Multilevel Oral Appliance Treatment for Obstructive Sleep Apnea
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 like a gasket 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 it is difficult to tolerate and very likely detrimental to glymphatic circulation. Mandibular advancement is well tolerated and has potential long-term facial growth benefits; but it's only effective in about half of those who try it. For the other half, new mechanisms can now be added to mandibular advancement appliances to also control the soft tissues at each level of the pharynx. A low-force silicone rubber soft palate elevator extends posteriorly from the palatal plate of the upper base appliance to "tent" the soft palate in order to draw its untouchable distal end antero-superiorly away from the obstruction in the nasopharynx, a novel tongue holding device grips the entire tongue body and the lateral borders of the tongue base between upper and lower tongue gripping plates covered with “tongue Velcro” to prevent it from dropping back and obstructing the oropharynx, and small adjustment mechanisms at the back of the upper tongue gripping surface can gradually and progressively pry the tongue base by its lateral borders antero-inferiorly away from the pharyngeal wall in the hypopharynx. For edentulous patients, the soft tissue controls can be carried on denture base plates (dentures without teeth); where the tongue holding is especially effective, because there are no teeth in the way, and the base plates require little retention, because they are constantly cushioned by the tongue.
RATIONALE - Current medical treatment for OSA is inadequate. Minor surgeries include cutting out hypertrophic soft tissue such as prominent tonsils or the distal end of the soft palate (uvulopalatopharyngoplasty, UPPP), advancing the genioglossus muscle, suspending the tongue base along with the hyoid bone from a suture tethered to a screw in the lingual plate of the symphysis,1-2 implanting an electrical stimulator in the hypoglossal nerve to dilate the pharynx by activating the genioglossus and geniohyoid muscles to protrude the tongue base during each inhalation,3 and radiofrequency ablation or surgical reduction of the tongue base. These each work on some people; but it's difficult to predict which people. Predictable success surgically requires multi-level treatment, such as maxillo-mandibular advancement to advance both upper and lower jaws by 8-10 mm.4 However, even such an extensive structural correction only brings AHI to under 5 in less than half of the patients, and its effect can wane over time if not accompanied by a supportive change in the activity of the jaw muscles.
Most OSA patients are treated with CPAP; but many find it difficult to tolerate; and the continuous positive pressure that is central to its operation is bound to reduce the intermittent negative pressure that powers the nightly drainage of cerebrospinal fluid (CSF) from the cranium through glymphatic circulation.5-10 During normal sleep, each inbreath produces enough negative pressure in the vessels to suck about half a drop of cerebrospinal fluid from the cranium. Applying continual positive pressure in the same vessels is bound to interfere with this drainage operation. Also, glymphatic circulation diminishes with age and as amyloid burden increases, and the biomarkers of most neurodegenerative diseases are first detected in the CSF, suggesting that loss of glymphatic drainage could be an important etiologic factor.
Current dental treatment is also inadequate. Mandibular advancement appliances are well tolerated, but they are only moderately effective, because the mandible is only attached to the tongue base by muscles, which lose their tonus during sleep. Therefore, even extreme mandibular advancement cannot prevent the tongue base from falling back and obstructing the airway - it just has a little further to fall; and mandibular advancement only cures about half of those treated, as shown by remarkably similar results in hundreds of studies. Attempts to identify which patients are likely to be in that half have been generally unsuccessful, so the high failure rate can make mandibular advancement appliances a hard sell. More effective treatment requires directly addressing the pathophysiology.
PATHOPHYSIOLOGY - OSA has complex anatomic, physiologic, and sensorimotor aspects; but the event at its core is choking on the tongue base, the gateway from the mouth to the trachea and the only structure in the pharynx that is thick and strong enough to plug the airway.12-14 It can obstruct the oropharynx by directly contacting the pharyngeal wall; it can obstruct the nasopharynx with the help of soft tissues getting sucked into the narrow gap between it and the pharyngeal wall like a gasket; and it can obstruct the hypopharynx by pushing the epiglottis closed - with considerable overlap between these obstruction mechanics and the different levels of the pharynx. 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 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
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 open during inhalation. In monkeys, airway obstruction triggers firing of the genioglossus in synchrony with inspiration.15 In humans, airway obstruction triggers a rapid increase in tonus of the pharyngeal dilator muscles (loop gain) until the arousal threshold is reached and breathing is restored. This arousal mechanism varies widely in its effectiveness. In some people, it opens the airway with each breath (the model for Inspire). In other people, it allows hypopneas but not apneas (upper airway resistance syndrome), because loop gain restores breathing before the airway is obstructed for long enough to produce hypoxia. Some people with high loop gain over-react, which destabilizes their ventilatory system and prevents 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 wearing 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 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; but that model fails as soon as the airway flow stops, because the Bernoulli forces also stop. That leaves only the weight of the soft tissues as the source of pressure in the chamber, which is far less than the pressure produced inside the tube by a diaphragm desperately trying to inhale. Maintaining the obstruction requires a stopper. The tube does not get sucked or squeezed closed; it gets plugged by a stopper; and the only structure inside the tube with enough physical integrity to form a stopper is the tongue base. Floppy pharyngeal tissues can fill in around the tongue base like a gasket that completes the stopper, but they can't obstruct the airway without the support of 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.
MANDIBULAR ADVANCEMENT - addresses the pathophysiology by applying anterior bias to the tongue base and all the other soft tissues attached to the mandible. Mandibular advancement has been shown to reduce resistance to airway flow through the pharynx, reduce AHI in clinical studies, and diminish the pressure at which the airway closes (defined as collapsibility) in experimental studies.
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 basic hardware was designed more than a century ago for bite jumping in children, and it is unnecessarily bulky and restrictive. The bolted connectors restrict lateral mandibular movements, which leads to frequent breakage; the downward vector of force on the mandible can lead to habitual mouth breathing; and adjustments require a special tool and have limited range. To solve those problems, Dr. Summer's new high-push Herbst (now in FDA review) has a lower profile, virtually unbreakable components, freely moveable connectors that cannot bind or restrict lateral movements, an upward vector of force on the mandible, and a ½ inch range of adjustment (more than you will ever need) without tools just by sliding the rod out of the tube, rotating the tubing assembly on the externally threaded offset connector arm, and re-inserting the rod into the tube to lock in the adjustment. To maintain support for the advancing mandible, the bite platform should extend anteriorly well beyond the labial surfaces of the upper anterior teeth, as shown right.
PALATE EXPANSION - can be included in the high push Herbst appliance by using detachable telescopic components. The upper appliance member, containing the expansion screw, is used by itself all day. Then every night, the lower appliance and telescopic components are hooked on. Some dexterity is required, but most people acquire the needed skills rapidly.
TITRATION - Increasing the advancement to a position of maximal tolerable benefit improves effectiveness, requiring adjustable mandibular advancement appliances. However, extreme advancement can damage the dentition; and its beneficial effects on airway dimensions diminish over time due to osseous remodeling at sites of large forces. Also, the new soft tissue controlling modalities now make extreme advancement unnecessary.
TESTING - After titrating a mandibular advancement appliance, its effectiveness should be tested; because even partial reductions of OSA can feel like successful treatment to the patient, but partial successes usually fade over time after the remaining incidents further stretch out the pharyngeal soft tissues. If OSA persists, more effective treatment requires also clearing the soft tissues from the different levels of the pharynx. The mechanics are described below.
USING THE SOFT PALATE ELEVATOR TO CLEAR THE NASOPHARYNX - In the nasopharynx, the loose pharyngeal soft tissues contribute to the obstruction by getting sucked into the narrow space between the tongue base and the posterior pharyngeal wall 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, swollen pharyngeal tissues can play a role, such as cryptic tonsils that trap food, but the loose pharyngeal soft tissues that contribute to the obstruction usually come from the distal end of the soft palate.
The soft palate's distal end 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 its center, where there are no gag reflexes, to “tent” the whole flaplike structure. The soft palate is a thin flap of muscles suspended from a keel-like midline aponeurosis, and they lose their tonus during sleep, leaving its distal end swinging back and forth due to airway flow around it.17 In this state, the midportion of the aponeurosis can be easily elevated by 1/4" or more using a silicone rubber bulb on the end of a thin flat arm. 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 # K211481.
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 in a patient who had previously undergone UPPP, 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. The resultant tightening of 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.
The soft palate elevator is usually employed together with mandibular advancement in the first phase of treatment, because the two modalities work better together than either one alone. Simply removing the gasket without also making changes in the functional environment that produced it 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 that combination of modalities is not effective, the next stage of the treatment involves holding the tongue to prevent it from sliding down and back into the oropharynx.
USING THE TONGUE HOLDING DEVICE TO CLEAR THE OROPHARYNX – The new tongue holding device (now in FDA review) holds the tongue between upper and lower tongue gripping plates formed by carpets of thousands of tiny pin points (AKA tongue velcro). The pin points are so closely packed that they feel like a fuzzy surface, and they are all slanted forward at a 45-degree angle to brace the tongue against backwardly directed forces.
THE UPPER TONGUE GRIPPING PLATE – Sewing needles were chosen for modeling the upper tongue gripping plate, because they fit almost perfectly between the filiform papillae that cover the tongue.
The 3,000 sewing needles for the model were shaped to fit the tongue and slanted forward at a 45-degree angle, as seen below left. To make an upper tongue gripping plate, the surface of the pin model is duplicated in dental acrylic, as shown below right.
The upper tongue gripping plate is split into anterior and posterior ends connected by torsion springs, as shown below right, to facilitate the wave of muscle contraction that occurs during swallowing.
THE LOWER TONGUE GRIPPING PLATE – Even smaller pins, 9,000 accupuncture needles, were chosen for modeling the lower tongue gripping plate, because the underside of the tongue is unkeratinized and therefore far more sensitive. The pins were shaped to fit the underside of the tongue and slanted forward at a 45 degree angle, as shown below left. Their surface is duplicated in dental acrylic, seen below right, to form a fuzzy mat which can also be reshaped to create a better fit just by dipping it in boiling water.
STEEL MODEL FOR MOLD FOR LOWER TONGUE GRIPPING SURFACE LOWER BASE APPLIANCE
SPRING LOADING – A very light compressive force from a thin wire spring is used to connect the tongue gripping plates with the base appliances to create a cushioned grip and prevent accidental tongue release during submaximal mandibular movements, including bruxism. Normally the upper tongue gripping plate is spring loaded in dentate patients, as shown below left; and the lower tongue gripping plate is spring loaded in edentulous patients, as shown below right. Under so little pressure, the tongue gripping plates effectively float on the tongue. Spring loaded upper and lower tongue gripping plates are shown on upper and lower denture base plates below.
UPPER TONGUE GRIPPING SPRING ON UPPER DENTURE BASE LOWER TONGUE GRIPPING SPRING ON LOWER DENTURE BASE
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. More advanced tongue positions are rarely necessary.
TARGET TONGUE POSITION
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 made of yellow acrylic, and the lower bite stops are made of green acrylic.
The X-rays below show a patient's tongue 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.
TONGUE IN RESTING POSTURE TONGUE BASE ADVANCED ABOUT 10 MM
The downward bias on the tongue base in the target tongue position works well together with the soft palate elevator to open the airway, because the two modalities separate the soft tissues that contact to produce the obstruction in the nasopharynx and the oropharynx.
CLEARING THE HYPOPHARYNX - If the OSA persists, small adjustment mechanisms called tongue base titraters can be added to the upper tongue gripping surface, which has been stabilized by the grip of the entire tongue body and the bite stops bracing the mandible, to shift its tail segments further down 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 effect of shifting the tongue base titraters down and back is shown above in X-rays of a patient's tongue painted with a radiopaque paste. The white V-shaped area marking the end of the upper tongue gripping surface and the end of the wire framework of the tongue base titrater has moved further down and back, increasing the sagittal width of the airway space in the lower oropharynx. The thin white line is made by the arm of a soft palate elevator.
The tongue base titraters can depress the tongue base in a range of directions that can be varied by up to 25 degrees, as illustrated below.
BEFORE ADJUSTMENT ADJUSTED DOWN-AND-BACK ADJUSTED DOWN-AND-FORWARD
This range of adjustment enables the tongue base titraters to first shift the tail segments down-and-back, to get them as far as possible behind the tongue base (below left), and then to rotate them forward (below right) to pry the tongue base anteriorly off the lower pharyngeal wall and away from the epiglottis. 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 are especially susceptible to OSA, because they lack a platform against which their mandible can be braced to prevent it from dragging the tongue base back into the pharyngeal airway 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 Studies have found that wearing dentures during sleep appears to reduce OSA in some of them but not in others.23-25
The new soft tissue controls can be carried on denture base plates and used without mandibular advancement to treat OSA in the edentulous. The base plates can extend well beyond the edentulous ridges, because they are not asymmetrically loaded in chewing and the constant light pressure from cushioning by the tongue keeps them seated. Also, the tongue gripping surfaces can extend all the way out to the cheeks. However, advancement of the tongue or mandible in its resting posture used during sleep could apply directional pressures to the edentulous ridges from passive stretch of the muscles, therefore the goal of treatment is just to hold the tongue up against the upper denture base plate to prevent it from dropping back into the pharynx. Treatment for denture patients is described in more detail under in a separate file under the tab SLEEP APNEA.
CLINICAL CONSIDERATIONS
VERTICAL DIMENSION - the height of an oral appliance, or the interarch space when the appliance is worn, affects facial growth and 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 to ensure 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 articular components, the joints and teeth. For patients with very strong jaw muscles and a restrictive anterior overbite, their mandibular advancement appliance can include a front flat bite plate to reduce the forces of nocturnal bruxism and redirect the remaining forces axially on the anterior teeth to gradually reduce the overbite. For patients with weak jaw muscles and excessive vertical dimension (usually accompanied by difficulty maintaining a lip seal at rest), any reduction of the natural vertical dimension that can be achieved by selectively grinding down teeth (equilibration) will make appliance wear more comfortable. Equilibration scares patients but rarely damages teeth.
MOUTH BREATHING - is a serious health problem. It prevents the nose from moistening, filtering, and warming the air before it hits the throat - making mouth breathers prone to upper respiratory problems. It also 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; and it reduces respiration, because the nose acts like a little lung. When volunteers temporarily wear nose clips to force mouth breathing, their arterial oxygen levels drop. Studies show that mouth breathing at night impairs sleep quality and exacerbates OSA.
OBLIGATE MOUTH BREATHERS - have nasal cavities that are too small to allow adequate resting nasal airway flow. They cannot maintain a lip seal for more than a couple of minutes. At rest and during sleep, their lips remain at least slightly parted to maintain an oral airway passage. Many people whose nasal cavities are barely large enough to allow adequate resting nasal airway flow become obligate mouth breathers whenever a slight allergy or rhinitis reduces the internal volume of their nasal cavity. In some of these people, restrictions to nasal airway flow produce turbulent airway flow downstream, which can move loose pharyngeal soft tissues into the pharynx.
In most obligate mouth breathers, adequate nasal airway flow can be restored by widening the palate non-surgically using a removeable expansion screw appliance. In adults, the two maxillary bones don’t separate at the midline suture, but they respond to light steady transverse forces by rotating relative to each other in a process that unfolds the upper jawbone like spreading a pair of wings, accompanied by lowering and adaptive remodeling of the midline suture.26 The expansion is maintained post-treatment by nightly wear of a retainer with a bite table that is broadly loaded during nocturnal bruxism and by ensuring a stable natural bite to function as a daytime retainer. Changing from mouth breathing to nose breathing can improve many sleep parameters; 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 mandibular resting posture due to a framework of bones and teeth (and sometimes the plastic of an oral appliance) that is longer vertically than the drape of skin and muscles hanging down from the forehead and temple areas to cover the face. When those muscles are relaxed, they can’t fully cover the face, causing the lips to part and creating an oral airway passage that becomes the habitual route for breathing.
Over time, habitual mouth breathers can become obligate mouth breathers due to the effects of mouth breathing on facial growth. Mouth breathing lowers mandible and tongue posture to create an oral airway passage, and postural forces provide the light steady forces that shape bones, therefore mouth breathing lowers the face. The lengthening of the face makes it grow narrow by pushing in on the cheeks. The ability of the cheeks to limit palate expansion can be seen in the ability of Frankel appliances to expand the palate using only plastic bumpers that hold the cheeks out away from the teeth.
Habitual mouth breathing can usually be eliminated by almost any way of holding the mouth closed and restoring the lip seal; including chin straps, medical tape (mouth taping), thick foam cervical collars, or interarch orthodontic elastics attached to oral appliances that fit on the teeth tightly enough to resist being pulled off by the weight of the mandible.
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 a cascade of physiologic events that include increases in autonomic sympathetic activity, tachycardia, supra-hyoid muscle tonus, and finally rhythmic masticatory muscle activity (RMMA) with tooth grinding or clenching and a rise in blood pressure. Nocturnal bruxism is intensified by stress, but not by bite conditions.28-29 It is also not correlated with TMJ disorders. In some people, nocturnal bruxism may be employed to prevent OSA by bracing the mandible against the cranium to prevent it from slipping back into the pharynx. In other people, nocturnal bruxism can be caused by OSA, because the obstructions increase sympathetic activity to trigger bodily movements in a physical struggle to restore breathing, and bruxism is one of those movements.
TMJ DISORDERS - usually resolve by middle age when OSA usually begins, so they are rarely significant barriers to oral appliance treatment. Many older mandibular advancement patients experience tight jaw muscles due to bite destabilization, because the bite is wired like a joint connecting the jawbones, and instability in any joint reflexively increases tonus in the muscles crossing that joint; but they rarely experience TMJ inflammation. The jaw muscle tightness can be treated by restabilizing the bite, as discussed below.
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 anteriorly on the lower dentition and posteriorly on the upper dentition by pushing the mandible forward off the maxilla. These forces can tip the teeth and/or move them bodily.
The other cause is the slow mandibular advancement that continues during adulthood. After the second decade of life, when elongation of the long bones stops, jawbone growth slows down 90 percent and then continues. The maxillary arch expands very slowly, while the V-shaped mandibular arch advances about twice as quickly, bringing a wider portion of the mandibular arch into contact with the directly widened portion of the maxillary arch and thereby keeping the upper and lower buccal segments in close alignment, even as the teeth wear down to their root tips.
One reason these jawbone growth processes were programmed to continue slowly during adulthood was to reduce resistance to airway flow in order to compensate for the loss of muscle strength, which continues at about 5% per decade during adulthood. Maxillary expansion reduces resistance in the nasal airway, and mandibular advancement reduces resistance in the pharyngeal airway. The reduction in resistance enables respiratory effort to remain constant with age.
The other reason these jawbone growth processes were designed to continue slowly during adulthood was to maintain a stable bite table despite tooth wear. Every micron of structure that was worn away from the biting surfaces was replaced, not just by eruption of the underlying teeth along with their sockets, but also by the movement of their basal bones. The forward translation and upward rotation of the mandibular corpus continually carried the roots of the lower teeth antero-superiorly into the upper teeth; 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 Today, in people who use mandibular advancement appliances on a long-term basis 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 natural adult mandibular advancement until it propels the mandibular corpus past the habitual bite.
The posterior open bites that commonly result from mandibular advancement are considered a serious negative side effect, because dental training has created such a box of thinking around centric relation that most dentists don't know how to adjust a bite anteriorly. When the loss of posterior support causes jaw muscle tightness; most dentists will use medications, physical therapy, or trigger point injections to treat the jaw muscles rather than restabilizing the bite by adjusting it anteriorly to eliminate the cause of the tightness. To try and prevent the bite from shifting anteriorly, many dentists have their mandibular advancement patients chew on hard gum or small wedges every morning (morning occlusal guides) to create an "occlusal return" or reprogramming process that forces the mandible back towards its previous central bite position. While use of these morning occlusal guides can trigger regressive remodeling that enables the condyles to seat more posteriorly than they otherwise would; simply adjusting the bite anteriorly to create a more anterior central bite position is much easier and healthier than trying to reverse growth that has already occurred or prevent further growth in a functional environment that stimulates it.
Furthermore, adjusting the bite anteriorly can significantly benefit OSA patients by shifting their mandibular resting postures anteriorly. The mandible always acquires a resting posture just beneath its central bite (intercuspal) position due to neuromuscular reflexes designed to maintain fast easy access to bracing, which was a critical protective feature in our evolution. The adaptation of the mandibular postural position to its bracing position has been demonstrated in numerous experiments.34-40 Adjusting the bite anteriorly shifts the mandibular resting posture anteriorly, which can improve resting airway flow during the day and reduce dependency on the appliance in our patients by preventing the mandible from dropping all the way back to its pre-treatment position if the mandibular advancement appliance is not worn for a short time, such as during a nap.
The most frequent mechanical barrier to natural mandibular advancement is incisor overbite, and a couple of millimeters can usually be removed from the labial-incisal edges of the mandibular incisors to allow significant mandibular advancement without damaging these 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 the mandible a few mm; and they don't need a perfectly intercuspated bite 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.
APPLIANCE THICKNESS - The unnecessary bulk, especially in the anterior regions, of nearly all current oral appliances works against our goals by distalizing tongue posture, which distalizes mandibular posture, which prevents natural mandibular advancement. A study of growing monkeys showed that a block of acrylic cemented in their palates lowered their tongue and mandibular posture, which caused them to grow long narrow faces. In humans, the center of rotation of the mandible is within the shortened ramus instead of far above it, therefore lowering tongue and mandibular posture also rotates the mandibular corpus down and back into the pharyngeal airway space. To provide space for the tongue's ideal resting posture up high in the front of the palate, all our oral appliances include a space carved out to fit the tongue tip (tongue tip hollow) just beneath the anterior bite table behind the maxillary incisors.
TIGHTNESS - The tightness of commercially made acrylic dental appliances also works against our goals. Resins shrink, which squeezes the upper teeth inward (palatally), especially the front teeth in the middle of the squeeze. The resulting pressure on the teeth reflexively increases jaw muscle tonus, just as noxious afferent input from any joint triggers increased tonus in the muscles which cross that joint. Healthy teeth at rest are delicately suspended in the middle of metabolically hyperactive sockets, which contain so many blood vessels that they give each tooth an individual arterial pulse and so many sensory nerves that they occupy an oversized portion of the brain. When the teeth remain in the middle of their sockets all night, these tissues remain passive. Displacement of a tooth from the middle of its socket by the pressure of an appliance triggers a collection of adaptive responses designed to make the socket once again fit the tooth position. One of those responses is increased jaw muscle tonus, which can add to the increased jaw muscle tonus caused by a TMJ disorder or an unstable bite.
Even if a dentist could fabricate a resinous oral appliance which 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 supporting tissues by limiting their functional ranges of motion. From its rest position, each tooth has a normal range of motion which extends about 1/4 mm vertically and bucco-lingually, and also about a tenth of that distance mesio-distally when adjacent teeth are present. An appliance that "hugs" a tooth restricts this range of motion. In the periodontal joints, like in all joints, restrictions to the normal range of motion prevent optimal functional circulation. What assures compliance in appliance wear is not tightness that makes an appliance difficult to remove, but comfort that makes the patients not want to remove it. An appliance should apply no pressure to teeth. It only needs enough mechanical retention to resist the forces of gravity.
ORTHODONTICS - for preventing or reducing OSA usually requires enlarging the craniofacial bony compartment to make room for the tongue by stimulating jawbone growth to expand the cross-sectional area of the airway. Palatal expansion creates space for the tongue to rest up high in the front of the palate, where it should fit well enough to produce a seal in resting posture; and mandibular advancement relative to the cervical spine (rather than the maxilla) is needed to increase the space available for the tongue base in the pharynx. Both of these growth processes are naturally dependent on jaw muscle strength, which also depends on bite stability. In some cases, bites can be stabilized by orthodontics, but it should not leave the teeth too steeply interdigitated to accommodate the slightly different directions of subsequent slow adult growth in upper and lower jawbones, leading to mechanical pressures that can move teeth and destabilize the bite post-treatment. Face height should remain stable in proportion to body height rather than steadily increasing with age, as is common today.
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) Holty JE, Guilleminault C. Maxillomandibular advancement for the treatment of obstructive sleep apnea: a systematic review and meta-analysis. Slep Med Rev 2020;14(5):287-297.
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) Tschopp S, Wimmer W, Caversaccio M, et al. Night-to-night variability in obstructive sleep apnea using peripheral arterial tonometry: a case for multiple night testing. J Clin Sleep Med. 2021:17(9):1751-1758.
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 onstructive 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) Berry DC. Occlusion: fact and fallacy. J Craniomandib Pract. 1986;4(1):54-64.
35) Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular disorders have a cause-and-effect relationship? J Orofac Pain 1997;11:15-23.
33) Forsberg CM. Facial morphology and ageing: a longitudinal cephalometric investigation of young adults. Eur J Orthod 1979;1(1):15-23.
34) 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.
35) 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.
36) 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.
37) Ingervall B, Thilander B. Activity of temporal and masseter muscles in children with a lateral forced bite. Angle Orthod. 1975;45:249-258.
38) Curtis D, Miller AJ, Mielsen OL, Kapila S. Lateral shifts in the occlusion of the Macaca mulatta monkey. J Dent Res. 1989;68:415.
39 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.
40) McNamara JA. Functional adaptations of the temporomandibular joint. Dent Clin North Am. 1975;19:457-471.