of the soft palate) from the obstruction without also making changes in the functional environment that produced the gasket invites formation of a new gasket, and simply changing the functional environment by advancing the mandible without also removing the gasket that completes the stopper may not produce enough anatomical change to restore airway flow. If the combination of mandibular advancement and soft palate elevation is not effective, the next stage of the treatment involves holding the tongue in an advanced position to prevent it from dropping back into the pharynx.
STAGE THREE - HOLDING THE TONGUE
The tongue holding device holds the tongue in a slightly advanced position by "pinning" it against the advanced mandible. The entire tongue body and the lateral borders of the tongue base, where there are no gag reflexes, are held in the space shown below between specialized upper and lower tongue gripping plates, each containing thousands of tiny plastic pin points (AKA tongue velcro), which are so closely packed that they feel like fuzz and all slanted forward at a 45 degree angle to prevent the tongue from sliding backward into the pharynx. The plates are anatomically shaped, but they can also be easily reshaped if necessary by dipping them in boiling water.
THE UPPER TONGUE GRIPPING PLATE – 4,000 sewing needles were used for modeling the upper tongue gripping plate, because they fit perfectly between the filiform papillae that cover the tongue, as seen below. When pushed gently into the dorsal surface of the tongue, the plastic points sink into the spaces between the papillae and thereby provide an excellent grip that requires very little pressure to hold the tongue securely all night.
The sewing needles were contoured and slanted, as shown below left; before making a mold and processing it in dental acrylic, to form a curved 2 mm thick plate, as shown below right.
The upper tongue gripping plate is then split into anterior and posterior ends connected by torsion springs (shown below left and middle) and attached by a length of tubing, as shown below right, to facilitate the wave of muscle contraction that passes posteriorly along the tongue during swallowing.
THE LOWER TONGUE GRIPPING PLATE – 10,000 accupuncture needles were used to make the model for the lower tongue gripping plate, because the underside of the tongue is unkeratinized and therefore much more sensitive. The pins were shaped to fit the underside of the average tongue and slanted forward at a 45 degree angle, as seen below left; and then their surface was duplicated in dental acrylic to form a 1.5 mm thick plate that can be attached to a lower base appliance, as seen below right.
STEEL MODEL FOR MOLD FOR LOWER TONGUE GRIPPING SURFACE LOWER BASE APPLIANCE
SPRING MOUNTING – A thin wire spring used to mount one of the tongue gripping plates provides a cushioned grip that prevents accidental tongue release during submaximal mandibular movements, including bruxism. Under so little pressure, the tongue gripping plates effectively float on the tongue. Spring mounted upper and lower tongue gripping plates are shown on upper and lower denture base plates below
UPPER TONGUE GRIPPING PLATE SPRING MOUNTED LOWER TONGUE GRIPPING PLATE SPRING MOUNTED
THE TARGET TONGUE POSITION - The tongue gripping plates are shaped and mounted to hold the patient's tongue in a target treatment position, with its tip between the incisors, as seen below. Because the tongue cannot escape during sleep, patients awake with the tongue in the same position. In the illustration below right, the tongue holding device is carried on a Herbst appliance to advance the tongue and mandible together. Because the mandible functions as the bone for the tongue, advancing them together is easier and more effective than advancing either one alone.
. TARGET TONGUE POSITION WITH HERBST APPLIANCE TO ADVANCE MANDIBLE
The tongue holding device for dentate patients includes bite stops, small flat stable plateaus of acrylic located over the disto-buccal cusps of the terminal molars, where they absorb all bite forces before those forces can hurt the tongue in a forceful clench. In the photo above left the upper bite stops are yellow, and the lower bite stops are green. In the photo below, the upper bite stops are shown in green.
The X-rays below show a patient's tongue coated with a radiopaque paint before and after inserting a tongue holding device. In the left side X-ray, the paint forms a puddle in the foramen cecum. In the right side X-ray, the paint forms a V shape where the tongue has curled around the end of the upper tongue gripping surface alongside the distal root of the second molar. Also the right side X-ray includes a soft palate elevator, the arm of which forms a white line. The soft palate elevator and tongue holding device are often combined to separate the soft tissues that commonly contact to form the nasopharyngeal obstruction.
TONGUE IN RESTING POSTURE TONGUE BASE ADVANCED ABOUT 10 MM
STAGE FOUR - CLEARING THE HYPOPHARYNX
If the OSA persists, small adjustment mechanisms (tongue base titraters) can be added to the back of the upper tongue gripping plate to shift its tail segments, which maintain contact with the lateral borders of the tongue base, gradually further away from the obstruction. The body of the upper tongue gripping plate, which has been stabilized by the grip of the tongue and the bite stops bracing the mandible, forms a good platform from which to continue shifting the tongue base. The tail segments can be shifted in progressive 1.3 mm increments, as shown below.
BEFORE SHIFT AFTER SHIFT
TONGUE BASE ADVANCED IN UPPER OROPHARYNX TONGUE BASE ADVANCEMENT EXTENDED INTO UPPER HYPOPHARYNX
The X-rays above show a patient's tongue painted with a radiopaque paste before (left) and after (right) using the tongue base titraters to shift the tail segments of the upper tongue gripping surface and the white V-shaped area marking the end of the upper tongue gripping plate further down and back, which has further increased the sagittal width of the airway space in the lower oropharynx. The thin white line is the arm of a soft palate elevator. The soft palate elevator and tongue holding device are often used together, because they separate the soft tissues that contact to obstruct the nasopharynx.
The tongue base titraters have a 25 degree range of adjustment, as shown below, which enables them to first shift the tail segments down-and-back, to get them as far as possible behind the tongue base before shifting them forward to pry the tongue base anteriorly off the lower pharyngeal wall and away from the epiglottis.
BEFORE ADJUSTMENT ADJUSTED DOWN-AND-BACK ADJUSTED DOWN-AND-FORWARD
The shift from down and back to down and forward is pictured below. The green acrylic build-ups over the third molars are the bite stops.
TAIL SEGMENTS DOWN AND BACK TAIL SEGMENTS DOWN AND FORWARD
The photos below show one tail segment rotated down-and-back and the other rotated down-and-forward.
EDENTULOUS - people have a much higher prevalence of OSA, because they have no platform against which to brace the mandible to prevent it from pushing the tongue base back into the pharynx during sleep. Also, edentulism has been shown to produce various functional and sensory deficiencies in the jaw system, increased collagen in the extracellular matrix of the superior pharyngeal constrictor muscle, and reduced tonicity in the pharyngeal musculature.18-22 However, the effect of losing the dentition also depends on how the bite had been affecting tongue posture. For example, if a deep anterior overbite had been crowding the tongue posteriorly, removing that restriction could enable the muscles to maintain an improved tongue posture. Wearing dentures during sleep reduces OSA in some people but not others.23-25
Edentulous OSA patients can’t tolerate mandibular advancement, because their soft tissues can’t withstand the pressures required to push the lower jawbone forward off the upper jawbone; but they can use new soft tissue controls carried on denture base plates (dentures without teeth). The denture base plates are continuously seated by the tongue acting like a big cushion, and they are not asymmetrically loaded in chewing, so they can extend well beyond the edentulous ridges. They can even be worn during sleep by some people who cannot wear dentures during the day.
Tongue holding is especially effective in the edentulous, because there are no teeth in the way of the tongue gripping plates, and there is no need to limit increases in vertical dimension. However, advancing the tongue during sleep could apply directional pressures to the edentulous ridges from the passive stretch of the jaw closing muscles, therefore the tongue is just held up against the upper denture base plate to prevent it from dropping back into the pharynx. To maintain the grip on the tongue, prevent accidental release during submaximal mandibular movements, and also help raise tongue posture; the lower tongue gripping plate can be mounted on a fine wire spring to gently and continuously push it up against the underside of the tongue, as shown on page 4. A chin strap may be needed in conjunction with the appliance to prevent the mandible from dropping open.
Treatment for denture patients is described in more detail under in a separate file under the tab SLEEP APNEA.
COMBINING SOFT PALATE ELEVATION AND TONGUE HOLDING – is also more effective than either one alone, because the two modalities separate the tissues that contact to obstruct the nasopharynx by pushing them in opposite directions. The tongue is pushed down and forward while the distal end of the soft palate is drawn upward and forward. In addition, combining these two modalities in the edentulous stabilizes the upper base plate between the superiorly directed pressure from the tongue and the inferiorly directed reciprocal pressure from the arm of the soft palate elevator.
CLINICAL CONSIDERATIONS
VERTICAL DIMENSION - the height of an oral appliance, which determines the interarch space when the appliance is worn, affects airway dimensions in a manner that varies widely depending on facial form. Increasing vertical dimension increases airway space in some people and decreases it in others. Most oral appliances should be no taller than necessary for structural integrity, because increasing the vertical dimension far enough to engage the passive stretch of the jaw closing muscles produces compressive forces that can damage the joints and teeth and make the perioral muscles strain to achieve a lip seal. Appliances for patients with very strong jaw muscles and a deep anterior overbite can include a front flat bite plate to reduce the forces of nocturnal bruxism and redirect the remaining forces axially onto the anterior teeth to gradually reduce the overbite. Patients with weak jaw muscles and excessive vertical dimension (usually accompanied by a gummy smile and difficulty maintaining a lip seal), are more likely to have problems with an appliance that significantly increases vertical dimension; and shortening their teeth (equilibration) can make appliance wear more comfortable. In full denture patients, vertical dimension increases can be used to better grip the tongue by passive stretch of the jaw closing muscles.
MOUTH BREATHING – impairs sleep quality and exacerbates OSA. It prevents the nose from moistening, filtering, and warming the air before it hits the throat. It prevents the release of nitric oxide from the paranasal sinuses into the lungs, where it is needed to help widen blood vessels and improve oxygen intake. It reduces glymphatic drainage through the cribiform plate, which normally accounts for 15-30 percent of the total drainage. It also reduces respiration, because the nose acts like a little lung. Wearing nose clips produces reduced arterial oxygen levels. Mouth breathing has been shown to decrease sleep quality and exacerbate OSA.
OBLIGATE MOUTH BREATHERS - have nasal cavities that are too small to allow adequate resting nasal airway flow, so their lips stay parted to maintain an oral airway passage. Many people with nasal cavities that are barely wide enough to allow adequate resting airway flow become obligate mouth breathers whenever a slight allergy or rhinitis swells their nasal cavity lining. Restrictions to nasal airway flow produce downstream turbulence, which can move loose pharyngeal soft tissues into the pharynx.
In most obligate mouth breathers, nasal breathing can be restored by slow non-surgical palate expansion using removeable expansion screw appliances. In adults, the two maxillary bones don’t separate at the midline suture, but they respond to light steady transversely directed forces by rotating outward in a process that unfolds the upper jawbone like spreading a pair of wings.26 The expansion must be maintained post-treatment by nightly wear of a retainer with a bite table that is broadly loaded during nocturnal bruxism and ensuring a stable natural bite to function as a daytime retainer. Better nasal airway flow can have downstream effects; but it rarely relieves OSA, because the expansion occurs so far from the obstruction.27
HABITUAL MOUTH BREATHERS - use an oral airway despite having an adequate nasal airway. Usually, the habit arises from an open-mouth resting posture due to a framework of bones and teeth (and sometimes the bite surfaces of a dual arch oral appliance) that is longer vertically than the drape of skin and muscles hanging down to cover the face. When the muscles relax, the lips part, which creates an oral airway passage that becomes the habitual route for breathing. The habit can usually be eliminated by almost any way of holding the mouth closed; including chin straps, medical tape (mouth taping), thick foam cervical collars, or interarch orthodontic elastics attached to oral appliances that tightly fit on the teeth.
Over time, habitual mouth breathers can become obligate mouth breathers due to the effects of mouth breathing on facial growth. Mouth breathing lowers mandibular posture to create an oral airway passage, and postural forces provide the light steady forces that shape bones. As a result, mouth breathing lengthens the face, which also narrows the face by pushing in on the cheeks. Conversely, strengthening the genioglossus muscle by means of exercises (myofunctional therapy) can increased its tonus, which may enable a return to nose breathing.
NOCTURNAL BRUXISM - occurs in everyone to some degree as a side effect of normal sleep, when the brain sends motor signals to the jaw muscles, usually following increases in sympathetic activity, heart rate, and supra-hyoid muscle tonus. It is intensified by stress, but not by bite conditions.28-29 It is also not correlated with TMJ disorders. In some people, it may be a behavior tiggered to prevent OSA by bracing the mandible to prevent it from dropping back into the pharynx. In other people, it can be caused by OSA, because the sympathetic arousals produced by the obstruction can trigger bodily movements in a physical struggle to restore breathing, and bruxism is one of those movements.
TMJ DISORDERS - usually resolve the inflammatory phase by middle age, so they are rarely significant barriers to oral appliance treatment. Jaw muscle tightness can occur as a subset of postural muscle tightness, because the mandible is an integral component of the head posture mechanism; or jaw muscle tightness can occur as a result of the bite destabilization that commonly occurs from mandibular advancement, because the bite is wired like a joint connecting the jawbones, and instability in any joint reflexively increases tonus in the muscles which cross that joint.
BITE CHANGES -The posterior open bites that commonly result from mandibular advancement are not due to shortening of the superior lateral pterygoid muscles, TMJ inflammation, or any other pathology. They have two causes. One cause is the forces generated by pushing the lower jawbone forward off the upper jawbone. These forces can tip the teeth and/or move them bodily. The other cause is adult mandibular growth. After the second decade of life, when elongation of the long bones stops, jawbone growth slows down about 90 percent, and then continues slowly.
Adult jawbone growth was programmed into our genetics, because it was needed to reduce resistance to airway flow during adulthood in order to compensate for the loss of muscle strength that invevitably occurs during adulthood at about 5% per decade, so our respiratory muscles do not have to keep increasing their effort as we age. Maxillary expansion reduces resistance in the nasal airway, and mandibular advancement reduces resistance in the pharyngeal airway.
Adult jawbone growth was also needed during evolution to compensate for whatever tooth wear occurred to maintain a stable facial height. While the teeth along with their sockets and the alveolar bone in which they are planted kept erupting into the bite table, the basal bones supporting them also kept shifting in the same direction. The forward translation and upward rotation of the mandibular corpus continually carried the lower teeth antero-superiorly toward the upper teeth surrounding them; and this growth process was stimulated by bite forces, so our ancestors who chewed extensively and experienced more tooth wear also underwent more growth to compensate for that wear.30-33
However, these horizontal growth processes are largely powered by bite forces, which have diminished by about half in the last couple of centuries due to our diet of soft foods. Esthetic orthodontics can further reduce bite forces and lead to muscle atrophy by making the teeth too tender for chewing at a critical age for jaw muscle development. Also these horizontal jawbone growth processes can be inhibited by steeply interdigitated teeth or an anterior overbite that locks the mandibular corpus, which cannot expand, to a maxilla, which cannot advance. Natural jawbone growth with age reqiuires some slippage in the occlusion.
Today, in people who use mandibular advancement appliances during sleep, the increased bite forces from passive stretch of the jaw closing muscles and the distraction osteogenesis created by holding the mandible down and forward all night can accelerate adult mandibular advancement until it propels the mandibular dentition past the maxillary dentition and out of the habitual bite. Dentists work hard to try and prevent this bite change, but their efforts are counter-productive, because we can take advantage of the bite change to improve long-term treatment. While the use of morning occlusal guides to force the mandible back towards its previous central bite position can trigger regressive remodeling that enables the condyles to seat more posteriorly than they otherwise would; adjusting the bite anteriorly is much easier and less likely to produce periodontal disease or root resorption34 than trying to reverse growth that has already occurred or prevent further growth in a functional environment that stimulates it.
Even more important, adjusting the bite anteriorly can significantly benefit OSA patients by shifting their mandibular resting postures anteriorly. The mandible reflexively acquires a resting posture just beneath its most stable bite position,35-44 so adjusting the most stable bite position anteriorly also shifts the mandibular resting posture anteriorly, which can improve daytime airway flow and reduce dependency on the appliance by preventing the mandible from dropping all the way back to its pre-treatment position during a short nap.
The most common mechanical barrier to mandibular advancement is incisor overbite, and a couple of millimeters can usually be removed from the labial-incisal edges of the mandibular incisors without damaging those teeth. In fact, the mandibular incisors benefit periodontally from the decreased crown/root ratio. Also, most of the patients who are wearing an oral appliance to treat OSA are not concerned with the small esthetic change that would result from permanently advancing their mandible a few mm. They rarely even notice a loss of posterior intercuspation. They don't need perfectly interdigitated teeth or dozens of simultaneous centric contacts. They just need a stable bite platform, with a few solid contacts on each side, which they can use for bracing and chewing.
The problem is that dental training has created such a box of thinking around centric relation that most dentists have never adjusted a bite anteriorly, and they won't even consider it as a treatment option. When mandibular advancement causes jaw muscle pain, they will use medications, physical therapy, and trigger point injections to treat the jaw muscles rather than restabilizing the bite. Some will even discontinue the mandibular advancement treatment to prevent further bite changes, leading to the suggestion that their patients will have the best bite in the cemetery.
APPLIANCE THICKNESS - The unnecessary bulk, especially in the anterior regions, of oral appliances works against our goals by distalizing tongue posture, which distalizes mandibular posture. In monkeys, a block of acrylic cemented in their palates lowered their tongue and mandibular posture to avoid the block, which caused them to grow long narrow faces. In humans, the center of rotation of the mandible is within the shortened ramus instead of above it, therefore lowering tongue and mandibular posture also rotates them down and back into the pharyngeal airway space. To enable a tongue posture up high in the front of the palate, all upper oral appliances should include a space hollowed out to fit the tongue tip (tongue tip hollow) just beneath the anterior bite table behind the maxillary incisors, as shown below.
APPLIANCE TIGHTNESS - relfexively causes increased jaw muscle tonus, which also works against our goals. Resins shrink when they set, which squeezes the upper teeth inward. Teeth at rest are delicately suspended in metabolically hyperactive sockets, and any displacement of a tooth from the middle of its socket triggers adaptive responses designed to make the socket once again fit the tooth. One of those responses is increased jaw muscle tonus, which can add to the increased jaw muscle tonus caused by an inflamed TMJ or an unstable bite. Oral appliances should fit passively without applying any pressure to teeth after they are seated. Also, even if an oral appliance perfectly fit all the teeth in their rest positions, a tight fit would feel uncomfortable; because it would impair circulation to the teeth and their sockets by limiting their natural ranges of motion, which extend about .15 mm vertically and bucco-lingually and a tenth that distance mesio-distally in the presence of adjacent teeth.
ORTHODONTICS - for preventing or reducing OSA usually requires increasing the cross-sectional area of the airway passage at multiple levels to enlarge the box that houses the tongue by stimulating horizontal jawbone growth to expand the upper jawbone and advance the lower jawbone relative to the cervical spine. During treatment, the mandible should not be locked back posteriorly. After treatment, the overbite should be left short and shallow to accomodate some future slippage in the occlusion; and the arches should not be left too steeply interdigitated for slippage to accommodate the slightly different directions of growth in upper and lower jawbones, leading to mechanical pressures that can move teeth and destabilize the bite post-treatment.
FOOTNOTES
1) Handler, E, Hamans E, Goldberg AN, Mickelson S. Tongue suspension: an evidence-based review and comparison to hypopharyngeal surgery for OSA. Laryngoscope, 2014; 124(1): 329-336.
2) Thaler E, Schwab R, Mauer J, et al. Results of the ADHERE upper airway stimulation registry and predictors of therapy efficacy. Laryngoscope 2020;130(5):1333-1338.
3) Hendricks R, Patel Z, Suleman L, et al. The role of the tongue base in obstructive sleep apnoea. Transactions of the Royal Society of South Africa, June 2024.
4) Ihsane Olakorede, Stefan Y Bögli, Zofia Czosnyka, Marek Czosnyka, Peter Smielewski, CSF production rate, resistance to reabsorption, and intracranial pressure: a systematic review and meta-analysis, Brain Communications January 2025; vol 7 (Issue 1)
5) Delaidelli A, Moiraghi, A. Respiration: A new mechanism for CSF circulation? Journal of Neuroscience 2017, 37 (30) 7076-7078.
6) Yiallourou TI, Damers MS, Kurtcuoglu V, Haba-Rubio J, Heinzer R, et al. Continuous positive airway pressure alters cranial blood flow and cerebrospinal fluid dynamics at the craniovertebral junction. Interdisciplinary Neurosurgery 2015;2(Issue 3):152-159.
7) Vinje, V., Ringstad, G., Lindstrøm, E.K. et al.Respiratory influence on cerebrospinal fluid flow – a computational study based on long-term intracranial pressure measurements. Sci Rep 9,9732 (2019).
8) Dreha-Kulaczewski S., Joseph AA, Merboldt KD, et al. Inspiration is the major regulator of human CSF flow. J Neurosci 2015;35:2485-2491.
9) Benveniste H, Liu X, Koundai S, et al. The glymphatic system and waste clearance with brain aging. Gerontology 2019;65:106-119.
10) Hladky SB, Barrand MA. The glymphatic hypothesis: the theory and the evidence. Fluids and Barriers of the CNS 2022;19(9):1-144.
11) Lee CH, Hong SL, Rhee CS, Kim SW, Kim JW. Analysis of upper airway obstruction by sleep videofluoroscopy in obstructive sleep apnea: a large population-based study. Laryngoscope. 2012 Jan;122(1):237-41.
12. Kuna S.T., Remmers J.E. Anatomy and Physiology of Upper Airway Obstruction. In: Kryger M.H., Roth T., Dement W.C., editors. Principles and Practice of Sleep Medicine. 3rd ed. WB Saunders; Philadelphia, PA, USA: 2000. pp. 840–858.
13. Isono S., Remmers J.E., Tanaka A., Sho Y., Sato J., Nishino T. Anatomy of pharynx in patients with obstructive sleep apnea and in normal subjects. J. Appl. Physiol. 1997;82:1319–1326.
14. Molnár V., Lakner Z., Molnár A., Tárnoki D.L., Tárnoki Á.D., Kunos L., Jokkel Z., Tamás L. Ultrasound and Magnetic Resonance Imaging of the Tongue in Obstructive Sleep Apnoea. Appl. Sci. 2022;12:9583.
15) Miller A, Vargervik K. Neural control of oral respiration in the rhesus monkey. P 133-156 in Muscle Adaptation in the Craniofacial Region. Carlson D and McNamara JA, eds. Monograph 8, Craniofacial Growth Series 1978.
16) Juge L, Knapman FL, Humburg P, et al. The relationship between mandibular advancement, tongue movement, and treatment outcome in obstructive sleep apnea. Sleep 2022;45(6).
17) Zhu JH, Lee HP, Lim KM, Lee SJ, et al. Passive movement of human soft palate during respiration: A simulation of 3D fluid/structure interaction. J Biomechanics 2012;45(11):1992-2000.
18) Sanders AE, Akinkugbe AA, Alade GD, et al. Tooth loss and obstructive sleep apnea signs and symptoms in the US population. Sleep Breath 2016;20(3):1095-1110.
19) Cillo JE, Schorr R, Dattilo DJ. Edentulism is associated with more severe obstrictive sleep apnea. J Oral and Maxillofac Surg. 2020;78(6):1013-1016.
20) Emami E, Sakah MH, Rompre P, et al. The nocturnal use of complete dentures and sleep stability in edentulous elders. J Dent. 2913;41(8);703-709.
21) Dantas DA, Mauad T, Silva LF, et al. The extracellular matrix of the lateral pharyngeal wall in obstructIve sleep apnea. Sleep 2012;35(4);483-490.
22) Owall B, Carlsson GE, Kayser AF. Prosthodontics principles and management strategies. Barcelona: Mosby-Wolfe 1996.
23) Bucca C, Carossa S, Pivetti S, et al. Edentulism and worsening of obstructive sleep apnea. Lancet. 1999;353(9147):121-122.
24) Bucca C, Cicolin A, Brussino L, et al. Tooth loss and obstructive sleep apnea. Respir Res. 2006;7(1):8.
25) Heidsieck, D.S.P., de Ruiter, M.H.T. & de Lange, J. Management of obstructive sleep apnea in edentulous patients: an overview of the literature. Sleep Breath 20, 395–404 (2016).
26) Ozbek MM, Memikoglu UT, Altug-Atac AT, Lowe AA. Stability of maxillary expansion and tongue posture. Angle Ortho. 2009 Mar;79(2):214-20).
27) Ribero AN, de Paiva JB, Rino-Neto J, Illiponti-Filho E, et al. Upper airway expansion after rapid maxillary expansion evaluated with cone beam computed tomography. Angle Orthod 2012;82(3):458-463.
28) Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28:1085-1091
29) Manfredini D, Lobezoo F. Relationship between bruxism and temporomandibular disorders: a systematic review of literature from 1998 to 2008. Oral Surg Oral Med Oral Pathol Oral Radiol Endodont. 2010;109(6):26-50.
30) Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepancies and nocturnal bruxism. J Prosthet Dent. 1984;51(4):548-553.
31) Bailey JO, Rugh JD. Effects of occlusal adjustment on bruxism as monitored by nocturnal EMG recordings. J Dent Res.1980;59(special issue):317.
32) Karcachi BJ, Bailey JO, Ash MM. A comparison of biofeedback and occlusal adjustment on bruxism. J Periodontol. 1978;49(7):367-372.
33) Pullinger AG, Seligman DA. The degree to which attrition characterizes differentiates patient groups of temporomandibular disorders. J Orofac Pain. 1993;7(2):196-208
34) Masoud, A.I., Alnoury, A.S. & Alsaggaf, D.H. Can the use of morning occlusal guides after oral sleep appliances cause root resorption similar to orthodontic jiggling?. Sleep Breath 29, 191 (2025).
35) Berry DC. Occlusion: fact and fallacy. J Craniomandib Pract. 1986;4(1):54-64.
36) Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular disorders have a cause-and-effect relationship? J Orofac Pain 1997;11:15-23.
37) Forsberg CM. Facial morphology and ageing: a longitudinal cephalometric investigation of young adults. Eur J Orthod 1979;1(1):15-23.
38) Troelstrup B, Moller E. Electromyography of the temporalis and masseter muscles in children with unilateral cross-bite. Scand J Dent Res. 1970;78:425-430.
39) Nerder PH, Bakke M, Solow B. The functional shift of the mandible in unilateral posterior crossbite and the adaptation of the temporomandibular joints: a pilot study. Eur J Orthod. 1999;21:155-166.
40) Tecco S, Tete S, Festa F. Electromyographic evaluation of masticatory, neck, and trunk muscle activity in patients with posterior crossbites. Eur J Orthod 2010;32(6):747-752.
41) Ingervall B, Thilander B. Activity of temporal and masseter muscles in children with a lateral forced bite. Angle Orthod. 1975;45:249-258.
42) Curtis D, Miller AJ, Mielsen OL, Kapila S. Lateral shifts in the occlusion of the Macaca mulatta monkey. J Dent Res. 1989;68:415.
43) Elgoyhen JC, Moyers RE, McNamara JA, Riolo MI. Craniofacial adaptation to protrusive function in young rhesus monkeys. Am J Orthod 1972;62(5):469-480.
44) McNamara JA. Functional adaptations of the temporomandibular joint. Dent Clin North Am. 1975;19:457-471.