Bites: Current Concepts

OCCLUSAL CONFUSION

Dentists in school are taught that occlusion is an act that must be carefully controlled to protect the teeth, but they are not taught that the bite table provides a platform for the mandible to rest on and exercise against.  They do not learn how the dental arches work orthopedically to provide a structural platform between the upper and lower jawbones, and how this platform affects craniofacial muscle tonus, facial growth, and body posture.  The bite platform is among the most stable of craniofacial growth landmarks in mammals, including our recent ancestors, while other craniofacial components fluctuate more widely around it.  However, when we industrialized our food supply, human bite platforms became much less stable structurally, more postero-inferiorly located, and more asymmetrical.  Those growth changes have had profound effects on our health, but dentists have been unable to connect them with the bite changes that cause them, because dentists have never come up with a functionally relevant way to measure bites.  We cannot even quantify bite stability.  As a result, studies that have tried to assess the effects of bite treatments have helped some subjects and harmed others.  We can't provide evidence-based treatment for bites, because we can't even collect relevant evidence about bites.  Therefore, instead of evidence-based treatment, clinical decisions today have to be based on rationale care, which is derived from understanding how bites function and dysfunction - subjects which are extensively described on this website.  

The inability of traditional dentistry to understand how bites work is revealed by the inadequacy of the clinical techniques  used to manage bite problems.  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 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), assuming that each stop must be carefully preserved; because reducing it could cause the existing bite to become lost and difficult or impossible to find again.  Therefore, bite changes are considered dangerous, because they are irreversible.  The reluctance to change a bite is so widespread in clinical dentistry today that successful phase one disk recapturing procedures using oral orthopedic appliances are usually followed by an attempt to return to the pre-treatment bite, even though that process causes more than half of the patients to undergo recurrence of the disk displacement and at least some recurrence of symptoms. 

Complaints of bite discomfort are assumed to be caused by factors other than bite strain if the bite meets conventional standards.  Patients who have become uncomfortable with the feel of their bite following dental work have been diagnosed as having occlusal disease, occlusal neurosis, occlusal dysesthesia,1 occlusal hyperawareness, positive occlusal sense, body dysmorphic disorder, somatoform disorder, monosymptomatic hypochondriacal psychosis,2 or phantom bite syndrome3. Studies of this condition have found that it is not associated with any recognized anatomical features or proprioceptive changes, such as altered interdental thickness discrimination.4-5 Treatments reportedly used for it 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   

Most of the clinical research on bites has attempted to locate the best single narrowly defined mandibular position for simultaneous contact of all the teeth, or at least all the back teeth, because the conceptual frameworks by which dentists evaluate bites grew out of laboratory techniques that employ a hinge articulator.  However,  mammalian bite tables always allow the mandible some horizontal freedom of movement within the central bite area.  In fact, that freedom of movement in a horizontal plane was the breakthrough that distinguished mammals from reptiles, because it enabled mammals to rub their teeth together in order to chew food rather than just tear and swallow it.  Thus the mammalian bite table functions as a platform that supports the mandible throughout a small area for bracing and a larger surrounding area for chewing.  Those areas are certainly smaller today than they were in our pre-industrial ancestors, but there is no reason to expect them to be zero, the goal of CR dentistry.

The bite table functions not as a wall, but as a dynamic articular surface.  Each tooth is constantly adapting its position to keep its articular surfaces aligned with functional forces. Normal healthy human teeth have a mobility of 50 - 100 microns,14-15 and they can adaptively shift position by hundreds of microns overnight to accommodate bite forces.  Therefore, reversing symptoms produced by a bite change does not require precisely reproducing all the critical support areas that existed before the change - it requires restoring the ability of the bite to provide a stable central bracing platform and a range of motion that is acceptable to the rest of the postural system. The barrier to using bite change therapeutically is our inability to predict the effects of altering a bite in any particular manner.  We know that the neuromusculature controlling mandibular movements and the cellular mechanisms controlling dento-alveolar remodeling are endowed with great adaptive capacity.  We just have not established what resting and functional forces are needed to promote healthy adaptation.  

BITES AND TMJ DISORDERS

Provocation studies provide strong evidence that bite features can have a causal role in TMJ disorders. Symptoms have been produced experimentally by adding high fillings (bite interferences) to centric stops,16-20 working side excursions,21-23  and balancing side contacts.24-31 In one subject, an experimental temporary bite interference only .25 mm tall caused symptoms that persisted for nine months until they were treated with a bite plate.32  It's reasonable to expect the bite to affect TMJ health, because it determines the location of the condyles when the mandible is braced and throughout its functional range of motion; and the location of the braced (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 their primary exercise template.  In other parts of the body, the physical features of the template against which muscles exercise affects the health of those muscles, and the jaw muscles have been shown to react almost immediately to even minute changes in the contours of their exercise template.33-38 

However, researchers have been unable to find a connection between TMJ disorders and bites.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 most bite parameters show no correlation with any functional condition.41-42  As a result of this failure to correlate, some researchers have concluded that the bite plays no significant role in TMJ disorders and therefore that evidence based treatment provides no justification for bite treatment. However, lack of evidence of a correlation is not evidence of lack of a correlation. It may be that we just don't know enough about bites or TMJ disorders to demonstrate the correlation between them.  

Indeed there is good evidence to support that explanation.  The parameters that we use to compare and contrast 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 chewing ability 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 is an uncontrolled variable.  Studies that attempt to evaluate the effect of altering bite parameters yield inconsistent results, because they are probably helping some people and hurting 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 measurable bite parameter that appears to have 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. Yet all these materials that must be interposed between the teeth are much too thick to give 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 teeth to hit and the subsequent contacts.

A third problem is the variability of mandibular closing trajectories.  The order of bite contacts at the termination of any closure of steeply intercuspated teeth 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 don't fully understand how natural bites function, they need techniques for managing bite problems and reconstructions in clinical practice.  The techniques that are currently used and the conceptual models that have been built to rationalize them are described below:  

CENTRIC RELATION 

Centric relation (CR), which is still 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 closing trajectory, the dentures remain stable during chewing and swallowing.  Later, when dentists needed to 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.  Centric relation was embraced by dentists and dental labs.  It seemed to work clinically, and it provided a consistent reference point for comparing different bites and changes to bites.

CR was embraced by the dental industry and its academia.  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 bracing 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 pull the mandible away from CR (a CR slide) to protect the teeth that interfered with access of the mandible to CR. 

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.  Some dentists performed full mouth rehabilitation on otherwise healthy patients just to create CR bites.  

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  Dentists promoted the belief that the ideal mandibular opening and closing trajectory was a pure hinge axis rotation like a hinge articulator, and each closing should terminate at 138 simultaneous tripodized bite contacts.  Researchers measured CR centric slides in .1 mm increments and tried to correlate them with TMJ disorders. 

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.  Grinding CR closure into a normal bite recreates Posselt's famous illustration of the envelope of mandibular movement, on the left side below, to fit CR theory, on the right side below.  Superimposing the two illustrations would see the apex at CRO created by grinding in CR.

FIGURE 1   -  REDRAWING THE ENVELOPE OF MANDIBULAR MOVEMENT     

                          POSSELT                                DAWSON

CCdawson posselt lowres.jpeg

Elaborate conceptual frameworks were concocted to explain why all other types of bites were unhealthy.  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 that muscle to pull the disk off the condyle, although only a small portion of that muscle is actually attached to the disk. 

These hypotheses were combined to produce an explanatory model of TMJ disorders that is still widely accepted today, even though it is completely fictional. A recent article summarized, “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

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 Anatomical 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 a mechanical abstraction; because, even in CR, the condyles do not operate like hinges.  All natural jaw movements combine 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 these centric slides 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". Okeson blamed the anterior shifting of the condyles in CR on pathological elongation of the temporomandibular ligaments. 57  Many researchers blamed lateral shifting of the condyles in CR on a pathology they named an "immediate side shift", which varies in length from 0 to 3 mm, yet it 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, some have redefined CR as a superior or superior-anterior condylar position instead of a posterior or supero-posterior one, and some advocate freedom in centric - either a long centric or a wide centric.   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 modern adults have a dislocated disk in at least one TMJ. Most authorities no longer recommend changing a functional and asymptomatic bite to fit CR theory.  Okeson simply advocates for a musculoskeletally stable mandibular position.

The repeatability of CR makes it convenient, but that does not make it a healthy treatment position. 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 become 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 used to limit jaw closing to one posteriormost opening and closing trajectory, but 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 borders 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 bite position.  

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 central mandibular bracing platform in all people.

CANINE GUIDANCE

For clinical work, dentists also need to choose mandibular pathways in and out of that central bracing platform.  Cusps that are too steep can collide.  Cusps that are too flat can prevent the cutting actions that are needed for effective chewing.   

In the 1960's, a researcher named D'Amico studied the skeletal remains of a 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.  He mistakenly concluded that this change in their bites was pathological.  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 in these tribes could be prevented by more overlap of their canines with their long roots, because "nature intended the canines to protect the posterior teeth by guiding the mandible into CR".  

Actually the changes in facial form that D'Amico saw as pathological were the natural results of mechanisms designed to compensate for wear, including a continual dento-alveolar eruption force of at least a few grams and an adult facial growth pattern that continually moves the lower dentition up and forward into the upper dentition just far enough to supply as much tooth structure as needed for the bite table to remain steady despite wear.79-84 In tribal people, face height generally maintained its proportion to body height throughout life.  To D'Amico, their faces seemed short.

D'Amico 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."   He advocated employing that reflex protective mechanism to reduce jaw muscle forces by increasing the steepness of the canine guidance to diminish tooth wear, because he had perceived excessive jaw muscle forces to be the problem that needed correcting in his Indian tribe. 

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.85-86  Thus canine guidance reduced functional jaw muscle forces, which the researchers took to be a justification for using canine guidance, because they believed that TMJ disorders were due to excessive jaw muscle forces.  However, the researchers were looking at the wrong muscle forces.  The problem in TMJ disorders is excessive jaw muscle resting forces, not excessive functional jaw muscle forces; and canine guidance only reduces jaw muscle functional forces.87

Steepening canine guidance shuts down functional masseter activity by triggering neuromuscular reflexes that are designed to protect the TMJs.  In apes, lateral movements of the mandible during chewing can thrust the molars laterally to 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 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 mandible posteriorly and thereby activate the posterior temporalis muscles earlier in the chewing cycle to pull it away from the canine contact.  In addition, while steepening canine guidance narrows the mandibular range of motion, there is good evidence that most people would be better served by a wider range of motion. 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. They are designed to work together with the other teeth to provide stable support for the mandible throughout its normal range of motion.

ANTERIOR GUIDANCE

The canine guidance concept was extended to include the anterior (front) teeth, because anterior guidance (unlike canine guidance) is found in all natural dentitions.  Insufficient anterior guidance is ICD 10 code M26.54.

MUTUAL PROTECTION

Combining CR with steep anterior and canine guidance led to an occlusal philosophy known as mutual protection, based on the belief that teeth should only receive forces axially (straight downward into their sockets).  The steep anterior and canine guidance protect the back teeth by preventing them from enduring all horizontal vectors of force, and stable CR contacts on the back teeth protect the front teeth from the powerful jaw closing forces produced during bracing.  Labwork is facilitated; because the back teeth just need to provide stable stops in one position and do not also require precise cusp and fossa interdigitation during gliding contacts, and the front teeth can be designed for esthetics without also requiring enough stability to provide an incisal bracing platform. 

BIOESTHETICS 

Some dentists took these concepts of mutual protection, centric relation, and canine and anterior guidance to their extremes in a bite philosophy that appeals to people who want to look younger by rebuilding all their teeth to their original unworn shapes, including CR contacts on the front teeth.  The proponents of bioesthetics claim that wear and nocturnal bruxism are pathologies that result from the bite being "out of balance", and these pathologies can be prevented by restoring balance to the bite. The clinical practice of bioesthetics usually involves increasing the steepness of the anterior and canine guidance.  

However, the foundational beliefs of bioesthetics also have no scientific basis. Nocturnal bruxism is a normal sleep behavior, usually associated with microarousals following increased sympathetic activity, 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 In fact, some tooth wear is probably normal and desireable.  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 provide a constant supply of ridges that helped to grate food and edges that cut food - not to maintain a continuous protective layer on teeth or limit the range of motion of the mandible.115. The teeth protect each other by sharing the loads they encounter in whatever direction the mandible moves.

Also, in all natural dentitions, teeth do not just receive forces axially - they have a healthy natural range of movement that helps keep them 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 a normal 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 narrow spaces lining the roots and into venous circulation, then release of the compression allows new blood to flow back into that area of 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.  Also like in synovial joints, alternating compression and release affects one area at a time; therefore a healthy functional range of motion for a tooth within its socket requires sufficient variability, including a vertical (axial) component, a transverse (bucco-liongual) component, and even a mesio-distal component which functions as an interproximal joint between adjacent teeth, complete with interproximal contact areas shaped to function as interproximal articular surfaces.

GROUP FUNCTION

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 rest of the teeth formed a bite table, 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. Omnidirectional group function gave the dentition longevity by evenly distributing wear. The teeth wore in together, and they wore out together.  Despite the attempts of dentists to establish canine guidance as the dominant occlusal scheme and their belief that canine guidance is natural and proper, most natural bites still operate in group function.123 

The trouble with group function is that it has been difficult to create prosthodontically with existing technology. 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 bite surfaces prosthodontically. 

NEUROMUSCULAR DENTISTRY

The "neuromuscular" bite philosophy is generally been posited as the alternative to CR, although it also has no scientific basis.  While CR and anterior and canine guidance techniques almost always shift the mandibular bracing position backward, "neuromuscular" techniques almost always shift the mandibular bracing position forward.  

Neuromuscular dentistry began in 1969 when a well know and respected researcher, Dr. Barney Jankelson, thought he had discovered a new way to locate and record CR by 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 the 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 advocated using the system to treat TMJ disorders.  When Dr. Jankelson was near the end of this life, the ADA awarded his equipment its seal of acceptance.  

Soon afterwards, scientific research undermined all the assumptions on which neuromuscular dentistry was based.  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 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 One study found that the myotronics diagnostic package was unable to even distinguish between TMJ disorder patients and "normals".129 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 pain which had been triggering muscle tightening.131-133   Applying TENS over the cheeks usually causes the mandible to shift anteriorly, because the muscles closest to the source are the superficial masseters, which are oriented in a more forward direction than the other elevator muscles. Treatment that brings the mandible anteriorly often provides relief of symptoms, because most TMJ disorders are caused by longstanding retrusion of the mandible, not because TENS has some special ability to relax the jaw muscles.  

Freed from all regulations, the company has become so successful at marketing that most dentists now believe that TENS relaxes the jaw muscles, although TENS is used in medicine for pain relief and not for muscle relaxation.  Today "neuromuscular dentistry" is being promoted to create a resinous "myoaligner" bite surface that is cemented over the back teeth, and then must be followed by new crowns that recreate biting surfaces engineered to fit the position determined by the non-diagnostic equipment. 

CONDYLAR POSITION ON X-RAY

There have also been attempts to determine the optimal mandibular bracing location by the radiographic positions of the condyles in the glenoid fossae in transcranial X-rays, but that parameter turns out to be much too variable to be useful clinically.142-143 Even in patients with unilateral disk disorders, 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 for evaluating condyle position, because the glenoid fossae are not inert frameworks.  They are attached to the condyles in many ways, 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 have generally been unsuccessful.146-148

OCCLUSAL SOLUTION

The most consistent and physiologically healthy mandibular closing trajectory occurs during swallowing.  Studies have indicated that swallowing reflexively recruits all of the jaw closing muscles in a way that appears less adaptive to bite interferences than the normal voluntary closure trajectory.  However, there is still natural variation in the mandibular closing trajectory 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 jaw muscles have been deprogrammed while tipping the head into different postural positions, and then integrating all this information digitally to mill or mold a platform that provides orthopedic support for the working side of the mandible throughout its functional range of motion. A proper orthopedic platform could also be generated functionally in acrylic or some other recording material.  

OCCLUSAL CONCLUSION

For almost 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 define a functional range of motion anteriorly and laterally.  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 single central bracing position does not even resemble natural jaw movement pathways, and it does not recognize the important role that jaw muscle exercise plays in the physiology and natural orthopedic function of the mandible.  

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.

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

  2. 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.

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

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

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

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

  7. 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.

  8. 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.

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

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

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

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

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

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

  15. 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.

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

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

  18. 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.

  19. 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.

  20. 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.

  21. 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.

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

  23. 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.

  24. 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.

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

  26. 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.

  27. 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.

  28. 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.

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

  30. 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.

  31. 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.

  32. 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.

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

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

  35. 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.

  36. 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.

  37. 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.

  38. 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.  

  39. 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.

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

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

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

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

  44. 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.

  45. 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.

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

  47. 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.

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

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

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

  51. 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.

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

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

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

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

  56. 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.

  57. 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).

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

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

  60. 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.

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

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

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

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

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

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

  67. 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.

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

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

  70. 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.

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

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

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

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

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

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

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

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

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

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

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

  82. 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.

  83. 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.

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

  85. 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.

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

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

  88. 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.

  89. 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.

  90. 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.

  91. 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.

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

  93. 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.

  94. 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.

  95. 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.

  96. 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.

  97. 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-  

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

  99. 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.

  100. 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.

  101. 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.

  102. American Academy of Sleep Medicine: International Classification of Sleep Diosorders, ed. 3. Darien IL: American Academy of Sleep Medicine, 2014. 
  103. 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.

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

  105. 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. 

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

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

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

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

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

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

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

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

  114. 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.

  115. 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.

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

  117. 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.  

  118. 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. 

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

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

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

  122. 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.

  123. 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.

  124. 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.

  125. 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.

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

  127. 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.

  128. 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.

  129. 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.

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

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

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

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

  134. 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.

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

  136. 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.

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

  138. 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.

  139. 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.

  140. 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.

  141. 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.

  142. 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.

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

  144. 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.

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