Bites: Current Concepts

OCCLUSAL CONFUSION

Unfortunately, dentistry still cannot treat TMJ disorders orthopedically, because it has never understood the role of the bite, so denstists treat TMJ disorders by managing the symptoms rather than curing the condition. Dentists in school are taught that biting (called occlusion) is an act that must be carefully controlled, but they are not taught why. They are taught all the exact contours of an ideal bite, but they are not taught how and why those contours affect jaw system health. Any bite that varies from these exact contours is called a malocclusion, but nearly all people have a malocclusion according to this standard. Dentists learn that each tooth should provide a centric bite stop, but they don't learn how those bite stops on multiple teeth work together to provide a platform for the mandible to rest on and exercise against, and how this platform affects craniofacial muscle tonus, facial growth, and body posture. 

Aside from the cranial base, the bite table is the most stable craniofacial growth landmark in mammals, including our recent ancestors, while other craniofacial components fluctuate more widely around it. However, when we industrialized our food supply, human bite tables became much less stable structurally, more postero-inferiorly located, and more asymmetrical. Those changes have had profound effects on our health, but dentists have been unable to connect the health impacts with the bite changes that have caused them, because the parameters by which dentists measure bites have no relevance to their orthopedic function or health.  

The inability of traditional dentistry to understand bites is revealed by the way they are managed clinically. Altering a bite has been described as "sailing into uncharted waters". Most dental authorities consider any bite treatment, even stabilizing a bite, to be invasive because it is irreversible, and therefore only to be used as a last resort. Clinical dentistry treats the bite table as a wall with a number of critical support areas (centric stops), each of which must be carefully preserved; because reducing any one of them could cause the existing bite to become lost and difficult or impossible to find again. For that reason, any bite adjustment is considered irreversible and therefore generally contraindicated.

If a bite that has been reconstructed perfectly according to conventional standards still causes chronic jaw discomfort, the conventional standards are not questioned, but the discomfort is generally assumed to be caused by some pathology other than bite strain. The diagnoses used to describe these  cases have included occlusal disease, occlusal neurosis, occlusal dysesthesia,¹ occlusal hyperawareness, positive occlusal sense, body dysmorphic disorder, somatoform disorder, monosymptomatic hypochondriacal psychosis,² and phantom bite syndrome^3.  Studies of these supposedly pathological conditions have found that they are not associated with any recognized anatomical features or proprioceptive changes, such as altered interdental thickness discrimination.^4-5 Treatments reportedly used for them have included cognitive behavioral therapy, counseling, psychotherapy, and medications including pimozide (a neuroleptic drug),^6-7 dothiepin (antidepressant),⁸ tricyclic antidepressants,^9-10 serotonin-selective reuptake inhibitors, seratonin-norepinephrine reuptake inhibitors,^9,11-12 monozide (anti-psychotic),¹³ mirtazapine (noradrenergic and specific serotoninergic antidepressant), and aripripazole (a dopamine partial agonist).⁹   

Nearly all of the clinical research on bites has attempted to locate the single best mandibular position for simultaneous contact of all the teeth, or at least all the back teeth, with light contacts between the front teeth; because the conceptual frameworks by which dentists evaluate bites grew out of laboratory techniques that employ hinge articulators, which open and close on one clearly defined and repeatable trajectory. However, natural mandibles do not work like hinges, even multi-adjustable hinges. In all mammals, the bite table functions as a platform that occupies an area, not a point. That area is certainly smaller today than it was in our pre-industrial ancestors, but there is no reason to expect it to be zero.

Also, while the bite table is treated clinically like a structural wall with a number of critical supports, it is actually a dynamic platform in which each supporting member is constantly adapting its position to fit functional forces. Normal healthy human teeth have a mobility of 100 - 150 microns,^14-15 and they can adaptively shift position by hundreds of microns overnight to accommodate bite forces. Reversing the symptoms produced by a problemmatic bite change does not require precisely recreating all the critical support areas that existed before the change - it requires restoring the ability of the bite to provide a stable platform in a location and surrounded by a range of motion that are acceptable to the rest of the jaw and postural systems. 

BITES AND TMJ DISORDERS

Bite strain can certainly cause TMJ disorders. Symptoms have been produced experimentally by adding a high filling (bite interference) to a centric stop,^16-20 a working side excursion,^21-23  or a balancing side contact.^24-31 In one subject, an experimental bite interference only .25 mm tall caused symptoms that persisted for nine months after removing the interference until the patient was treated with a bite plate.³²  It's reasonable to expect the bite to affect TMJ health, because it determines the fully seated (braced) location and functional range of motion of the condyles; and the location of the close packed position and the functional range of motion of the articulating bones in other joints affects their health. It's also reasonable to expect the bite to affect the health of the jaw muscles, because it provides the platform they rest on and exercise against. The jaw muscles have been shown to react almost immediately to even minute changes in the contours of the bite table.^33-38 

Despite those obvious connections, researchers have been unable to find any correlations between TMJ disorders and bite parameters.^39-40 A few bite parameters (deep overbite, anterior open bite, loss of posterior support, and unilateral cross-bite) show weak correlations with TMJ disorders at extreme values; but normal variants show no correlation with any functional condition.^41-42 As a result of this failure to correlate bite parameters and symptoms, some researchers have concluded that the bite must play no significant role in TMJ disorders.

However, lack of evidence of association is not evidence of lack of association. It may be that we just don't know enough about bites or TMJ disorders to demonstrate the association between them. Indeed there is good evidence to support that explanation. The parameters that we use to compare different bites include static measurements of spatial relationships between upper and lower teeth and some measurements of sliding and incidental tooth contacts, however none of those parameters has ever been well correlated with jaw system health or TMJ disorder symptoms. For decades we have known that some people with chronic TMJ disorder symptoms and difficulty chewing have textbook perfect bites, while other people with very irregular bites have excellent jaw system health and function. In research, the bite has been an uncontrolled variable. Studies that have attempted to evaluate the effects of bite treatments have yielded inconsistent results, because the bite treatments used, (mostly equilibration or restoration in CR), helped some people and hurt others. Even balancing side interferences are correlated with TMJ disorder symptoms in some studies,^43-44 and not in others.^45-47 

BITE STABILITY

The only currently measurable bite parameter that has any functional relevance is stability.⁴⁸ On average, people with TMJ disorders have less stable bites than normals.⁴⁹ However even that relationship has been difficult to demonstrate, because our techniques for measuring bite stability are so crude compared with the sensitivity of the system. There are three problems with our current techniques for measuring bite stability.  

One problem is the thickness of the measuring device. Bite stability is measured as the ability to evenly distribute biting pressure on a 100 micron thick piezoelectric film sensor (Tek Scan or Accura) or a slightly thinner and less sensitive plastic sheet (Prescale Occluzer System), to mark bite surfaces with 40 to 60 micron thick carbon paper or inked cloth, or to penetrate a sheet of thin wax. These materials are much too thick to provide clinically relevant information. The neuromusculature of the masticatory system reacts to interferences less than 8 microns tall,^50-52 yet even the thinnest marking device is at least twice that thick, and most are several times that thick.

A second problem is tooth mobility. Teeth at rest are so delicately suspended in the middle of their sockets that they move easily over small distances.⁵³ When a patient bites, the first teeth to contact shift to allow other teeth to contact, and our marking devices cannot distinguish between the first contacts and subsequent contacts.

A third problem is the variability of mandibular closing trajectories. The teeth that first contact at the termination of any jaw closure depends on the precise closing trajectory, which depends on variables such as posture and mental state. It only becomes consistent after a series of consecutive mandibular closures has allowed the jaw muscles to hone in on whatever bracing position provides the most stable bite platform after the teeth have shifted in any way they need to provide maximal stability in that bracing position.  

BITE PHILOSOPHIES - Even if dentists can't measure the functional aspects of bites or understand how they work with the rest of the body, they need techniques for managing bite problems and reconstructing bites in clinical practice. The techniques that are currently used and the conceptual models that rationalize them are described below:  

CENTRIC RELATION - CR, the most commonly held bite philosophy and a deeply held belief system among many dentists, is a conceptual model that grew out of the use of hinge articulators to set denture teeth a century ago. Dentists learned that, if the mandible is pushed back as far as possible, it can be made to consistently rotate open and closed like a hinge around an axis drawn between the TMJs; and, if the denture teeth are set to all contact at the same height on that hinge-axis trajectory, the dentures remain stable during chewing and swallowing. Later, when dentists needed to also construct effective chewing surfaces for making crowns and bridges, they found that making the teeth fit together on that same hinge axis trajectory seemed to enable effective chewing and also prevent the rapid periodontal breakdown that sometimes occurred when other positions were used to build the bite. 

CR was embraced by academic and clinical dentistry. A bite in which all the teeth contact simultaneously in CR was considered to be the only proper bite. People who sometimes use a more forward bite position were assumed to be "posturing" for psychological reasons or suffering from some other pathology, such as spasm of the superior lateral pterygoid muscles. People who did not have a stable bite in CR were assumed to have a malocclusion characterized by CR interferences that triggered chronic firing of the superior lateral pterygoid muscles to avoid striking the interferences by pulling the mandible anteriorly away from CR (the CR slide). 

As dentistry became more precise, CR became more narrowly defined. Dawson described CR as a point -"a definite apex from which no forward or backward movements of the condyle-disk assemblies can occur unless they move down on the bony slope of the fossa".⁵⁴  The ideal mandibular opening and closing trajectory was thought to be a pure hinge axis rotation, like a hinge articulator, which terminates at 138 simultaneous perfectly tripodized (three point) bite contacts. Researchers measured CR centric slides in .1 mm increments and unsuccessfully tried to correlate them with TMJ disorders. 

CR philosophy spread to all areas of dentistry. Periodontists removed centric interferences to diminish tooth mobility. TMJ specialists designed nightguards and splints to provide stable contacts in CR. Orthodontists pushed back the upper teeth to fit closely around the lower teeth when the mandible is in CR. Equilibration techniques, in which dentists perfected techniques for locating and removing all interferences to CR closure, became the popular way to treat TMJ and bite disorders, with some dentists even performing full mouth rehabilitation on otherwise healthy patients just to create CR bites, and others grinding CR closure into normal bites, which changes the normal envelope of mandibular movement (Posselt), seen on the left side below, by grinding into it an apex point (CRO) to fit CR theory, as seen on the right side below. This equilibration process, which is how most studies of bite treatment have been conducted, removes the natural posterior guidance from the dentition.

FIGURE 1   -  REDRAWING THE ENVELOPE OF MANDIBULAR MOVEMENT     

                          POSSELT                                DAWSON

Elaborate conceptual frameworks were concocted to explain why CR bites must be healthier than other types of bites. Dawson claimed that CR is the only mandibular position which is stable, because it is braced by bone; and therefore it is the only mandibular position that allows full relaxation of the superior lateral pterygoid muscles. Ramfjord claimed that the jaw muscles function with harmonious low level activity when the teeth contact evenly in CR.⁵⁵ Other researchers hypothesized that centric interferences cause spasm or hyperactivity of the superior lateral pterygoid muscles by denying access to CR, and that chronic hyperactivity of the superior lateral pterygoid muscles displaces the TMJ articular disks by pulling them antero-medially off the condyle. Medical illustrations were drawn with the entire superior lateral pterygoid muscle attached directly to the front edge of the disk in a manner that would enable it to pull the disk off the condyle. 

These hypotheses were combined to produce an explanatory model of TMJ disorders that is still widely accepted today. For example, one author write, “Any sort of hit-and-slide from CR into MI will cause the condyles to translate down and forward out of the fossae. Once the condyles are positioned down and forward on the slippery slope of the eminentiae, the inferior belly of the lateral pterygoid muscle must contract to hold the condyles in this down and forward position, while the superior belly of the lateral pterygoid must also contract to keep the disc properly positioned between the condyle and eminence. Periods of prolonged contraction of the lateral pterygoid result in fatigue or spasm of the muscle, which can be experienced as pain and discomfort to the patient. These symptoms can be exacerbated if the patient has a clenching or bruxing habit because the temporalis, medial pterygoid, and masseter elevator muscles will be highly active and will be in direct contrast to the already contracted lateral pterygoid muscles. This dysfunction and constant opposition between the elevator muscles and condyle positioning muscles will further increase the fatigue and strain on all of the muscles of mastication. Also, constant tension within the superior belly of the lateral pterygoid muscle (the portion of the lateral pterygoid with attachments to the articular disc) will result in continuous stretching of the ligaments that attach the disc to the posterior surface of the condyle. This constant stretching can eventually create an unstable condyle-disk assembly, resulting in a disc that can click or pop off of and onto the lateral pole of the condyle during function.”⁵⁶

However, research has undermined all these assumptions. Provocation experiments found that centric interferences are as likely to decrease jaw muscle activity as to increase it.^67-68 MRI studies showed that disk displacements occur in many different directions and not usually in the path of the superior lateral pterygoid muscles.⁶⁹ Anatomy studies showed that 80% to 85% of the superior lateral pterygoid fibers attach to the condyle rather than the disk, making it unlikely that they could pull the disk off the condyle anyway.^70-71 Radio telemetry showed that, even after removing all CR interferences, CR is rarely used.^60-63  Intrajoint catheters showed that CR is the only mandibular position that produces increased intra-articular fluid pressure.⁶⁴ EMG studies showed that retruding the mandible causes increased elevator muscle tension⁶⁵ and hyoid instability.⁶⁶ Kinematic studies showed that the concept of a pure hinge axis closure was an abstraction; because all condylar movements involve some combination of rotation and translation. 

Supporters of CR had to explain why most people with perfectly healthy masticatory systems lack the characteristics of an ideal or even a good bite according to CR theory. Centric slides can be found in all pre-industrial human dentitions,^72-73 and they are still found in 90% of modern dentitions.^74-76  When patients have full mouth reconstruction to eliminate their centric slide, it usually returns.⁷⁷  Dawson claimed that the centric slides that are common in apparently perfectly healthy jaw systems were due to an "adaptive centric posture", which occurs when "deformed TMJs have adapted to a degree that they can comfortably accept firm loading". The ability of condyles to shift anteriorly in CR was blamed on pathological elongation of the temporomandibular ligaments.⁵⁷ The ability of condyles to shift laterally in CR was blamed on "immediate side shift", a phenomenon that varies in length from 0 to 3 mm and appears to have no clinical significance.^58-59 

Even the plausible sounding warning that condyles should not be held down on the slopes of the articular eminences for more than very short intervals turned out to be baseless when dentists treating sleep apnea learned that mandibles can be held in extreme protrusion all night without causing problems in most people.

Recently, as a result of the problems sometimes associated with the clinical application of CR, supporters of CR have softened their positions. Most have stopped pushing the mandible backward so forcefully. The glossary of prosthodontic terms has 7 definitions for CR, with the most recent moving the focus away from the interdigitation of the teeth by defining CR as a disk-condyle relationship, even though about thirty percent of adults have a dislocated disk in at least one TMJ. Some CR dentists have redefined CR as a superior or superior-anterior condylar position instead of a posterior or supero-posterior one. Other CR dentists advocate freedom in centric - either a long centric or a wide centric. 

The repeatability of CR makes it convenient for lab work, but that does not make it healthy. The repeatability is due to the fact that CR is a border position. Border positions in joints are not functional positions – they provide movement limitations that protect the joint structures from injury. The ligaments that protect the TMJs by becoming taut when the mandible reaches its posterior border position are designed to function passively as restraining devices, not to enter actively into joint function. They can be manipulated posteriorly into that border position in order to artificially limit jaw opening and closing to one trajectory, but that border position cannot be considered a functional position. Joints need a range of motion that ensures adequate circulation to all areas of their articular surfaces to stay healthy, and it's difficult to envision how confining the mandibular range of motion to its posterior border position could benefit the TMJs. The optimal location for stable mandibular bracing is probably, on average, about 1 mm to 1.5 mm forward from CR, but even that varies too much to provide a guide for choosing a good central bite area. Also, some people need freedom from centric, their mandibles need freedom from being forced into the posterior end of its range of motion. They need the centric slide and posterior guidance that forms the upper rear end of Posselt's illustration of the envelope of mandibular movement, seen on the previous page.

Restoring dentitions in CR usually works clinically, because CR is located close to the posterior border of the functional mandibular range of motion, where the jaw muscles automatically bring the mandible for power crushing and therefore where teeth are most vulnerable to damage by extreme chewing forces. A tooth that contacts prematurely near CR is more likely to be injured than a tooth that contacts prematurely in a more forward mandibular position, where jaw muscle forces are lower.  If a facial pain condition is due to frequent activation of neuromuscular reflexes protecting a hypersensitive molar from bite trauma, eliminating a CR interference on that tooth can relieve TMJ disorder symptoms. However, the success that CR dentistry has occasionally had in those types of patients is certainly not an indication that CR is the ideal or even a desireable location for the most stable bite platform.

CANINE GUIDANCE - For clinical work, dentists also need to choose mandibular pathways in and out of the most stable bite platform. Cusps that are too steep can collide. Cusps that are too flat can prevent the cutting actions that are needed for effective chewing. Canine guidance provided a solution that facilitated dental laboratory work and became widely accepted in clinical dentistry as an adjunct to CR. 

The concept of canine guidance was introduced in the 1960's by a researcher named D'Amico who studied the skeletal remains of one tribe of American Indians and saw that they, like all tribal people, lose their overbite and overjet to acquire end to end occlusion as their teeth wear down with age; but he mistakenly concluded that this change in their bites was a pathological loss of vertical dimension. His reasoning was, "If the edge to edge relation of the anterior teeth were a hereditary functional relation, it would be seen in man today, with unabraded normal tooth structure".⁷⁸ He went on to hypothesize that the tooth wear which caused the pathological loss of vertical dimension could be prevented by more overlap of their canines, because "nature intended the canines to protect the posterior teeth by guiding the mandible into CR". However, he was diagnosing the tribal people he studied as having lost vertical dimension, because he was comparing them to his patients, many of whom had excessive face height. Actually these tribal people maintained very stable facial height in proportion to body height throughout life due to mechanisms that effectively compensated for whatever wear they experienced, as described fully in chapter 2 of ETIOLOGY.^79-84 

D'Amico had correctly observed that canine guidance decreases functional jaw muscle forces. He said, "contact of the upper cuspids by the opposing mandibular teeth during eccentric excursions causes transmission of periodontal proprioceptive impulses to the mesencephalic root of the fifth cranial nerve, which in turn alters the motor impulses transmitted to the musculature." Later other researchers using EMG affirmed his finding that canine contact reduces biting forces. They found that group function contacts caused both the ipsilateral temporalis and the masseter to fire; but a canine contact only triggered firing in the ipsilateral temporalis.

However, D'Amico had used his finding of decreased functional muscle forces in the presence of canine guidance to advocate for steepening canine guidance, because he believed, as others did at that time, that TMJ disorders were due to excessive jaw muscle forces.^85-86 Now we know that he was looking at the wrong muscle forces. Canine contact shuts off functional jaw muscle forces, because it triggers neuromuscular reflexes that are designed to protect the TMJs,⁸⁷ but the problem in TMJ disorders is excessive jaw muscle resting forces (tonus), not functional forces.  In apes, lateral mandibular thrusts during chewing produce a powerful grinding action, while the contacts between the backward facing surfaces of the lower canines and the forward facing surfaces of the upper canines protect the mandible from posteriorly directed forces. In modern humans, lateral mandibular thrusts produce contacts between the forward facing surfaces of the lower canines and the backward facing surfaces of the upper canines, which can drive the ipsilateral mandibular condyle posteriorly and thereby activate a protective response by the ipsilateral posterior temporalis muscle to pull the mandible away from the distally driving canine contact. In addition, while steepening canine guidance narrows the mandibular range of motion, there is good evidence that wider ranges of motion are healthier. When jaw muscles are rehabilitated and bites are stabilized, the functional mandibular range of motion naturally widens.^100-102  

The canines provide important contributions to the anchorage of natural dentitions, but they do not play a unique role in the bites of hominids¹⁰³, and they are not specially designed to remove all horizontal forces from the other teeth, like advocates of canine guidance still preach. The canines are designed to work together with the other teeth to provide stable support for the mandible throughout its normal range of motion. They are the primary support for the mandible only when it moves antero-laterally.

ANTERIOR GUIDANCE

The guidance concept was extended to include the anterior (front) teeth, the primary support for the mandible when it moves anteriorly. Anterior guidance is found in all healthy natural dentitions, when the mandible moves anteriorly up onto the palatal surfaces of the upper front teeth and onto a stable bite platform there. Insufficient anterior guidance is ICD 10 code M26.54.

MUTUAL PROTECTION

Combining stable CR contacts on the back teeth with steep anterior and canine guidance at the front teeth led to an occlusal philosophy known as mutual protection. Its advocates claim that teeth should only receive forces axially (straight downward), that steep anterior and canine guidance protect the back teeth by preventing them from all horizontal vectors of force, and that stable CR contacts on the back teeth protect the front teeth from the powerful jaw closing forces produced during bracing. It is a convenient philosophy for dental lab work; because the back teeth just need to provide stable centric stops in one mandibular position without requiring simultaneous sliding contacts; and the front teeth can be designed for esthetics without also requiring enough incisal edges uniform enough to provide an incisal bracing platform. 

BIOESTHETICS 

Some dentists have taken the concept of mutual protection to such an extreme that they claim the teeth should all be restored to their original unworn shapes, with the kind of bite they achieve when they first eupt, with CR contacts even on the front teeth. They believe that nocturnal bruxism results from the bite being "out of balance", and it can be prevented by restoring balance to the bite, usually by increasing the steepness of the anterior and canine guidance. 

However, these basic tenets of bioesthetics are nonsense. Nocturnal bruxism is a normal sleep behavior, and it reflects no particular bite condition.¹⁰⁶ It cannot be caused by bite problems or eliminated by bite treatment,^107-108 and it is not correlated with TMJ disorders.^109-113 Also, normal degrees of tooth wear cannot be considered pathological. In fact, most species of mammals do not even achieve effective chewing function until wear has reduced the complex arrangement of cusps and fossae that cover the biting surfaces of newly erupted teeth into a series of closely fitting facets that crush food between the facets and cut food at the facet edges.¹¹⁴ Our unworn enamel covered bite surfaces were designed to align the dental arches and then wear away to produce sharp edges and grinding surfaces - not to maintain a continuous protective layer on teeth or limit the range of motion of the mandible.¹¹⁵ The teeth are designed to protect each other by sharing the loads they encounter in whatever direction the mandible moves, like the walls of a socket.

Also, in all natural dentitions, teeth do not just receive forces axially - they have a healthy natural range of movement in all directions, which they need to stay healthy.  The concept that teeth should only move straight up and down defies biologic common sense. All joints, including the dento-alveolar (periodontal) joints between the tooth roots and their sockets, are designed to benefit from hydrostatic forces generated by their functional range of movement. The extensive network of small vessels and anastomoses that fill the tooth sockets communicate directly with surrounding bone marrow spaces. During healthy mastication, these vessels act like hydraulic lines to absorb shocks and circulate fluids.^116-118 Compression of a tooth pumps fluids out of the socket and into venous circulation, then release of the compression allows new blood to flow back into the socket with an articular pulse that gradually returns the tooth to its rest position.¹¹⁹ The circulatory benefit from alternating compression and release probably explains why reducing or eliminating masticatory forces causes atrophic periodontal changes,^120-121 much like immobilizing synovial joints causes degenerative arthritic changes in those joints. Also like in synovial joints, alternating compression and release of a tooth affects one portion of the socket at a time. A healthy functional range of motion requires sufficient variability to keep the entire socket replenished; including a vertical (axial) component, a transverse (bucco-liongual) component, and even a mesio-distal component between adjacent teeth, complete with interproximal contact areas shaped to function as interproximal articular surfaces.

GROUP FUNCTION - is the natural state of the bite in all mammals, including humans.¹²² Until the industrialization of our diet in the last couple of centuries, canine guidance was only present temporarily in some newly erupted dentitions, where its role was to provide enough early coupling between the diverse growth patterns in the maxilla and the mandible to maintain the proximity of the dental arches in a sagittal plane despite their diverse growth patterns. Once the bite table was formed, the front teeth did not restrict or "guide" mandibular movements but cooperated with the neighboring teeth to provide a stable bracing platform for the mandible in whatever directon it moved anteriorly or antero-laterally. The canines were the primary supports only when the mandible slid out antero-laterally. Omnidirectional group function gave the dentition longevity by evenly distributing wear. The teeth wore in together, and they wore out together. 

Today most natural bites still operate with some degree of group function,¹²³ but it is difficult to create prosthodontically with the hinge articulators that are still used by dental labs. In the near future, a computerized mandibular movement simulator will recreate the complex functional movements of the mandible and take into account the independent movements of teeth within their sockets and even the bending of the mandible and the compression and release of the circum-maxillary sutures in order to reproduce mandibular movements accurately enough to enable us to build group function bites in the dental laboratory. 

NEUROMUSCULAR DENTISTRY

The "neuromuscular" bite philosophy is generally posited as the alternative to CR, although it also has no scientific basis. While CR techniques always shift the bite platform backward, "neuromuscular" techniques always shift it forward.  

Neuromuscular dentistry began in 1969 when a well know and respected researcher, Dr. Barney Jankelson, thought he had discovered an accurate technique for locating and recording the ideal bite position. He used to say, "if you can measure it, it's a fact. If you can't measure it, it's an opinion." His technique involved placing a pulsing TENS (transcutaneous electrical nerve stimulation) source directly over the motor root of the trigeminal nerve to fire all the jaw closing muscles evenly, and then increasing the TENS to electronically close the mandible directly into its ideal bite - the so-called myocentric position. He claimed that this myocentric position is so important that the pathways into and out of it do not matter, and he used articulators that had only straight vertical opening and closing movements. He coupled the pulsing TENS source with a jaw tracking system and a surface EMG recorder in a package that he claimed could be used to diagnose and treat TMJ and bite related disorders. When Dr. Jankelson was near the end of this life, the ADA awarded his equipment its seal of acceptance.  

However, scientific research undermined all the assumptions on which neuromuscular dentistry was based. Anatomical studies using needle electrodes showed that the pulsing TENS does not cause the jaw muscles to fire evenly but simply stimulates the muscle fibers that are closest to the source.^127-128  It usually advances the mandible, because the muscles closest to the source are the superficial masseters, which are oriented more anteriorly than the other jaw closing muscles. Treatment that brings the mandible anteriorly often provides relief of symptoms, because most TMJ disorders are caused by a bite that forced the mandible posteriorly, not because TENS has some special ability to relax the jaw muscles.  TENS is used in medicine to provide pain relief, not muscle relaxation,¹³⁰ and there is no good evidence that it actually relaxes jaw muscles, except as a secondary effect of diminishing the pain which had been triggering muscle tightening.^131-133

Also, the diagnostic equipment, which was included to quantify the beneficial effeccts of the treatment, was useless. The jaw tracking is not precise enough to identify a mandibular position with any accuracy, and researchers showed that small changes in the location of the EMG electrodes caused significant differences in the results – making any longitudinal monitoring useless.^125-126 One study found that the myotronics diagnostic package was unable to even distinguish between TMJ disorder patients and "normals".¹²⁹   

CONDYLAR POSITION ON X-RAY

There have also been attempts to determine the optimal mandibular bracing location by the positions of the condyles in the glenoid fossae as seen on transcranial X-rays, but that parameter turned out to be much too variable to be useful clinically.^142-143  Condyles are often displaced in unexpected directions and distances.^144. In addition, the positions of the condyles relative to the glenoid fossae are poor reference points, because the glenoid fossae are not inert frameworks. They are attached to the condyles, and they relocate with the condyles in response to functional forces.¹⁴⁵ Attempts to change the positions of the condyles relative to the glenoid fossae by full mouth reconstruction, equilibration, or orthodontics were generally unsuccessful.^146-148

SWALLOWING

The most consistent and physiologically healthy mandibular closing trajectory occurs during swallowing. Studies have indicated that swallowing is accompanied by a relatively consistent and uniform jaw closing muscle firing which appears less adaptive to bite interferences than the normal closure trajectory. (Ingervall B, Thilander B. Activity of temporal and masseter muscles in children with a lateral forced bite. Angle Orthod. 1975;45:249-258)(Celar A, Siejka E, Schatz J, Furhauser R, Piehslinger E. Mandibular reference position: chin-point guided closure vs, final deglutition. J Craniomand Pract. 1996;14(1):42-45.)

However, there is still natural variation in the mandibular closing trajectories used during swallowing, and that variation defines an area rather than a point. Therefore to reproduce the contours of an ideal mandibular bracing area would require recording a large number of swallowing events after the relaxed jaw muscles have been deprogrammed while tipping the head into different postural positions. The data could be integrated digitally to mill or mold a platform that provides orthopedic support for the working side of the mandible throughout its functional range of motion, like one large ball-and-socket joint. When the ball moves in any direction within the socket, it rides up on the socket walls in that direction, anteriorly, laterally, and posteriorly.  

OCCLUSAL CONCLUSION

For a century, dentists have reconstructed bite tables by choosing one mandibular bracing position, stabilizing it with as many simultaneous tooth contacts as possible, and then surrounding it with sloping walls of tooth structure that "guide" the mandible into it. Such a simple mechanical approach was useful when dental lab work was dependent on simple hinge devices to reproduce jaw movements; however, building a bite table around a point does not even resemble natural jaw movement pathways, and it does not recognize the important role that jaw muscle exercise and range of motion play in the physiology and natural orthopedic function of the mandible. The mandible needs support, not guidance, in a central bracing area and oon its working side throughout its range of motion. 

FOOTNOTES

1.Melis M, Zawawi KH. Occlusal dysesthesia: a topical narrative review. J Oral Rehabil. 2015;42:779-785.

2.Marbach JJ. Psychosocial factors for failure to adapt to dental prostheses. Dent Clin North Am. 1985;29:215-233.

3. Marbach JJ,Varscak JR, Blank RT, Lund P. Phantom bite; classification and treatment. J Prosthet Dent. 1983;49:556-559.

4. Baba K, Aridome K, Haketa T, Kono K, Ohyama T. Sensory perceptive and discriminative abilities of patients with occlusal dysesthesia. J Jpn Prosthodont Soc. 2005;49:599-607.

5. Tsukiyama Y, Yamada A, Kuwatsuru R, Koyano K. Bio-psycho-social assessment of occlusal dysaesthesia patients. J Oral Rehabil. 2012;39:623-629.

6. Clark GT, Minakuchi H, Lotaif AC. Orofacial pain and sensory disorders in the elderly. Dent Clin North Am. 2005;49:343-362.

7. Jagger RG, Korszun A. Phantom bite revisited. Br Dent J. 2004;197:241-243.

8. Wong MTH. Phantom bite in a Chinese lady. J Hong Kong Med Assoc. 1991;43:105-107.

9. Watanabe M, Umezaki Y, Suzuki S, Miura A, Shinohara Y, et al. Psychiatric comorbidities and psychopharmacological outcomes of phantom bite syndrome. J Psychosom Res. 2015;78:255-259.

10. Toyofuku A. A clinical study on the psychosomatic approaches in the treatment of serious oral psychosomatic disorders under hospitalization: evaluation of “behavior restriction therapy” for oral psychosomatic disorders and consideration of its pathophysiology. Jpn J Psychosom Dentist. 2000;15:41-71.

11. Bathia NK, Bathia MS, Bathis NK, Singh HP. Occlusal dysesthesia responded to Duloxetine. Delhi Psychiatr J. 2013;16:453-454.

12. Toyofuku A, Kikuta T. Treatment of phantom bite syndrome with milnacipran – a case series. Neuropsychiatr Dis Treat. 2006;2:387-390.

13. Shetti SS, Chougule K. Phantom bite – a case report of a rare entity. J Dent Allied Sci. 2012;1:82-84.

14. Berry DC, Singh BP. Daily variation in normal occlusal contacts. J Prosthet Dent. 1983;50:386-391.

15. O'Leary TJ. Tooth mobility. Dent Clin N Am. 1969;13:567-579.

16. Christensen LV, Rassouli NM. Experimental occlusal interferences. part 2. Masseteric EMG responses to an intercuspal inteference. J Oral Rehabil. 1995;22:521-531.

17. Ferrario VF, Sforza C, Serrao G, Colombo A, et al. The effects of a single intercuspal interference on electromyographic characteristics of human masticatory muscles during maximal voluntary teeth clenching, J Cranio Pract. 1999;17(3):184-188.

18. Christensen LV, Rassouli NM. Experimental occlusal interferences. part 1. A review. J Oral Rehabil. 1995;22:515-520.

19. Magnusson T, Enbom L. Signs and symptoms of mandibular dysfunction after introduction of experimental balancing side interferences. Acta Odontol Scand. 1984;42:129-135.

20. Riise C, Sheikholeslam A. The influence of experimental interfering occlusal contacts on the postural activity of the anterior temporal and masseter muscles in young adults. J Oral Rehabil. 1982;9:419-425.

21. Shiau YY, Ash MM. Immediate and delayed effects of working interferences on EMG and jaw movement. In Electromyography of jaw reflexes in man, Van Steenberghe D, De Laat A, (eds.) 1989;311-326.

22. Hannam AG, Wood WW, De Cou RE, Scott JD. The effects of working-side occlusal interferences on muscle activity and associated jaw movements in man. Arch Oral Biol. 1981;26:387-392.

23. Besler UC, Hanam AG. The influence of altered working-side occlusal guidance on masticatory muscles and related jaw movement. J Prosthet Dent. 1985;53(3):406-413.

24. De Boever J. Experimental occlusal balancing-contact interference and muscle activity. Paradontaologie 1969;23:59-69.

25. Karlsson S, Cho S-A, Carlsson GE. Changes in mandibular masticatory movements after insertion of nonworking side interference. J Craniomand Disorder Facial Oral Pain 1992;6:177-183.

26. Baba K, Yugami K, Yaka T, Ai M. Impact of balancing side tooth contact on clenching induced mandibular displacements in humans. J Oral Rehabil. 2001;28:721-727.

27. Okano N, Baba K, Akishige S, Ohyama T. The influence of altered occlusal guidance on condylar displacement. J Oral Rehabil. 2002;29:1091-1098.

28. Okano N, Baba K, Ohyama T. The influence of altered occlusal guidance on condylar displacement during submaximal clenching. J Oral Rehabil. 2005;32:714-719.

29. Okano N, Baba K, Igarashi Y. The influence of altered occlusal guidance on masticatory muscle activity during clenching. J Oral Rehabil. 2007;34:679-684.

30. Karlsson S, Cho S-A, Carlsson GE. Changes in mandibular masticatory movements after insertion of nonworking-side interference. J Craniomandib Disord Facial Oral Pain 1992;(6):177-183.

31. Ingervall B, Carlsson GE. Masticatory muscle activity before and after elimination of balancing side occlusal interference. J Oral Rehabil 1982;9:183-192.

32. Randow K, Carlsson K, Edlund J, Oberg T. The effect of an occlusal interference on the masticatory system. An experimental investigation. Odont Revy. 1976;27:245-256.

33. DeBoever JA, Carlsson GE, Klineberg IJ. Need for occlusal therapy and prosthodontic treatment in the management of temporomandibular disorders. Part 1. Occlusal interferences and occlusal adjustment, J Oral Rehabil. 2000;27:367-379.

34. Riise C, Sheikholeslam A. Influence of experimental interfering occlusal contacts on the activity of the anterior temporal and masseter muscles during mastication. J Oral Rehabil. 1984;11:325-333.

35. Bakke M, Moller E. Distortion of maximal elevator activity by unilateral premature tooth contact. Scand J Dent Res. 1980;80:67-75.

36. Miralles R, Manns A, Pasini C. Influence of different centric functions on electromyographic activity of elevator muscles. J Craniomandib Pract. 1988;6:26-33.

37. Manns A, Miralles R, Valdivia J, Bull R. Influence of variation in anteroposterior occlusal contacts on electromyographic activity. J Prosthet Dent. 1989;61:617-623.

38. Miralles R, Bull R, Manns A, Roman E. Influence of balanced occlusion and canine guidance on electromyographic activity of elevator muscles in complete denture wearers. J Prosthet Dent 1989;61:494-498.

39. Riolo M, Brandt D, Tenhave T. Associations between occlusal characteristics and signs and symptoms of TMJ dysfunction in children and young adults. Am J Orthod. 1987;92:467-477.

40. Seligman DA, Pullinger AG. The role of functional occlusal relationships in temporomandibular disorders. A review. J Craniomand Disorder Facial Oral Pain. 1991;5:265-279.  

41. Pullinger AG, Seligman DA. Quantification and validation of predictive values of occlusal variables in temporomandibular disorders using a multifactorial analysis. J Prosthet Dent. 2000;83(1):66-75.

42. Seligman DA, Pullinger AG. Association of occlusal variables among refined TM patient diagnostic groups. J Craniomandib Disord Facial Oral Pain. 1989;3227-236.

43. McNamara JA, Seligman DA, Okeson JP. Occlusion, orthodontic treatment, and temporomandibular disorders: a review. J Orofacial Pain. 1995;9:73-90.

44. Geering AH. Occlusal interferences and functional disturbances of the masticatory system J Clin Periodontol 1974;1:112-119.

45. Shields JM, Clayton JA, Sindledecker LD. Using pantographic tracings to detect TMJ and muscle dysfunctions. J Prosthet Dent 1978;39:80-87.

46. Lederman KH, Clayton JA. Restored occlusions. Part 2: The relationship of clinical and subjective symptoms to varying degrees of TMJ dysfunction. J Prosthet Dent 1982;47:303-309.

47. Roberts CA, Tallents RH, Katzberg RW, Sanchez-Woodworth RE, Handelman SL. Comparison of internal derangements of the TMJ with occlusal findings. Oral Surg Oral Med Oral Pathol 1987;63:645-650.

48. Bakke M: Mandibular elevator muscles: physiology, action, and effect of dental occlusion. Scand J Dent Res. 1993;101(5):314-331.

49. Moller E, Sheikholeslam A, Lous I. Response of elevator muscle activity during mastication to treatment of functional disorders. Scand J Dent Res. 1984;92:64.

50. Anderson DJ, Hannam AG, Matthews B. Sensory mechanisms in mammalian teeth and their supporting structures. Physiol Rev 1970;50:171-195.

51. Turp JC, Schindler H. The dental occlusion as a suspected cause of TMDs: epidemiological and etiological considerations. J Oral Rehabil. 2012;39:502-512.

52. McNamara D. Occlusal adjustment for physiologically balanced occlusion. J Prosthet Dent. 1977;38:284-293.

53. Riise C, Ericsson SG. A Clinical study of the distribution of occlusal tooth contacts in the intercuspal position at light and hard pressure in adults. J Oral Rehabil. 1983;10:473-480.

54. Dawson PE. Evaluation, diagnosis, and treatment of occlusal problems, ed 2. St. Louis 1989, Mosby.

55. Ramfjord SP. Dysfunctional temporomandibular joint and muscle pain. J Prosthet Dent. 1961;11:353-362.

56. Wolfe MD. Functional considerations of the masticatory system during prosthodontic procedures. www.insidedentistry.net January 2017.

57. Okeson JP. Management of Temporomandibular Disorders and Occlusion. ed 7, 2013, Mosby.` p. 75. 

58. Goldenberg BS, Hart JK, Sakumura JS. The loss of occlusion and its effect on mandibular immediate side shift. J Prosthet Dent. 1990;63(2):163-6.

59. Taylor T. Avinash SB. Nazarova E. Wiens JP. Clinical significance of immediate mandibular lateral translation: A systematic review. J Prosthet Dent. published online 12/23/2015. Also (Journal of Prosthetic Dentistry (vol 115(4) pp 412-418).

60. Gillings B, Kohl J, Zander H. Contact patterns using miniature radio transmitters. J Dent Res. 1963;42:177.

61. Pameijer JH, Glickman L, Roeber FW. Intraoral occlusal telemetry. Tooth contacts in chewing, swallowing, and bruxism. J Periodontol. 1969;40:253-258.

62. Pameijer JH, Brion M, Glickman L, Roeber FW. Intraoral occlusal telemetry. Effect of occlusal adjustment upon tooth contacts during chewing and swallowing. J Prosthet Dent. 1970;24:492-497.

63. Glickman JI, Martigoni M, Haddad A, Roeber FW. Further observation on human occlusion monitored by intraoral telemetry [abstract 612] IADR. 1970;201.

64. Roth T, Goldberg J, Behrents R. Synovial fluid pressure determination in the temporomandibular joint. Oral Surg Oral Medicine Oral Pathol. 1984;57:583-588.

65. Ingervall B, Egermark-Eriksson I. Function of temporal and masseter muscles in individuals with dual bite. Angle Orthod 1979;49:131.

66. Ingervall B, Carlsson G, Helkimo M. Change in location of hyoid bone with mandibular positions. Acta Odont Scand. 1970;28(3):337-362.

67. Pruzansky S. Applicability of electromyographic procedures as a clinical aid in the detection of occlusal disharmony. Dent Clin N Am. 1960;3:117-130.

68. Moss M. Functional analysis of centric relation. Dent Clin N Am. 1975;19(3):436.

69. Tasaki MM, Westesson PL, Isberg AM, Ren YF, Tallents RH. Classification and prevalence of temporomandibular joint disk displacement in patients and symptom-free volunteers. Am J Orthod Dentofacial Orthop. 1996;109(3):249-262.

70. Heylings DJ, Nielsen BL, McNeill C. Lateral pterygoid muscle and the temporomandibular disc. J Orofacial Pain 1995;9:9-16.

71. Begg PR, Kesling PC. Begg's Orthodontic Theory and Technique, 2nd ed., WB Saunders, Philadelphia, 1971.

72. Ainamo J, Talari A. Eruptive movements of teeth in human adults. In: The Eruption and Occlusion of Teeth. DFG Poole and MV Stack (eds). Butterworths, London, pp 97-107. Colston papers No. 27 1976.

73. Weinberg L, Chastian J. New TMJ clinical data and the implication on diagnosis and treatment JADA;120(3):305-311.

74. Posselt U. Movement areas of the mandible. J Prosthet Dent.1957;7:375-385.

75. Agerberg G, Sandstrom R. Frequency of occlusal interferences: C clinical study in teenagers and young adults. J Prosthet Dent 1988;59(20:212-217.

76. Celenza F. The centric position: replacement and character. J Prosthet Dent. 1973;30:591-598.

77. D'Amico A. The canine teeth - normal functional relation of the natural teeth of man. J Southern Calif Dent Assoc. 1958;261:198.

78. Kaidonis J. Tooth wear: the view of the anthropologist. Clinical Oral Investig. 2008;12(Suppl 1): 21-26.

79. Poole DFG. Evolution of mastication. In: Anderson DJ, Matthews B, eds. Mastication, Bristol, England, 1976, John Wright and Sons.

80. Brace CL. Occlusion to the anthropological eye. In The Biology of Occlusal Development, Monograph 7, Craniofacial Growth Series. University of Michigan, Ann Arbor 1977.

81. Murphy T. The changing pattern of dentine exposure in human tooth attrition. Am J Phys Anthropol 1959;17:167-178.

82. Ainamo J. Relationship between occlusal wear of the teeth and periodontal health. Scand J Dent Res. 1972;80:505-508.

83. Panek H, Matthews-Brzozowska T, Nowakowska D, et al. Dynamic occlusions in natural permanent dentition. Quintessence Int. 2008;39(4):337-342.

84. Williamson EH, Lundquist DO. Anterior guidance: Its effects on electromyographic activity of the temporal and masseter muscles. J Prosthet Dent.1983;49(6):816-823.

85. Shupe RJ, Mohamed SE, Christiensen LV, Finger IM, Weinberg R. Effects of occlusal guidance on jaw muscle activity. J Prosthet Dent 1984;51:811-818.

86. Pruzansky S. Applicability of electromyographic procedures as a clinical aid in the detection of occlusal disharmony. Dent Clin N Am. 1960;3:117-130.

87. Yemm R. Comparison of the activity of left and right masseter muscles of normal individuals and patients with mandibular dysfunction during experimental stress. J Dent Res. 1971;50:1320-1323.

88. Weinberg L, Chastian J. New TMJ clinical data and the implication on diagnosis and treatment JADA;120(3):305-311.

89. Sheikholeslam A, Moller E, Lous I. Pain, tenderness, and strength of human mandibular elevators. Scand J Dent Res 1980;88:60-66.

90. Gervais RO, Fitzsimmons GW, Thomas NR. Masseter and temporalis electromyographic activity in asymptomatic, subclinical, and temporomandibular joint dysfunction patients. J Craniomandib Pract. 1989;7(1):52-57.

91. Helkimo E, Carlsson GE, Carmeli Y. Bite force in patients with functional disturbances of the masticatory system. J Oral Rehabil. 1975;2(4):397-406.

92. Kogawa EM, Calderon PS, Lauris JR, Araujo CR, Conti PC. Evaluation of maximal bite force in temporomandibular disorder patients. J Oral Rehabil. 2006;33:559-565.

93. Sheikholeslam A, Moller E, Lous I. Postural and maximal activity in the elevators of the mandible before and after treatment of functional disorders. Scand J Dent Res. 1982;90:37.

94. Lous I, Sheikholeslam A, Moller E. Postural activity in subjects with functional disorders of the chewing apparatus. Scand J Dent Res. 1970;78:404

95. Hansson T, Oberg T. Arthrosis and deviation in form in the temporomandibular joint, a macroscopic study on human autopsy material. Acta Odont Scand. 1977;35(1-3):167-174.

96. Kurita H, Ohtsuka A, Kobayashi H, Kurashina K. Resorption of the lateral pole of the mandibular condyle in temporomandibular disc displacement. Dentomaxillofacial Radiol. 2001;30:88-91.

97. Hansson T, Oberg T. Arthrosis and deviation in form in the temporomandibular joint: A microscopic study on human autopsy material. Acta Odontol Scand 1977;35:167-174.

98. Axelsson S, Fitins D, Hellsing G, Holmlund A. Arthrotic changes and deviation in form of the temporomandibular joint – an autopsy study. Swed Dent J. 1987;11:195-200.

99. Besler UC, Hannam AG. The influence of altered working side occlusal guidance on masticatory muscles and related jaw movement. J Prosthet Dent. 1985;53(3):406-  

100. Clayton JA. Border positions and restoring occlusion. Dent Clin N Am. 1971;15:525 -  

101. Moller E, Sheikholeslam A, Lous I. Response of elevator muscle activity during mastication to treatment of functional disorders. Scand J Dent Res. 1984;92:64.

102. Rugh J, Graham G, Smith J, Ohrback R. Effects of canine versus molar occlusal splint guidance on nocturnal bruxism and craniomandibular symptomatology. J Craniomand Pract. 1989;3:203-210.

103. Thumati P, Manwani R, Mahantshetty M. The effect of reduced disclusion time in the treatment of myofascial pain dysfunction syndrome using immediate complete anterior guidance development protocol monitored by digital analysis of occlusion. J Craniomandib Pract. 2014;32(4):289-299.

104. American Academy of Sleep Medicine: International Classification of Sleep Diosorders, ed. 3. Darien IL: American Academy of Sleep Medicine, 2014. 

105. Kerstein RB. Treatment of myofascial pain dysfunction syndrome with occlusal therapy to reduce lengthy disclusion time – a recall evaluation. J Craniomandib Pract. 1995;13(2):105-115.

106. Lobbezoo F, Naeije M. Bruxism is mainly regulated centrally, not peripherally. J Oral Rehabil. 2001;28:1085-1091.

107. 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. 

108. Rugh JD, Barghi N, Drago CJ. Experimental occlusal discrepancies and nocturnal bruxism. J Prosthet Dent. 1984;51(4):548-553.

109. Bailey JO, Rugh JD. Effects of occlusal adjustment on bruxism as monitored by nocturnal EMG recordings. J Dent Res.1980;59(special issue):317.

110. Karcachi BJ, Bailey JO, Ash MM. A comparison of biofeedback and occlusal adjustment on bruxism. J Periodontol. 1978;49(7):367-372.

111. Pullinger AG, Seligman DA. The degree to which attrition characterizes differentiates patient groups of temporomandibular disorders. J Orofac Pain. 1993;7(2):196-208.

112. Berry DC. Occlusion: fact and fallacy. J Craniomandib Pract. 1986;4(1):54-64.  

113. Lobbezoo F, Lavigne GJ. Do bruxism and temporomandibular disorders have a cause-and-effect relationship? J Orofac Pain 1997;11:15-23.

114. Murphy T. Mandibular adjustment to functional tooth attrition. Aus Dent J. 1958;3(3):171-178.

115. Bien SM. Hydrodynamic damping of tooth movement. J Dent Res. 1966;45:907-914.

116. Kardos TB, Simpson LO. A theoretical consideration of the periodontal membrane as a collagenous thixotropic system and its relationship to tooth eruption. J Periodont Res. 1979;14:444-445.

117. Ng GC. Walker TW. Zingg W. Burke PS. Effects of tooth loading on the periodontal vasculature of the mandibular fourth premolar in dogs. Arch Oral Biol. 1981;26:189-195.

118. Anneroth G. Ericsson SG. An experimental histological study of monkey teeth without antagonist. Odont Revy. 1967;18:345.

119. Levy GG, Mailland ML. Histologic study of the effects of occlusal hypofunction following antagonist tooth extraction in the rat. J Periodont. 1980;51(7):393-399.  

120. Motokawa M, Terao A, Karadeniz EI, Kaku M, et al. Effects of long term occlusal hypofunction and its recovery on the morphogenesis of molar roots and the periodontium in rats. Angle Orthod. 2013;83:597-604. 

121. Beyron H. Occlusal relations and mastication in Australian Aborigines. Acta Odont Scand.1964;22:597-678.

122. Woda A, Vigneron P, Kay D. Nonfunctional and functional occlusal contacts: a review of the literature. J Prosthet Dent. 1979;42:335

123. Rugh JD, Drago CJ. Vertical dimension. A study of clinical rest position and jaw muscle activity. J Prosthet Dent. 1981;45:670-675.

124. Klasser GD, Okesson JP. the clinical usefulness of surface electromyography in the diagnosis and treatment of temporomandibular disorders. J Am Dent Assoc. 2006;137(6):763-771.

125. Rugh JD, Santos JA, Harlan JA, Hatch JP. Distribution of surface EMG activity over the masseter muscle. J Dent Res. 1988 67 (special issue), abstr 1790;513.

126. Dao T, Feine J, Lund J. Can electrical stimulation be used to establish a physiologic occlusal position. J Prosthet Dent.1988;60(4):509-514.

127. DeSantana JM, Walsh DM, Vance C, Rakel BA, et al. Effectiveness of transcutaneous electrical nerve stimulation for treatment of hyperalgesia and pain. Curr Rheumatol Rep. 2008 Dec; 10(6): 492–499.

128. Bessette RW, Quinlivan JT. Electromyographic evaluation of the myo-monitor. J Prosthet Dent. 1973;30:19-24.

129. Wieselmann-Penkner K, Janda M, Lorenzoni M, Polansky R. A comparison of the muscular relaxation effect of TENS and EMG-biofeedback in patients with bruxism. J Oral Rehabil. 2001;28(9):849-853.

130. Lund J, Widmer C, Feine J. Validity of diagnostic and monitoring tests used for temporomandibular joint disorders. J Dent Res. 1995;74(4):1133-1143.

131. Lund JP, Widmer C. Evaluation of the use of surface electromyography in the diagnosis, documentation, and treatment of dental patients. J Cranio Dis Fac Oral Pain. 1989;3:125-137.

132. Ricketts RM. Abnormal function of the temporomandibular joint Am J Orthod 1955;41:435-441.

133. Weinberg L A. Posterior unilateral condylar displacement: its diagnosis and treatment. J Prosthet Dent. 1977;37:559-569.

134. Farrar WB. Diagnosis and treatment of anterior dislocation of the articular disc. N.Y Dent J 1971;41:348-351.

135. Weinberg L A. Correlation of temporomandibular dysfunction with radiographic findings. J Prosthet Dent 1972;28:519-539.

136. Mongini F. Abnormalities in condylar and occlusal positions. In Solberg WK and Clark GT (eds) Abnormal Jaw Mechanics: Diagnosis and Treatment. Quintessence Publ Co. Chicago pp 23-43.

137. Blaschke DD, Blaschke TJ. Normal TMJ bone relationships in centric occlusion. J Dent Res. 1981;60:98-104.

138. Dumas AL, Moaddab MB, Willis HB, Homayoun NM. A tomographic study of the condyle/fossa relationship in patients with TMJ dysfunction. J Craniomandib Pract. 1984;2(4):315-325.

139. Owen AH. Orthodontic/orthopedic treatment of craniomandibular pain dysfunction part 2: Posterior condyle displacement. J Craniomandib Pract. 1984;2(4):333-349.

140. Pullinger, AG, Solberg WK, Hollender L, Guichet D. Tomographic analysis of mandibular condyle position in diagnostic sub-groups of temporomandibular disorders. J Prosthet Dent. 1986;55:723–729.

141. Pullinger AG, Hollender L, Solberg WK, Petersson A. A tomographic study of mandibular condyle position in an asymptomatic population. J Prosthet Dent.1985;53(5):706-713.

142. Westesson PL. Double-contrast arthrography and internal derangement of the temporomandibular joint. Swed Dent J (suppl 13) 1982:1-23. Markovic M, Rosenberg H. Tomographic evaluation of 100 TMJ patients. Oral Surg 1976;42:838-846.

143. Ronquillo HI, Guay J, Tallents RH, Katzberg RW. Comparison of condyle-fossa relationships with unsuccessful protrusive splint therapy. J Craniomandib Disord Facial Oral Pain 1988;2:178-180.

144. Pirttiniemi P, Kantomaa T, Tuominen M. Associations between the location of the glenoid fossa and its remodeling. An experimental study in the rabbit. Acta Odontol Scand. 1991;49:255-259.

145. Breitner C. Bone changes resulting from experimental orthodontic treatment. Am J Orthod. 1940;26:521-546.

146. Dahan J, Dombrowsky KJ, Oehler K. Static and dynamic morphology of the temporomandibular joint before and after functional treatment with activator. Trans Eur Orthod Soc. 1969;255-273.

147. Johnston LE. Gnathologic assessment of centric slides in post-retention orthodontic patients. J Prosthet Dent. 1988;60:712.