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 stopper in the nasopharynx; and sometimes with the epiglottis under the weight of the tongue base functioning as the stopper 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 prevents the negative pressure during inspiration from sucking the tongue back into the pharynx, and ballooning out the pharynx makes it too large to get obstructed at any level above the epiglottis; but compliance with CPAP is poor, and continuous positive pressure is likely to interfere with glymphatic drainage, which relies on intermittent negative pressure. Mandibular advancement is more tolerable than CPAP; but it's not always effective, because the mandible is only loosely attached to the tongue.
Now ineffective mandibular advancement appliances can be amended with mechanical devices that also directly control the soft tissues involved in the obstruction - the tongue and the soft palate. A new type of tongue holding device "pins" the tongue body and lateral borders of the tongue base to the advanced mandible between upper and lower tongue gripping surfaces made of thousands of forward slanted bristles that prevent it from slipping backward into the pharynx. For patients who need finer control of their tongue base, the upper tongue gripping surface can be fitted with tongue base titraters to gradually pry the tongue base off the pharyngeal wall. Also, to address nasopharyngeal obstructions, 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 obstruction posteriorly.
In denture wearers, tongue holding is especially effective, because the tongue gripping surfaces can extend all the way out to the cheeks, and the light steady pressure from the cushioning of the tongue keeps the denture base plates seated. However, any advancement would apply pressure to the edentulous ridges, therefore the tongue is simply held to prevent it from dropping back into the pharynx. The FDA clinical study in denture patients with untreated obstructive sleep apnea runs from April 2024 until April 2025.
CURRENT MEDICAL TREATMENT - for OSA is still problemmatic. Sometimes simple measures like nasal cones or EPAP work, and sometimes nothing works. Minor surgeries include genioglossus advancement, suspending the tongue base along with the hyoid bone from a suture tethered to a bone screw in the front of the mandible,3-4 implanting an electrical stimulator in the hypoglossal nerve to dilate the pharynx by activating the genioglossus and geniohyoid muscles,5 uvulopalatopharyngoplasty (UPPP), tongue reduction surgery, and palatal stiffeners. These each work on some people, but it's difficult to predict which people. Predictable success surgically requires multi-level treatment, usually involving bone reconstruction, such as maxillo-mandibular advancement; but even such an extensive structural correction only brings AHI to under 5 in 43% of patients.6 Also, the advancement of the jawbones 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, because it is usually effective in those who can tolerate it; but compliance is poor. In addition, continuous positive pressure is bound to inhibit the intermittent negative pressure that powers the nightly drainage of cerebrospinal fluid from the cranium through glymphatic circulation.7-12
PATHOPHYSIOLOGY - OSA has complex anatomic, physiologic, and sensorimotor aspects; but the obstruction event at its core is choking on the tongue base and/or the epiglottis just beneath it - the only pharyngeal structures with the physical features necessary to form a stopper capable of plugging the airway. Imaging has found the location of the obstruction too variable to provide a basis for targeted treatment.2 Studies using drug induced sleep videoendoscopy (DISE) have found that, when all muscle tonus is eliminated, the obstruction occurs most frequently in the velum (nasopharynx), but it also occurs frequently in the oropharynx, behind the tongue, and at the epiglottis. It can even seesaw back and forth between these locations at different times. In the oropharynx, the tongue base can directly contact the pharyngeal wall to plug the airway. In the nasopharynx, loose soft tissues can fill in the narrow gap between the tongue base and the pharyngeal wall like a gasket. In the hypopharynx, the weight of the tongue base can close the epiglottis like closing a trap door (floppy epiglottis), which may not respond to CPAP.
Some researchers blame OSA on non-anatomical factors, primarily an inadequate neuromuscular arousal mechanism - commonly described as the muscles relaxing too much during sleep, and they target the neuromusculature for treatment. The patency of the unsupported portion of the pharyngeal airway is maintained by the tonus of the pharyngeal dilator muscles, which respond to increasing carbon dioxide levels by increasing their tonus as much as necessary during inspiration. Experimental airway obstruction in monkeys causes the genioglossus to pulse in synchrony with inspiration.1 In humans, studies show that 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. Some people are able to use this adaptive muscle response system effectively to open the airway with each breath (the model for Inspire). Other people undergo hypopneas when loop gain leads to enough arousal to restore breathing, but they rarely undergo apneas. Other people with high loop gain over-react to the increased carbon dioxide levels, which destabilizes the ventilatory system, leads to more disturbances, 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. Precision medicine can be used to identify and treat individual sleep apnea disorders by providing medications that alter arousal threshold and loop gain, but an inadequate neuromuscular response cannot be considered the cause of the problem, because muscles normally relax during sleep. The goal of OSA treatment should be to provide an adequate airway passage at rest that does not depend on adaptive muscle activity.
Other researchers blame OSA on “collapse” of the pharyngeal walls. They cite the model of a Starling resistor, in which the rate of flow through a collapsible 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 this case, the pressure in the chamber surrounding the collapsible tube is the weight of the soft tissues surrounding the pharynx, which is much less than the negative pressure produced by a diaphragm desperately trying to inhale, therefore the airway flow through the pharynx in OSA does not fit the model of a Starling resistor. The pharynx is a collapsible tube, and studies show that it can only withstand a certain amount of negative pressure (Pcrit) before it becomes obstructed. This obstruction is described as a collapse of the pharyngeal walls, but the physics are more accurately described as a plugging of the tube. It occurs when the pharynx gets plugged by a stopper, which must have more physical integrity than the pharyngeal walls. Endoscopic viewing make some obstructions appear concentric, with the airway surrounded by a circle of tissues that seems to keep becoming smaller until the airway flow stops completely; but loose pharyngeal tissues cannot just tighten around the airway like a noose. People don't choke on loose tissues, they choke on a piece of meat. The piece of meat in OSA is the 6 cm thick slab of muscle that forms tongue base. The Pcrit is the pressure needed to suck it into the airway.
NASOPHARYNGEAL OBSTRUCTION - occurs when the loose soft tissues in the area, like the distal end of the soft palate, get sucked into the narrow space between the tongue base and the pharyngeal wall to form a seal like a gasket that prevents airway flow. In these situations, airway flow can usually be restored by removing the loose soft tissues from the site of the obstruction. In children, tonsillectomy is often effective. In adults, uvulopalatopharyngoplasty (UPPP) can be used to cut off the distal end of the soft palate, or barbed pharyngoplasty can be used to cut and reposition it. However, removing the gasket from the obstruction must be considered only a short term solution, because other soft tissues can later get stretched out and form a new gasket.
TENTING THE SOFT PALATE - is an easy way to remove the gasket from most nasopharyngeal obstructions. The soft palate is a flexible flap-like structure made of extrinsic and intrinsic muscles which lose their tonus during sleep, leaving its distal end swinging back and forth due to airway flow. A keel-like aponeurosis runs along its midline. The new soft palate elevator employs a silicone rubber bulb on the end of a thin flexible arm to elevate the central portion of this apnoneurosis, where there are no gag reflexes, in order to draw its untouchable distal end, which is full of gag reflexes, antero-superiorly out of the narrow gap between the tongue base and the pharyngeal wall. The soft palate elevator employs so little force that patients are unaware of its presence, and the arm's flexibility enables it to easily accommodate the functional movements of the soft palate during swallowing, when breathing stops anyway. It can elevate the center of the soft palate 1/4" all night without causing any discomfort.
The elevation of the center 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
Elevating the center of the soft palate also tightens the nearby soft tissues, 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 purple lines on the left side photo to become curved on the right side photo. Such tensioning of the pharyngeal wall makes the soft tissues there less easily sucked into the pharynx or vibrating during snoring.
The soft palate elevator is usually employed together with mandibular advancement in the first phase of treatment; because simply elevating the soft palate to remove the gasket without also making changes in the functional environment that led to it invites relapse due to reproduction of a gasket by other loose soft tissues, and simply changing the functional environment by advancing the mandible may not produce enough change in the anatomy to restore airway flow without removing the gasket.
ADVANCING THE TONGUE BASE
Addressing the root cause of OSA requires shifting the tongue base anteriorly away from the pharyngeal wall, both in the short-term to restore airway flow and in the long-term to gradually reduce resistance to airway flow with age. Such anterior shifting of the front of the airway was designed to continue during adulthood in humans in order to compensate for the gradual loss of muscle strength that also occurs during adulthood in humans and thereby maintain a stable airway. However horizontal facial growth, including the anterior shifting of the front of the airway, is largely powered by chewing forces, which have diminished radically since the advent of processed foods. As a result, horizontal facial growth has been redirected vertically. On average, our mandibles now rotate backward rather than forward. Some people have strong enough jaw closing muscles to prevent excessive vertical facial growth, so their mandibles cannot rotate backward; but their mandibles are instead simply locked back behind a steep overbite, where they remain posteriorly positioned, along with the tongue base. Short term treatment involves shifting the tongue base anteriorly far enough to restore airway flow, and long term treatment involves ensuring that the mandible and tongue base keep growing anteriorly away from the cervical spine and the pharyngeal wall just in front of it.
One way to move the tongue base away from the cervical spine is by shifting the mandible anteriorly. Mandibular advancement appliances can have a beneficial effect on AHI in clinical studies, and they have been shown to increase Pcrit in experimental studies. In addition to increasing the space in front of the tongue, the mechanisms by which mandibular advancement can improve pharyngeal airway flow may include repositioning the origins of the suprahyoid and genioglossus muscles anteriorly, stretching the palatoglossus and palatopharyngeal muscles, repositioning the pharyngeal arches laterally, and shifting the hyoid bone anteriorly and superiorly.
However, mandibular advancement does not always advance the tongue base into the enlarged space anteriorly, because the mandible is only attached to the tongue by muscles, which naturally lose 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 solves the problem for about half of the patients treated, as shown by a remarkable similarity of results in hundreds of studies. Attempts to identify anatomical features that indicate which patients are likely to respond well to mandibular advancement have been generally unsuccessful, so the high failure rate makes mandibular advancement appliances a hard sell.
Another way to move the tongue base away from the pharyngeal wall is by extreme advancement of the tongue tip. The Tongue Stabilizing Device, Tongue Retaining Device, and Good Morning Snore Solution employ a silicone rubber squeeze bulb that uses suction to grasp the tongue tip and hold it out in front of the lips, where there is room for the bulb. Unlike mandibular advancement appliances, these appliances can be used in denture wearers; but the tongue tip is far from the tongue base where the choking occurs, so they are only about as effective as mandibular advancement, and the extreme tongue advancement they require is difficult for most people to tolerate.13 Also, in some people, pulling the tongue very far forward pulls a thicker portion of the tongue base up into the area of obstruction and exacerbates the problem.
In dentate patients, the most effective way to move the tongue base away from the pharyngeal wall just far enough to restore flow is to slightly advance the entire front of the airway, including the whole tongue structure and the mandible. Because the mandible functions as the supporting framework and base of operation for the tongue, advancing the tongue and mandible together is easier than advancing either one alone. Previously there have been attempts to combine mandibular and tongue advancement, but the available technologies required different materials. For example, the silicone rubber used for the tongue holding bulbs does not attach to acrylic.
Now a new tongue holding technology made entirely of dental acrylic enables advancing the mandible and tongue together. In dentate patients seeking treatment, the first stage of treatment involves mandibular advancement and soft palate elevation. The second stage of treatment involves "pinning" the tongue against the advanced mandible. The third stage of treatment involves adding tongue base titraters to gradually pry the tongue base away from the pharyngeal wall.
ADVANCING THE MANDIBLE - can be performed with a variety of currently available oral appliances. Dorsal fin, EMA, Silent Night, and Herbst appliances that are made of acrylic (rather than nylon) can also be used for the subsequent stages of multi-level treatment. Monobloc and TAP appliances cannot be used for subsequent stages of multi-level treatment, because they do not allow mouth opening.
Herbst appliances have the longest history of effective treatment for OSA and the best control of mandibular position; but the bolted connectors of previous Herbst appliances are unnecessarily bulky, and they restrict lateral mandibular movements, which leads to frequent breakage. In addition, their downward vector of push on the mandible can open the lips and lead to habitual mouth breathing. To solve those problems, Dr. Summer's high push Herbst appliance has a much lower profile, freely moveable connectors that cannot bind or restrict lateral movements, and a vector of force on the mandible directed upward and forward, rather than downward and forward. The high push Herbst appliance is almost unbreakable, and each side can be adjusted in 1/3 mm increments 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.
COMPONENTS SEPARATED COMPONENTS ASSEMBLED INTERNALLY THREADED TUBING
BEFORE ADVANCING AFTER ADVANCING
PALATE EXPANSION - can be included in the high push Herbst appliance by using removeable offset connectors. The upper member of the appliance (the palatal expander with embedded anchors) can be worn by itself all day. Then, every night before bed, the patient can hook on the offset connectors and attached tubing assemblies along with the lower member of the appliance. Some dexterity is required, but most people acquire the needed skills rapidly. After the expansion, the components will no longer need to be separated, and the offset connectors can be crimped on for use just at night.
TITRATING - the 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 bite platform greatly increases the forces applied to the posterior connectors and can thereby lead to breakage of any Herbst appliance.
TESTING - Whatever type of mandibular advancement appliance is used for stage one treatment, its effectiveness should be tested after titration. Even a 50% reduction in AHI can feel like successful treatment to the patient, but such limited improvements often do not last, because the remaining incidents keep stretching out the pharyngeal tissues until they reform a gasket that once again obstructs the airway. Multi-night home sleep testing eliminates any first night effect and the normal night-to-night variability in results.14
EXTREME ADVANCEMENT - Many dentists have gone to extreme mandibular advancement to try and relieve the OSA in some of their patients. However, extreme advancement can damage teeth or their supporting structures, and its beneficial effects on the shape of the airway are bound to diminish over time, because the large forces used to advance the mandible will be gradually accommodated by osseous remodeling that reduces the pressure on the tissues. In addition, holding the entire tongue against a slightly advanced mandible is likely to be a safer and more effective way than extreme mandibular advancement to shift the tongue base away from the pharyngeal wall.
THE NEW TONGUE HOLDING DEVICE - Holds the body of the tongue and the lateral borders of the tongue base against the advanced mandible between specialized upper and lower tongue gripping surfaces that have thousands of forward slanted bristles, which function like directional tongue velcro to prevent the tongue from dropping backward into the pharynx.
The upper tongue gripping surface is a sheet of up to 4,000 (depending on size) bristles that are sized to fit between the filiform papillae that cover the dorsal surface (top) of the tongue. The sheet is curved to fit each patient's tongue. The lower tongue gripping surface is a sheet of up to 10,000 (depending on size) accupuncture needle sized points (shown left) which form a carpet of "tongue velcro." The carpet is shaped to fit the inner border of the mandible and the lower dentition and then bonded to the lower base appliance, where the tiny points grip the sensitive tissues on the underside of the tongue like a non-skid surface, as seen below right.
STEEL MODEL FOR MOLD FOR LOWER TONGUE GRIPPING SURFACE LOWER BASE APPLIANCE
To prevent accidental release of the tongue during sleep, at least one of the upper tongue gripping surfaces (the upper for patients with teeth and the lower for denture patients) is mounted in a continual biasing mechanism that creates a cushioned grip which persists throughout the submaximal mandible and tongue movements that occur during sleep, including bruxism. The cushioned grip continues until the mouth is opened wide enough to release the tongue. The illustration below shows a spring loaded upper tongue gripping surface; in which the tongue stays gripped in the middle figure with the mouth partly open, and then the tongue is only released in the bottom figure at wide opening.
FULLY CLOSED
PARTLY OPEN
FULLY OPEN
The target tongue position is normally with the tip of the tongue between the incisors and the lips comfortably closed around it, as seen in the tongue holding device carried on a Herbst appliance below. Because the tongue cannot escape during sleep, patients go to sleep with the tongue in its target position, and they awake with the tongue in the same position.
The tongue gripping surfaces are added together with bite stops, small flat stable plateaus of acrylic located over the terminal molars where they absorb all bite forces before those forces can hurt the tongue. In the photo below, the upper bite stops are made of yellow acrylic, and the lower bite stops are made of green acrylic.
TONGUE BASE TITRATERS
If further treatment is needed, tongue base titraters are added to the upper tongue gripping surface of the tongue holding device to gradually pry the tongue base off the pharyngeal wall in progressive 1.3 mm increments as the patient gets used to them. The tongue base is pushed down and forward away from its obstructing contact with the distal end of the soft palate while the distal end of the soft palate is drawn upward and forward away from its obstructing contact with the tongue base. The upper tongue gripping surface, which has been stabilized by gripping the tongue body and bracing the mandible against the bite stops, provides good anchorage from which to titrate the position of the tongue base. The tongue base titraters have the flexibility to accommodate the natural movements of the tongue base during swallowing, when breathing stops anyway.
BEFORE SHIFT AFTER SHIFT
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
Shifting the tongue base titraters down-and-back 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) inserting a tongue control device; and then after (bottom) using the tongue base titraters to shift the tongue base further down-and-back. 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 in the middle X-ray. However, in the middle X-ray, the airway is still restricted in the lower oropharynx and upper hypopharynx. 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, seen between the arrows.
HYPOPHARYNX
A hypopharyngeal obstruction is treated by using 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 rotate them forward (below right) in two steps to pry the tongue base anteriorly off the lower pharyngeal wall and away from the epiglottis. The photos below show this rotation of the tail segment adjusters from down-and-back to down-and-forward. 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 (DENTURE) PATIENTS - Generally cannot tolerate mandibular advancement; therefore treatment for OSA in this population involves just "pinning" the tongue against an upper denture base plate to prevent it from dropping back into the pharynx, and then adding a soft palate elevator if necessary. Tongue gripping is especially effective in these patients, because the tongue gripping surfaces can extend almost all the way to the cheeks, and the cushioning force from light compression of the tongue keeps the base plates fully seated on the edentulous ridges. In addition, the base plates do not require retention, because they don't have to withstand chewing forces. However, the goal of treatment is not advancement, which would apply pressure to the soft tissues. The goal of treatment is just to hold the tongue against the relatively stable upper denture base plate to prevent it from dropping back into the pharynx.
In most edentulous patients, resilient mounting of one of the tongue gripping surfaces to produce a cushioned grip is unnecessary, because the increase in vertical dimension that results from wearing the denture base plates together with the tongue gripping surfaces produces enough passive stretch of the jaw closing muscles to hold the tongue. The amount of passive stretch that the appliance produces depends on its vertical dimension, which can be easily controlled. It can also be enhanced by a chin strap.
If a cushioned grip is needed to prevent tongue release during submaximal opening, the lower tongue gripping surface, (rather than the upper tongue gripping surface as in dentate patients), is "spring loaded". It is attached to the lower denture base plate by a polyester mesh anterior tether and a pair of 3/8” long orthodontic elastics on each side that connect a cleat on the posterior portion of the lingual flange of the lower tongue gripping surface with a ball clasp on the buccal side of the posterior portion of the lower denture base plate. The elastics bias the lower tongue gripping surface continually upward into the underside of the tongue. The bias is maintained until the cleats reach the same plane as the bite table. Any further opening releases the tongue. The release point is controlled by the location of the cleats on the lingual flanges.
ELASTICS BOTTOM ENDS ON CLEATS TOP ENDS ON BALL CLASPS ELASTICS SUSPEND LOWER TONGUE GRIPPING SURFACE
If the lower denture base plate is too unstable to function as a base from which the lower tongue gripping surface can be pushed upward into the underside of the tongue, both the upper and lower tongue gripping surfaces are bonded to the upper and lower denture base plates, and the base plates are connected by interarch elastics attached to buttons, cleats, or ball clasps on their buccal walls. Then, if the mandible drops out of the unstable lower denture base plate, the tongue stays gripped, and the airway remains protected.
CLINICAL CONSIDERATIONS
GROWTH EFFECTS - While short-term treatment success requires simply reopening the airway, long-term treatment success also requires redirecting the slow facial growth of adulthood horizontally to gradually increase the size of the airway passage and decrease resistance to airway flow, just as muscles naturally become weaker with age, in order to maintain a stable resting airway flow. Horizontal growth in the maxilla involves expansion which enlarges the nasal airway, and horizontal growth in the mandible involves anterior translation of the corpus, which enlarges the pharyngeal airway. Many people have an adult facial growth pattern that slowly but continuously rotates the mandibular corpus down and back into the space needed for the pharyngeal airway, thereby increasing resistance to airway flow and triggering forward head posture to reduce it.
VERTICAL DIMENSION, the height of an oral appliance, affects the shape of the airway, but its effect depends on facial form. Increasing vertical dimension at the dentition increases airway space in some people and decreases it in others. For most patients with a normal facial form, their appliance should be no taller than necessary to ensure its 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 or the TMJs.
For patients with very strong jaw muscles and short anterior faces, especially in the presence of deep overbite, their mandibular advancement appliance should include a front flat bite plate (extending from canine to canine for stability) in order to lower nocturnal bruxism forces to prevent the jaw muscles from further reducing facial height and redirect them to gradually reduce the overbite that inhibits mandibular advancement. Including the canines in the front flat bite plate provides stability, while preventing contact between the posterior teeth reduces the forces used in nocturnal bruxism by about half.
For patients with very weak jaw muscles and long anterior faces (usually accompanied by difficulty maintaining a lip seal at rest), their jaw muscles may need to be stretched and rehabilitated before they can tolerate even a 2 mm increase in vertical dimension continuously for eight hours. Also, in these people, 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 - is detrimental to health. 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 prevents the release from the paranasal sinuses into the lungs of nitric oxide, which has antibacterial properties, a vasodilating effect, and a role in ensuring good endothelial health. It also impairs the effectiveness of respiration, because the nose is so vascular that it acts like a little lung. In one study, volunteers who wore nose clips to force mouth breathing for a couple of hours developed lowered arterial oxygen levels.
Obligate mouth breathers have nasal cavities that do not allow adequate resting nasal airway flow, and they must keep their lips slightly parted to maintain an oral airway passage. Many people with a nasal cavity that is barely large enough to allow adequate airway flow become obligate mouth breathers whenever a mild allergy or rhinitis causes nasal swelling that slightly reduces the cross-sectional diameter of the nasal cavity. In obligate mouth breathers, palate expansion can be employed at any age to widen the nasal airway and raise tongue posture.16 The expansive force triggers adaptive remodeling throughout the midface. The resulting increase in nasal airway size can be maintained post-treatment by wearing a retainer nightly and stabilizing the 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.17
Habitual mouth breathers use an oral airway despite having an adequate nasal airway. Frequently the habit arises from an open-mouth resting posture due to a framework of bones and teeth at the front of the face that has grown too long to be comfortably covered by the drape of relaxed soft tissues hanging down from the front of the cranium, causing the lips to part when the facial muscles are at rest. During swallowing, the perioral muscles show visible strain trying to form a lip seal. During sleep, the parted lips create an oral airway passage that offers less resistance than the nasal airway passage, and it can become the habitual route for breathing.
Mouth breathing then sustains itself due to its influence on facial growth, because it lowers mandibular posture, and postural forces provide the light steady forces that shape bones. The lowered mandibular posture makes the face grow vertically long and narrow, which prevents the nasal cavity from growing wide enough to create an adequate nasal airway passage, which leads to more mouth breathing. Monkeys forced to mouth breathe by experimentally plugging their nostrils grew long narrow faces, because their mandibles acquired a lowered posture to maintain an oral airway. Humans forced to mouth breathe by a restricted nasal airway grow long narrow retrusive faces, because lowering the human mandible also rotates it down and back.
Habitual mouth breathing can be triggered by wearing an oral appliance that increases the vertical dimension far enough to part the lips, and it can usually be eliminated in these cases 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.
NOCTURNAL BRUXISM - is a side effect of normal sleep, when the brain sends motor signals to the jaw muscles, usually during arousals that mark a transition to a lighter sleep stage; and it reflects no particular bite condition.18 It cannot be caused by bite problems or eliminated by bite treatment,19-20 and it is not correlated with TMJ disorders.21-27 In some people, nocturnal bruxism may be an adaptive response that prevents OSA by bracing the mandible to prevent it from slipping back into the pharynx. In other people, nocturnal bruxism can be a result of OSA, because the obstructions trigger sympathetic activity to stimulate bodily movement to restore breathing, and bruxism is one of those movements. Therefore oral appliances should be designed to withstand bruxism in patients treated for OSA.
TMJ DISORDERS - usually resolve by middle age when OSA begins, so they are rarely significant barriers to gradual mandibular advancement or other oral appliance treatments for OSA. The bite destabilization that results from mandibular advancement can cause increased jaw muscle tonus, just as instability in any joint reflexively increases tonus in the muscles crossing that joint, because the bite is wired like a joint between the jawbones. In such cases, the bite can be easily restabilized by extending it anteriorly, as described below.
BITE CHANGES - The posterior open bites that frequently result from mandibular advancement can reduce chewing effectiveness and confound dentists, so they are treated as an adverse side effect that can even warrant discontinuing the treatment; but they can be easily managed in a way that restores chewing ability and increases the long-term effectiveness of the treatment. The posterior open bites that commonly result from mandibular advancement are often blamed on pathologies such as contracture of the superior lateral pterygoid muscles or inflammation in the TMJs; but the cause is not pathological. Advancement of the mandibular corpus throughout life is the natural pattern of adult human facial growth. In our ancestors, it helped compensate for the tooth wear that they also experienced throughout life by continuous bringing the lower dentition antero-superiorly into the upper dentition. In addition, it was stimulated by bite forces, so that individuals who chewed extensively and experienced more tooth wear also underwent more jawbone growth to compensate for that wear.26-27 Today, it continues although it is rarely needed, and it can be accelerated by the bite forces produced by an oral appliance that is tall enough to create passive stretch of the jaw closing muscles or by the distraction osteogenesis created by holding the mandible down and forward all night.
The loss of the previous central bite position has been difficult for dentists to accept, because it tramples on a deeply held belief system in dentistry that the center of all biting activity and the reference point for all clinical dental work should be the rearmost mandibular position. To prevent loss of this reference point, many dentists who use mandibular advancement appliances today have their patients chew on hard gum or small wedges (morning occlusal guides) every morning to create an "occlusal return" or "reprogramming" process that forces the mandible back towards its previous central bite position. Such forced mandibular retrusion can trigger regressive remodeling that enables the condyles to seat more posteriorly than they otherwise would, but simply adjusting the bite forward is much easier than trying to reverse growth that has already occurred or prevent further growth in a functional environment that stimulates it.
In addition, shifting the bite anteriorly can facilitate long-term treatment, because it shifts the mandibular postural position anteriorly, which facilitates airway passage in upright posture and can also reduce dependency on the appliance by preventing the mandible from dropping all the way back and causing sleep to deteriorate to pre-treatment levels right away if the mandibular advancement appliance is not worn for a short time, such as during a nap. In the OSA population, esthetics is rarely a barrier to mandibular advancement; and most people only need enough bite stability to chew comfortably, not a perfectly located and precisely defined centric position. After relatively rapid mandibular advancement to accomplish short-term treatment goals (eliminating the OSA), gradual mandibular advancement can continue, because it grows in that direction anyway.
THICKNESS - The unnecessary bulk, especially in the anterior regions, of nearly all current oral appliances can exacerbate airway problems by distalizing tongue posture. 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 facial growth vertically, causing them to grow long narrow faces. Humans have a shorter ramus and a more inferior center of rotation, therefore lowering tongue and mandibular posture also rotates the mandibular corpus down and back into the pharyngeal airway space. To avoid impinging on tongue posture, all upper oral appliances should include a space hollowed out to fit the tongue tip (tongue tip hollow) just beneath the anterior bite table at the front of the palate behind the maxillary incisors, as shown below.
TIGHTNESS - Nearly all acrylic dental appliances force the upper teeth inward (palatally) due to the shrinkage of acrylic, especially on the labial wall of the anterior region at the center of that shrinkage. In a healthy dentition at rest, each tooth is suspended in the middle of a dynamically 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 oversize portion of the brain. When the teeth remain in the middle of these sockets all night, the tissues lining the sockets remain passive. Displacement of a tooth from its rest position triggers a collection of adaptive responses designed to make the socket once again fit the tooth's rest position. One of those responses includes an increase in jaw muscle tonus, because noxious afferent input from any joint triggers increased tonus in the muscles which cross that joint, the periodontium is wired like a joint between the tooth roots and their sockets, and the jaw closing muscles cross that joint. As a result, pressure on the teeth automatically increases tonus in the jaw muscles; which can add to the jaw muscle tightness caused by increased central nervous system stress or an appliance with a vertical dimension that produces passive stretch of the jaw closing muscles.
Even if a dentist could obtain a perfectly accurate impression of the dentition in its resting state and fabricate an oral appliance which perfectly fit the model made on that impression, the 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 should have a range of motion of about 1/4 mm vertically and bucco-lingually and about a tenth of that distance mesio-distally in the presence of adjacent teeth. The movement of the teeth throughout their ranges of motion enhances periodontal circulation during functional activities like chewing by flushing out blood with each compression and then allowing arterial circulation to replenish it with each rebound. An appliance that "hugs" a tooth restricts its range of motion and thereby also its 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 only needs enough mechanical retention to resist the forces of gravity. It can fit around an undercut for retention; but, once fully seated, it should apply no pressure to teeth, leaving each tooth in its natural rest position and allowing at least a slight range of motion.
FOOTNOTES
1) 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.
2) 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.
3. Mickelson SA. Hyoid advancement to the mandible (hyo-mandibular advancement). Operative Techniques in Otolaryngology. 2012:23, 56-59.
4. 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.
5) 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.
6) 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.
7) Delaidelli A, Moiraghi, A. Respiration: A new mechanism for CSF circulation? Journal of Neuroscience 2017, 37 (30) 7076-7078.
8) 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.
9) 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).
10) Dreha-Kulaczewski S., Joseph AA, Merboldt KD, et al. Inspiration is the major regulator of human CSF flow. J Neurosci 2015;35:2485-2491.
11) Benveniste H, Liu X, Koundai S, et al. The glymphatic system and waste clearance with brain aging. Gerontology 2019;65:106-119.
12) Hladky SB, Barrand MA. The glymphatic hypothesis: the theory and the evidence. Fluids and Barriers of the CNS 2022;19(9):1-144.
13) Zhang W, Song X, Masumi SI, et al. Effects of head and body positions on 2- and 3- dimensional configuration of the oropharynx with jaw protruded: a magnetic resonance imaging study. Oal Surg Oral Med Oral Pathol. 2011;111(6):778-84.
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) 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.
16) Ozbek MM, Memikoglu UT, Altug-Atac AT, Lowe AA. Stability of maxillary expansion and tongue posture. Angle Orthod. 2009 Mar;79(2):214-20).
17) 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. The role of the Nose in Pharyngeal Obstructions,pp 181-193 in The Role of Epiglottis in Obstructive Sleep Apnea. pub January 2024.
18) American Academy of Sleep Medicine: International Classification of Sleep Disorders, ed. 3. Darien IL: American Academy of Sleep Medicine, 2014.
19 Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28:1085-1091
20) 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.
21) Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepancies and nocturnal bruxism. J Prosthet Dent. 1984;51(4):548-553.
22) Bailey JO, Rugh JD. Effects of occlusal adjustment on bruxism as monitored by nocturnal EMG recordings. J Dent Res.1980;59(special issue):317.
23) Karcachi BJ, Bailey JO, Ash MM. A comparison of biofeedback and occlusal adjustment on bruxism. J Periodontol. 1978;49(7):367-372.
24) Pullinger AG, Seligman DA. The degree to which attrition characterizes differentiates patient groups of temporomandibular disorders. J Orofac Pain. 1993;7(2):196-208
25) Berry DC. Occlusion: fact and fallacy. J Craniomandib Pract. 1986;4(1):54-64.
26) Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular disorders have a cause-and-effect relationship? J Orofac Pain 1997;11:15-23.
27) Kulmer S, Hattmannstorfer R, Niedermoser A, et al. Cephalometric changes after orthodontic treatment and fixed oral rehabilitation in adult patients: 23 years of follow-up. J Oral Health Dent Sci 2019;3:402
28) Forsberg CM. Facial morphology and ageing: a longitudinal cephalometric investigation of young adults. Eur J Orthod 1979;1(1):15-23.