Multilevel 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 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 it splints the tongue base anteriorly and makes the pharynx too large to be obstructed at any level above the epiglottis; but it is poorly tolerated. Mandibular advancement is more tolerable than CPAP; but it's not always effective, because the mandible is only loosely attached to the tongue base and soft tissues that produce the actual obstruction. Now ineffective mandibular advancement appliances and denture base plates can be amended with mechanical devices that also control the positions of the soft palate, tongue body, and tongue base. A new low-force silicone rubber soft palate elevator "tents" the center of the soft palate, where there are no gag reflexes, in order to draw its untouchable distal end antero-superiorly away from the nasopharyngeal obstruction. Specialized tongue gripping surfaces that contain thousands of forward slanted bristles hold the tongue body and lateral borders of the tongue base to prevent the tongue from slipping backward into the oropharynx. If the apnea persists, the tail segments of the upper tongue gripping surface can be gradually shifted in 1.3 mm increments further down-and-back or down-and-forward in order to pry the tongue base off the pharyngeal wall in the hypopharynx. For edentulous patients, the soft tissue controls can be carried on denture base plates, the mandible is supported rather than advanced, and the tongue holding is especially effective, because the tongue gripping surfaces can extend all the way out to the cheeks.
RATIONALE - Current medical treatment for OSA is inadequate. Minor surgeries include cutting out areas of soft tissue, 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 uvulopalatopharyngoplasty (UPPP), 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, which can advance the tongue base by 8-10 mm in both upper and lower jaws.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 people do not use it, and the continuous positive pressure must eliminate or at least reduce the intermittent negative pressures that power nightly drainage of cerebrospinal fluid from the cranium with each inbreath through glymphatic circulation.5-10
Current dental treatment is also inadequate. Dentists make a variety of mandibular advancement appliances, which reduce AHI in clinical studies and increase Pcrit in experimental studies, and they are well tolerated; but they have limited effectiveness, because the mandible is only attached to the tongue base by muscles, which naturally lose tonus during sleep. Therefore, even extreme mandibular advancement cannot prevent the tongue base from falling back and obstructing the airway - it just has further to fall; and mandibular advancement has only a 50% success rate, as shown by remarkably similar results in hundreds of studies. Attempts to identify which patients are likely to respond have been generally unsuccessful, so the high failure rate makes mandibular advancement appliances a hard sell.
Now there are new oral appliance modalities that can also control the soft tissues that actually obstruct the airway. The soft palate can be elevated centrally to draw its distal end antero-superiorly out of the nasopharynx, the tongue body can be held to prevent it from dropping back into the oropharynx, and the tongue base can be pried by its lateral borders antero-inferiorly away from the pharyngeal wall in the hypopharynx. The new modalities are added one at a time to ineffective mandibular advancement appliances or denture base plates until follow-up sleep testing shows that the problem is eliminated.
PATHOPHYSIOLOGY - OSA has complex anatomic, physiologic, and sensorimotor aspects; but the event at its core is choking on the tongue base. The tongue base is the gateway of airway passage between the oropharynx and the trachea and the only structure in the area that is thick enough and strong enough to plug the airway. It is also long enough to plug the airway at different levels. Usually it obstructs the oropharynx by directly contacting the pharyngeal wall, the nasopharynx with the help of soft tissues getting sucked into the narrow gap between it and the pharyngeal wall, and the hypopharynx by pushing the epiglottis just beneath it closed like a trap door. Imaging has found the location of the obstruction too variable to provide a basis for targeted treatment. 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 It can even seesaw back and forth between these locations at different times.
Some researchers blame OSA on an inadequate neuromuscular arousal mechanism - commonly described as the muscles relaxing too much during sleep, and they target the neuromusculature for treatment, but muscles normally relax during sleep. As soon as a person with a healthy airway falls asleep, the tonus in all their pharyngeal dilator muscles plunges. However, in response to airway obstruction, the muscles stay on guard, and their tonus increases as much as necessary to restore airway flow. In monkeys, experimental nasal airway obstruction causes the genioglossus to pulse in synchrony with inspiration.12 In humans, the increased carbon dioxide levels trigger a rapid increase in tonus of the pharyngeal dilator muscles (loop gain), until the arousal threshold is reached and breathing is restored. This neuromuscular arousal mechanism varies widely in its effectiveness. In some people, it successfully opens the airway with each breath (the model for Inspire). In other people, it allows hypopneas but prevents apneas, because rapid loop gain produces arousal that restores breathing before the airway is obstructed for long enough to produce hypoxia. Some people with high loop gain over-react to the increased carbon dioxide levels, which destabilizes the ventilatory system and prevents the return of normal breathing. Still other people with low arousal thresholds have their sleep repeatedly disturbed by minor desaturations or by events that are not associated with desaturation, such as snoring or wearing a CPAP mask. Precision medicine can be used to identify and treat some OSA by providing medications that alter arousal threshold and loop gain, but an inadequate neuromuscular response to the problem should not be considered the cause of the problem, and the goal of OSA treatment should be to provide an adequate resting airway passage that does not require a protective 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. However, in airway flow through the pharynx, the pressure in the chamber is only the weight of the soft tissues surrounding the pharynx, which is much less than the pressure produced inside the tube by a diaphragm desperately trying to inhale. Thus, it is not the pressure in the chamber surrounding the tube that stops the flow through the tube. It is a plug inside the tube. The tube does not get squeezed closed from pressure outside it; it gets plugged from within by a stopper; and the only structure inside the tube with enough physical integrity to form a stopper is the tongue base. People don't choke on loose tissues like floppy pharyngeal walls, they choke on a piece of meat. The piece of meat in OSA is the 6 cm thick slab of muscle that forms the tongue base. The loose pharyngeal soft tissues can contribute to the obstruction by getting sucked into the narrow space between the tongue base and the 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, they usually come from the distal end of the soft palate. Removing the gasket is one way to at least temporarily restore the airway.
"TENTING" THE SOFT PALATE - The distal end of the soft palate is untouchable, because it is full of gag reflexes; but it can be drawn away from the obstruction by elevating its center, where there are no gag reflexes. The soft palate is a flexible flap of thin muscles suspended from a keel-like midline aponeurosis, and its muscles lose their tonus during sleep, leaving its distal end swinging back and forth due to airway flow.13 In this condition, a silicone rubber bulb on the end of a thin flexible arm can elevate the central portion of the aponeurosis about 1/4" all night without causing any discomfort. The distal end of the soft palate probably only moves a fraction of that distance, but that small movement can restore airway flow. The arm of the soft palate elevator is flexible enough to comfortably accommodate the functional movements of the soft palate during swallowing, when breathing stops anyway. Most patients don’t even know it’s there.
The "tenting" of the soft palate 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.
BEFORE INSERTING THE SOFT PALATE ELEVATOR AFTER INSERTING THE SOFT PALATE ELEVATOR
Tenting the soft palate also tightens the nearby pharyngeal wall, as was demonstrated below 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.
The soft palate elevator is usually employed together with mandibular advancement in the first phase of treatment, because these two modalities work better together than either one alone. Simply removing the gasket without also making changes in the functional environment that led to gasket formation invites relapse due to formation of a new gasket, and simply changing the functional environment by advancing the mandible may not produce enough change in the anatomy to restore airway flow without also removing the gasket.
ADVANCING THE MANDIBLE – is the simplest way to change the functional environment that regulates airway flow through the pharynx. The mandible serves as the basal bone for the tongue, so advancing the mandible exerts an anterior bias on the tongue and creates space anterior to the tongue, but it cannot advance the tongue into the space created, because the mandible is only attached to the tongue by muscles, which naturally lose their tonus during sleep. As a result, even extreme mandibular advancement cannot prevent the tongue base from falling back into the airway - it just has a little further to fall; and mandibular advancement only cures about half of the patients treated, as shown by remarkably similar results in hundreds of studies. Attempts to identify anatomical features that indicate which patients are likely to respond to mandibular advancement have been generally unsuccessful, so the high failure rate makes mandibular advancement appliances a hard sell.
HERBST APPLIANCES - have 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. When it is used for adults with OSA, the bolted connectors protrude into the lips and restrict lateral mandibular movements, which leads to frequent breakage; the downward vector of force on the mandible can open the lips and lead to habitual mouth breathing; and adjustments require a special tool and have limited range. To solve those problems, Dr. Summer has developed and tested (now in FDA review) improved telescopic hardware. The high-push Herbst has a lower profile (doesn't push into the lower lip), freely moveable connectors that cannot bind or restrict lateral movements, an upward vector of force on the mandible that has less tendency to push the mouth open, and an unlimited range of adjustment 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.
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, with telescopic components attached, is added. Some dexterity is required, but most people acquire the needed skills rapidly.
TITRATING - mandibular advancement to a position of maximal tolerable benefit improves effectiveness, therefore mandibular advancement devices should be adjustable. For people with a history of TMJ problems, treatment should begin with minimal advancement and increase gradually. To maintain support anteriorly for the mandible as it advances, the bite platform should extend anteriorly well beyond the labial surfaces of the upper anterior teeth, as shown in the photos below; because loss of anterior support when the mandibular anterior teeth advance past the anterior bite platform greatly increases the forces applied to the connectors and can thereby lead to breakage of any Herbst appliance.
TESTING - After titrating a mandibular advancement appliance, its effectiveness should be tested. Even partial reductions of OSA can feel like successful treatment to the patient, but partial successes usually fade over time, because the remaining incidents keep stretching out the pharyngeal soft tissues. Multi-night home sleep testing eliminates any first night effect and the normal night-to-night variability in results.14
EXTREME ADVANCEMENT - can damage teeth or their supporting structures, and its beneficial effects on the shape of the airway diminish slowly over time due to osseous remodeling. Holding the tongue body is safer and probably more effective than extreme mandibular advancement.
PREVIOUS TONGUE HOLDING MECHANISMS - Until now, there have only been a couple of different kinds of tongue holding appliances. The Tongue Stabilizing Device, Tongue Retaining Device, and Good Morning Snore Solution all employ a silicone rubber squeeze bulb that uses suction to grasp the tongue tip; however the bulb is too large to fit in the mouth so it must be held all the way out in front of the lips, producing extreme tongue advancement that is difficult to tolerate; and the tongue tip is far from the obstruction, so they are only about as effective as mandibular advancement. Also, pulling the tongue forward pulls a thicker portion of the tongue base up into the area of obstruction and thereby exacerbates the apnea in some people. The Full Breath Solution and Zyppah Appliances push down on the middle of the tongue base, which can move it down and away from an obstructing contact superiorly, but into an obstructing contact inferiorly; and they have limited posterior reach, because they contact the tongue base in its midline, where the gag reflexes are located.
THE NEW TONGUE HOLDING DEVICE – holds the entire tongue body and the lateral borders of the tongue base between upper and lower tongue gripping surfaces, which each contain thousands of tiny bristles that are all slanted forward at a 45 degree angle, to prevent the tongue from shifting posteriorly into the pharynx. The bristles on the upper tongue gripping surface are sized to fit between the filiform papillae that cover the dorsal surface of the tongue, and the tiny bristles on the lower tongue gripping surface grip the sensitive tissues on the underside of the tongue like a non-skid surface. Upper and lower carpets of this “tongue Velcro” are molded to fit each patient's anatomy.
STEEL MODEL FOR MOLD FOR LOWER TONGUE GRIPPING SURFACE LOWER BASE APPLIANCE
Their grip is so effective that the only compressive force they need to hold the tongue between them without discomfort all night is provided by a thin wire spring that biases one tongue gripping surface toward the other, (the upper in dentate patients and the lower in edentulous patients). The tongue gripping surfaces float on the surfaces of the tongue, while a flexible anterior tether prevents posterior shifting. The lightweight spring is long enough to create a cushioned grip which persists until the mouth is open wide, so it cannot be interrupted by the submaximal mandible and tongue movements that occur during normal sleep, including bruxism. Opening wide releases the tongue, as shown in the bottom illustration below.
MOUTH CLOSED
PARTLY OPEN
MOUTH WIDE OPEN
The tongue gripping surfaces 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 can be used, but they are rarely necessary.
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 the photo above right, the upper bite stops are made of yellow acrylic, and the lower bite stops are made of green acrylic.
EDENTULOUS PATIENTS
Edentulous people have greater prevalence and severity of OSA, because the mandible lacks a platform to brace against to prevent it from dropping back into the pharyngeal airway during sleep. Also, edentulism produces 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.15-19 Wearing dentures during sleep appears to reduce OSA in some people.20-22 Tongue gripping surfaces carried on denture base plates are especially effective, because there’s much more room for them without teeth in the way, and the constant light pressure from cushioning by the tongue keeps the denture base plates well seated. However, advancement of the tongue or mandible could apply directional pressures to the tissues from passive stretch of the muscles, therefore the goal of treatment is just to hold the tongue up against the upper base plate to prevent it from dropping back into the pharynx; and the cushioned grip is produced by biasing the lower tongue gripping surface upward rather than biasing the upper tongue gripping surface downward, as in dentate patients. In the photo below, a polyester mesh tether attaches the anterior end of the lower tongue gripping surface to the lower denture, and the posterior end of the lower tongue gripping surface is biased upward by a pair of orthodontic elastics that each connect a cleat on the lingual flange of the lower tongue gripping surface with a ball clasp on the buccal side of the lower denture. The bias is maintained until the cleats reach the same plane as the bite table, as seen in the right-side photo below. Any further opening releases the tongue.
BOTTOM ENDS OF ELASTICS ON CLEATS TOP ENDS OF ELASTICS ON BALL CLASPS ELASTICS SUSPEND LOWER TONGUE GRIPPING SURFACE
TONGUE BASE TITRATERS - If further treatment is needed for dentate or edentulous patients, the upper tongue gripping surface can be amended with tongue base titraters - small adjustment mechanisms that can gradually shift its tail segments further down and back or down and forward off the body of the upper tongue gripping surface, which has been stabilized by the grip of the tongue and the bite stops to brace the mandible, in progressive 1.3 mm increments, as the patient gets used to them.
BEFORE SHIFT AFTER SHIFT
The tongue holding device can move the tongue base away from an obstruction in the oropharynx, as shown below in X-rays of a patient's tongue painted with a radiopaque paste before (top) and after (middle) insertion. The small white radiopaque puddle in the foramen cecum in the top X-ray has been replaced by a larger white V shape where the tongue has curled around the end of the upper tongue gripping surface alongside the distal root of the second molar in the middle X-ray. In the bottom X-ray, the tongue base titraters have shifted the tail segments of the device and thereby also the tongue base further down-and-back, which has shifted 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 in the same direction and has further increased the sagittal width of the airway space in the lower oropharynx, seen between the arrows. The middle and bottom X-rays also contain a thin white line made by the arm of a soft palate elevator.
PHARYNX AT REST
PHARYNX WITH TONGUE HOLDING DEVICE
PHARYNX WITH TONGUE BASE TITRATER DOWN AND BACK
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
HYPOPHARYNX
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.
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. Appliances that are tall enough to engage the passive stretch of the jaw closing muscles can produce sustained compressive forces that can damage the dentition and the TMJs. For patients with very strong jaw muscles and significant 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 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 vertical dimension that can be achieved by selectively grinding down teeth will make appliance wear more comfortable. Equilibration scares patients but rarely damages teeth.
MOUTH BREATHING - 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 from the paranasal sinuses of nitric oxide, which helps widen blood vessels and improve oxygen intake in the lungs. Volunteers who wear nose clips to force mouth breathing develop lower arterial oxygen levels.
Obligate mouth breathers have nasal cavities that are too small to allow adequate resting nasal airway flow, and they cannot sit comfortably with their lips sealed for more than a couple of minutes. At rest, their lips remain 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 allergy or rhinitis reduces the cross-sectional area of the nasal cavity.
One way to treat obligate mouth breathing is to widen the palate non-surgically using a removeable expansion screw appliance. In adults, the maxillary bones don’t separate at the midline suture, but they respond to light steady expansion forces by reshaping and unfolding, accompanied by lowering of the midline suture.23 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, including respiration; but it rarely relieves OSA, because the expansion occurs so far from the obstruction.24
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) at the front of the face that is too long to be comfortably covered by the drape of relaxed soft tissues hanging down from the forehead and temple areas, causing the lips to part when the facial muscles are at rest, which creates an oral airway passage during sleepthat can easily become the habitual route for breathing.
Habitual mouth breathing 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. As a result, lowered mandible and tongue posture makes the face grow vertically long; and lengthening the face vertically also makes it grow narrow by pushing in on the cheeks. This effect can be seen dramatically in the ability of Frankel appliances to expand the palate using only plastic bumpers that hold the cheeks out away from the teeth. The long narrow facial growth pattern produced by lowered mandible and tongue posture frequently prevents the nasal cavity from growing wide enough to create an adequate nasal airway passage.
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 orthodontic ball clasps, cleats, or buttons on upper and lower appliances that fit on the teeth tightly enough to resist being pulled off by the weight of the mandible. Obligate mouth breathers cannot tolerate those interventions until they undergo structural improvement.
NOCTURNAL BRUXISM - occurs in everyone as a side effect of normal sleep, when the brain sends motor signals to the jaw muscles, usually during transitions to lighter sleep stages. It is intensified by stress, but it is not affected by bite conditions.25-26 Nocturnal bruxism is also not correlated with TMJ disorders.27-29 In some people, nocturnal bruxism may be an adaptive response that prevents 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 trigger sympathetic activity to stimulate bodily movement 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 appliances for OSA treatment. It's rare to find an inflamed TMJ beyond middle age. Many older people being treated for OSA with a mandibular advancement appliance experience muscle pain due to bite destabilization, because instability in any joint reflexively increases tonus in the muscles crossing that joint, and the periodontium is wired like a joint between the jawbones.
TMJ DISORDERS - usually resolve by middle age when OSA usually begins, so they are rarely significant barriers to oral appliances for OSA treatment. It's rare to find an inflamed TMJ beyond middle age. Many older people being treated for OSA with a mandibular advancement appliance experience muscle pain due to bite destabilization, because instability in any joint reflexively increases tonus in the muscles crossing that joint, and the periodontium is wired like a joint between the jawbones.
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. The obvious cause is the tipping and bodily movement of teeth due to the posteriorly directed forces on the upper dentition and the anteriorly directed forces on the lower dentition that are always produced by mandibular advancement. An equally important cause is continuing adult jawbone growth. After the second decade of life, when elongation of the long bones stops, jawbone growth slows down 90 percent and then continues at a 10 percent rate.
The most salient feature of continual adult jawbone growth is continual advancement of the mandibular corpus, with gradual reduction of overbite and overjet throughout life, which can be seen in all museum collections. Mandibular advancement during adulthood was built into our genetics, because it reduces resistance to airway flow as muscles slowly lose strength with age during adulthood. It also helped compensate for continuous tooth wear in our ancestors by continuously bringing the lower dentition antero-superiorly into the upper dentition; and it was stimulated by bite forces, so that individuals who chewed extensively and experienced more tooth wear also underwent more mandibular advancement 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 stimulate natural adult mandibular advancement and propel the mandibular corpus past the habitual bite.
The loss of a stable habitual central bite position has been difficult for dentists to accept, because it removes the normal reference point for clinical dental work; therefore, many dentists see it as a serious adverse side effect, and they try to prevent it by having their mandibular advancement patients chew on hard gum or small wedges for an hour 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 is much easier than trying to reverse growth that has already occurred or prevent further growth in a functional environment that stimulates it. However, dental training has created such a box of thinking around centric relation that most dentists have never adjusted a bite anteriorly. Instead of restabilizing the bite, they will use medications, physical therapy, and trigger point injections to treat the jaw muscle tightness that was caused by the bite destabilization.
In most of our patients, the mechanical barrier to natural mandibular advancement is incisor overbite, and a couple of millimeters can be removed from the labial-incisal edges of the mandibular incisors to allow some mandibular advancement without requiring anesthesia or causing any damage. In fact, those teeth 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 at least a few contacts on each side, which they can use for bracing and chewing. It’s time to get over our fear of adjusting the bite.
More important, 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 bracing position due to neuromuscular reflexes that maintain fast easy access to bracing, which was an important protective feature in our evolution. The adaptation of the mandibular postural position to its bracing position has been demonstrated in experiments. Children with unilateral cross-bite show a parallel shift of mandibular posture, which normalizes after correction of the cross-bite.34-37 Monkeys fitted with crowns to experimentally displace the mandible immediately undergo a parallel shift of mandibular posture.38-40 The more anterior mandibular resting posture that can be acquired by shifting the bite anteriorly improves resting airway flow during the day, and it can 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.
PREVENTION – requires optimizing adult jawbone growth. In most facial types, it involves encouraging or at least enabling gradual natural mandibular advancement and even more gradual maxillary expansion. These horizontal jawbone growth processes are designed to continue slowly with age in order to gradually reduce airway resistance as muscles naturally weaken with age; but they are largely powered by chewing forces, which have diminished radically since we adopted a diet of processed foods. In addition, horizontal jawbone growth can be further restricted by deep or steep overbites which lock the mandibular corpus to a maxilla that grows by expanding rather than advancing. Much of the jawbone growth that has been restrained horizontally has been redirected vertically. When the mandibular corpus cannot advance, it typically rotates down and back into the space needed for the pharyngeal airway, thereby increasing resistance to pharyngeal airway flow and triggering forward head posture to reduce it. In some people, strong jaw closing muscles are able to prevent the downward component of jawbone growth, but the mandible remains locked back behind a steep and usually deep overbite. Removing the barriers to natural horizontal jawbone growth as early in life as possible provides the easiest prevention. Stimulating natural horizontal jawbone growth as early in life as possible provides the best prevention.
APPLIANCE THICKNESS - The unnecessary bulk, especially in the anterior regions, of nearly all current oral appliances can work 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 to avoid the block, which redirected their facial growth vertically, causing 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 prevent such adverse effects on facial growth, our upper oral appliances include a space hollowed out to fit the tongue tip just beneath the anterior bite table at the front of the palate behind the maxillary incisors.
TIGHTNESS - The tightness of commercially made acrylic dental appliances also works against our goals by squeezing the upper teeth inward (palatally) due to the shrinkage of acrylic, especially the front teeth in the middle of the squeeze. Healthy teeth at rest are each suspended in the middle of a metabolically hyperactive socket; which contains so many blood vessels that it exhibits an individual arterial pulse and such an extensive network of sensory nerves that it occupies 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, because noxious afferent input from any joint triggers increased tonus in the muscles which cross that joint. As a result, any pressure on the teeth increases tonus in the jaw closing muscles; 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 impair the functional circulation to the teeth and their supporting tissues by limiting their functional ranges of motion. From its rest position, each tooth needs to be able to move about 1/4 mm vertically and bucco-lingually and about a tenth of that distance mesio-distally in the presence of adjacent teeth. An appliance that "hugs" a tooth restricts its range of motion, which makes it feel uncomfortable, and probably also prevents optimal circulation, like immobilization of other joints. A thin layer of rubber, like a silicone liner, make a removeable appliance feel more comfortable, because it allows those movements. What assures compliance in appliance wear is not tightness that makes it 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.
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) 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.
13) 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.
14) 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.
15) 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.
16) 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.
17) 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.
18) 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.
19) Owall B, Carlsson GE, Kayser AF. Prosthodontics principles and management strategies. Barcelona: Mosby-Wolfe 1996.
20) Bucca C, Carossa S, Pivetti S, et al. Edentulism and worsening of obstructive sleep apnea. Lancet. 1999;353(9147):121-122.
21) Bucca C, Cicolin A, Brussino L, et al. Tooth loss and obstructive sleep apnea. Respir Res. 2006;7(1):8.
22) 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).
23) Ozbek MM, Memikoglu UT, Altug-Atac AT, Lowe AA. Stability of maxillary expansion and tongue posture. Angle Ortho. 2009 Mar;79(2):214-20).
24) 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.
25) Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28:1085-1091
26) 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.
27) Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepancies and nocturnal bruxism. J Prosthet Dent. 1984;51(4):548-553.
28) Bailey JO, Rugh JD. Effects of occlusal adjustment on bruxism as monitored by nocturnal EMG recordings. J Dent Res.1980;59(special issue):317.
29) Karcachi BJ, Bailey JO, Ash MM. A comparison of biofeedback and occlusal adjustment on bruxism. J Periodontol. 1978;49(7):367-372.
30) Pullinger AG, Seligman DA. The degree to which attrition characterizes differentiates patient groups of temporomandibular disorders. J Orofac Pain. 1993;7(2):196-208
31) Berry DC. Occlusion: fact and fallacy. J Craniomandib Pract. 1986;4(1):54-64.
32) 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 evaluaton 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.