Occlusion: Current Concepts



Dentists manage occlusions using clinical techniques that usually provide acceptable results for reasons we have never understood. Most of the clinical research on occlusion has been focused on locating one mandibular position at which all the posterior teeth contact simultaneously. However the techniques for locating that position attained popularity because of convenience and marketability rather than anatomical or physiologic considerations, and the occlusal ideals to which they aspire are never found in pre-industrial dentitions – even those with minimal occlusal wear. While unworn teeth can be made to interdigitate in a way that defines a precise spatial position, the occlusions of all mammals are designed to have some play or transverse movement (freedom in centric) in the bracing (intercuspal) area of the occlusal table. In the average modern human masticatory system, it is certainly smaller than it was in our pre-industrial ancestors, but there is no good reason to expect it to be zero.


The conceptual frameworks by which dentists evaluate occlusions grew out of techniques for setting denture teeth and observations of newly erupted teeth rather than any understanding of natural occlusal function. In fact, our conceptual frameworks for understanding occlusion provide so little guidance for effectively managing occlusion in clinical practice that most dental authorities consider any occlusal treatment to be an invasive procedure which should only be used as a last resort because it is irreversible, in spite of the fact that we can easily replace very small amounts of tooth structure with adhesive bonding of resin, metal, or porcelain.

Sometimes the clinical techniques based on our conceptual frameworks just do not work. Patients who have become uncomfortable with the feel of their occlusion following dental work and remain uncomfortable despite occlusal adjustment according to accepted standards may become “fixated” on their occlusion and develop a condition known as occlusal disease, occlusal neurosis, occlusal dysesthesia,1 occlusal hyperawareness, positive occlusal sense, body dysmorphic disorder, somatoform disorder, monosymptomatic hypochondriacal psychosis,2 or phantom bite3. Studies of this condition have found that it is not associated with any recognized occlusal parameters, anatomical features, or 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,9 seratonin-norepinephrine reuptake inhibitors,9,11-12 monozide (anti-psychotic),13 mirtazapine (noradrenergic and specific serotoninergic antidepressant),9 and aripripazole (a dopamine partial agonist).9

In research, occlusion is an uncontrolled variable; because our inability to categorize different types of occlusions according to their functional features makes it impossible to control for their effects. When any occlusal change accompanies an experimental treatment, it may be improving masticatory system function in some subjects and impeding it in others.

In clinical work, occlusion is treated as an uncontrollable variable, because there is an assumption that each patient's existing occlusion may be a critical feature which must be carefully preserved and that changing it even a small amount may cause it to become lost and difficult or impossible to find again. Altering an occlusion has been described as "sailing into uncharted waters." Dentists are so reluctant to change an occlusion that successful phase one disk recapturing procedures using oral orthopedic appliances are usually followed by an attempt to return to the pre-treatment occlusion, even though that process is almost certain to result in recurrence of the disk displacement and likely to result in recurrence of symptoms, which are then managed with physical therapy, home care, medications, and cognitive behavioral therapy.


It is difficult to prosthodontically reproduce numerous occlusal contacts that occur as precisely and simultaneously as they do in well established natural healthy functional masticatory systems; but the problem with occlusal change is not the lack of precision that can be achieved.  Normal healthy teeth have a mobility of 50 - 100 microns,14-15 and they can adaptively shift position by hundreds of microns overnight to accomodate occlusal forces. Within that margin of error, we can create any occlusal interface desired.  

The barrier to using occlusal change therapeutically is our inability to predict the effects of altering an occlusion 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 conditions are needed to promote healthy adaptation.

Provocation studies provide strong evidence that occlusal features can have a causal role in TMJ disorders. Symptoms can be produced by adding high fillings (occlusal interferences) to centric stops,16-20 working side excursions,21-23  or balancing side contacts.24-31 In one subject, an occlusal interference only .25 mm tall caused symptoms that persisted after it was removed for nine months until they were treated with a bite plate.32   

It's also reasonable to expect the occlusion to affect TMJ health, because it determines the location of the condyles when the mandible is braced and throughout its functional range of motion.  In other synovial joints, the location of the braced (close packed) position and the functional range of motion of the articulating bones affects health.  

It's also reasonable to expect the occlusion 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, in spite of these good reasons to expect a connection between TMJ disorders and occlusion, researchers have been unable to find one.39-40 A few occlusal parameters (deep overbite, anterior openbite, loss of posterior support, and unilateral cross-bite) show weak correlations with TMJ disorders at extreme values; but most occlusal parameters show no correlation with any functional condition.41-42  As a result of this failure to correlate, some researchers have concluded that occlusion plays no significant role in TMJ disorders and therefore that evidence based treatment provides no justification for occlusal treatment. Other researchers have pointed out that lack of evidence of an association is not evidence of lack of an association. It may be that we just don't know enough about dental occlusion or TMJ disorders to demonstrate the association between them.  Indeed there is good evidence to support that explanation.

One major flaw in all our studies of occlusion is that we cannot even measure functional aspects of occlusion. The parameters that we use to compare and contrast different occlusions include static measurements of spatial relationships between maxillary and mandibular 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. Even balancing side interferences are correlated with TMJ disorder symptoms in some studies,43-44 and not in others.45-47 For decades we have known that some people with chronic TMJ disorder symptoms and difficulty chewing have textbook perfect occlusions and ideal occlusal parameters, while other people with very irregular occlusions and extreme occlusal parameters have excellent masticatory system health and function.


The only occlusal parameter that appears to have functional relevance is stability.48  On average, people with TMJ disorders have less occlusal stability than normals.49  However it's been difficult to even demonstrate that relationship, because our techniques for measuring occlusal stability are so crude compared with the sensitivity of the system.  There are three problems with our current techniques for measuring occlusal stability.  

One problem is the thickness of the measuring device.  Occlusal stability is measured as the ability to evenly distribute biting pressure on a 100 micron thick electronic wafer  (Tek Scan) or a slightly thinner and less sensitive plastic sheet (Prescale Occluzer System), to mark occlusal surfaces with 20 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 occlusal marking device is at least twice that thick, and most are several times that thick.

A second problem is tooth mobility. Teeth are so delicately suspended at rest that they move easily from that rest position over distances that have significant implications for occlusion. Increasing the bite force increases the number of occlusal contacts by displacing prematurely contacting teeth.53  Occlusal marking devices cannot distinguish between the initial contacts and subsequent contacts that occur only after the initially contacting teeth have shifted.

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

As a result of these problems, our clinical tools are better suited for optimizing the distribution of chewing forces than creating stable mandibular bracing contacts. Widespread distribution of chewing forces protects the teeth when masticating a thin resistant bolus, but bracing is central to masticatory system health and function. The most accurate way to assess the stability of bracing contacts is still the sharpness of the sound they make.  


Despite our inability to measure functional aspects of occlusion, dentists need techniques for managing occlusal problems and reconstructions in clinical practice. Unfortunately, instead of deducing techniques from a plausible conceptual model, we have built conceptual models to provide rationalization for techniques that were either discovered to facilitate laboratory work or developed to market products. The only technique deduced from a conceptual model (condylar concentricity) is not useful clinically. These techniques and philosophies are described below:  


Centric relation (CR) is an occlusal philosophy built around the use of mechanical articulators to set denture teeth. CR was first discovered nearly a century ago when 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. The position of the mandible at that posterior-most location became known as CR. Within a few decades, dentists found that making crowns and bridges occlude in CR also yields successful clinical results. Teeth do not fracture, and the periodontium does not break down. CR dentistry became widely accepted.

As dentistry became more precise, CR became more narrowly defined. Dawson described it 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  Initial opening from that point was thought to be a pure hinge axis rotation. Hinge axis closing was expected to terminate at 138 simultaneous pinpoint occlusal contacts in CR.

A dental occlusion in which all the teeth contact simultaneously in CR became known as centric relation occlusion (CRO), and many dentists considered that to be the only proper occlusion. People who sometimes use a more anterior 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 or dual bite. People who could not achieve CRO were thought to have a malocclusion characterized by CR interferences that caused the mandible to slide (centric slide) anteriorly or antero-laterally from CR into maximal intercuspation (MI). Researchers measured centric slides in 1/10 mm increments and tried to correlate them with TMJ disorders.

Dawson redrew Posselt's famous illustration of the envelope of mandibular movement to make it fit CR theory, as shown in figure 1. The centric slide (MI-CR) was removed from the illustration on the left below by extending the CR arc superiorly until it intersects the occlusal plane, much like centric slides are removed clinically by grinding away all occlusal contacts which had been interfering with a superior extension of the hinge axis closure.



                          POSSELT                                DAWSON

CCdawson posselt lowres.jpeg




CR philosophy spread to other fields of dentistry. Periodontists removed centric interferences to diminish tooth mobility. TMJ specialists designed nightguards and splints to provide stable contacts in CR. Orthodontists retruded the maxillary arch to fit closely around the mandibular arch in CR. Dawson claimed that there is hardly any aspect of clinical dentistry that is not adversely affected by a disharmony between MI and CR. 

Elaborate conceptual frameworks were concocted to explain the importance of CR. Dawson claimed that CR is the only mandibular position which is stable because it is braced by bone, and therefore 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 Many researchers hypothesized that the jaw muscle pain in TMJ disorders is caused by spasm or hyperactivity of the superior lateral pterygoid muscles in response to centric interferences.  Some went on to hypothesize that superior lateral pterygoid muscle hyperactivity pulls TMJ articular disks antero-medially off the condyle and thereby cause disk displacements. Medical illustrations were drawn with the entire superior lateral pterygoid muscle attached directly to the front edge of the disk.

These hypotheses were combined to produce an explanatory model of TMJ disorders that is still widely accepted today. 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

The conceptual frameworks that had been built around CR had to be modified to explain why many people with perfectly healthy masticatory systems lack the characteristics of an ideal or even a good occlusion according to CR theory. Dawson claimed that they have an "adaptive centric posture", which occurs when "deformed TMJs have adapted to a degree that they can comfortably accept firm loading". Okeson claimed that the ability of many condyles to shift anteriorly from CR without also moving inferiorly was due to pathological elongation of the temporomandibular ligaments. 57  Other researchers claimed that the ability of many condyles to shift laterally from CR without also moving inferiorly was due to "immediate side shift", and they looked in vain for pathological processes that could cause it.58 Studies found that it varies in length from 0 to 3 mm, yet it appears to have no clinical significance.59   

Although CR can serve as a useful anatomical landmark to denote the posterior border position of the mandible, research was never able to support using CR as a treatment position. It is not even a normal functional mandibular position for most people. 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 the condyles combine rotation and translation in all natural jaw movements. 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 75% to 80% 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 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.

It seems unlikely that a symmetrical and well supported centric slide is pathological.  Centric slides were present 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 anyway.77

Recently, as a result of the problems sometimes associated with the clinical application of CR, supporters of CR have modified their positions.  Most have stopped pushing the mandible so far posteriorly, 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.  Okeson advocates for a musculoskeletally stable mandibular position. 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 occlusion to fit CR theory.

The repeatability of CR makes it convenient, but that does not make it the ideal mandibular bracing 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. The fact that they can be used to locate a consistently repeatable mandibular closing trajectory braced against the temporal bone is not reason to think that such a closing trajectory leads directly to an ideal or even a functional mandibular bracing position.  Joints need a range of motion that ensures adequate circulation to all areas of their articular surfaces, and it's difficult to envision how confining the mandibular range of motion to pathways directly into and out of 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 anterior from CR, but even that varies too much to provide a guide for choosing a mandibular bracing position.  

CR works well in many clinical situations, because it 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 anterior mandibular position where elevator forces are lower.  If a facial pain condition is due to frequent activation of neuromuscular reflexes protecting a hypersensitive posterior tooth from occlusal trauma, eliminating a CR interference on that tooth can relieve the symptoms by also eliminating the occlusal contacts that occur on that tooth when the mandible is power-crushing mode, which occurs very close to CR. Also centric interferences are frequently balancing side interferences on the palatal cusps of the terminal maxillary molars, and eliminating balancing side intereferences can often provide rapid relief of symptoms. However, the success of CR dentistry in sometimes eliminating dental and muscular symptoms is certainly not an indication that CR is a healthy or desireable location for mandibular bracing.


For clinical work, in addition to a bracing platform, dentists also need to choose mandibular pathways in and out of that platform.  Cusps that are too steep can collide.  Cusps that are too flat can diminish masticatory effectiveness.  Canine guidance is an occlusal philosophy that was built largely on top of CR philosophy and has merged with it.

In the 1960's, a researcher named D'Amico studied the skeletal remains of American Indians and saw that they lose their overbite and overjet to acquire end to end occlusion as their teeth wear down with age.78 He mistakenly concluded that this change of occlusion was an adverse consequence of loss of vertical dimension caused by occlusal wear.  Actually our pre-industrial ancestors maintained a relatively constant vertical dimension and facial height during adulthood because of mechanisms designed to compensate for occlusal wear.79-85  These mechanisms included a continual dento-alveolar eruption force that we can measure but not explain and a continual adult facial growth pattern that was designed to maintain a continual supply of tooth structure at the occlusal table by continually moving the roots of the mandibular dentition further toward the maxillary dentition.

D'Amico then hypothesized that occlusal wear and loss of face height in these Indian tribes could have been prevented by overlap of their canines.  He claimed that the canines are uniquely suited for withstanding lateral forces because of their long roots, dense surrounding bone, and distance from the center of force of the elevator muscles.  He went on to preach that "nature intended" the canines to protect the posterior teeth by guiding the mandible into CR.  His reason for concluding that canine guidance must be the normal state of a healthy natural dentition 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."  Although the rationale was unsupportable, canine guidance became widely accepted.  

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."   He promoted canine guidance to diminish the rate of occlusal wear, which he saw as the problem.

Later other researchers used EMG to quantify the drop in functional jaw muscle forces that results from canine contacts during lateral excursions.86-87  They found that, in group function, both the ipsilateral temporalis and the masseter fired; but, in canine guidance, only the ipsilateral temporalis fired. They promoted canine guidance to diminish jaw muscle activity, which they saw as the problem because it was generally assumed at that time that TMJ disorders were due to jaw muscle hyperactivity and therefore that any reduction in jaw muscle activity would be helpful.

However, these early researchers were all targeting the wrong jaw muscle activity.  It is resting jaw muscle forces, not functional jaw muscle forces, that are too high in TMJ disorder patients.88 People with TMJ disorders generally have weaker jaw muscles than people without TMJ disorders,89-96 and therefore they should benefit from treatments that strengthen, not weaken, the jaw muscles. Canine guidance reduces jaw muscle functional forces, not resting forces, which are controlled by more central mechanisms.

Steepening canine guidance probably shuts down functional masseter activity by triggering neuromuscular reflexes that protect the TMJs.  In apes, lateral excursions of the mandible can pivot around a canine stop and thrust the molars laterally to produce a powerful grinding action, while the contact between the distal surface of the lower canine and the mesial surface of the upper canine protects the mandible from retrusive forces, even at rest. Hominid canines withdrew into the occlusal table to increase adaptability by allowing a mandibular range of motion to develop in any direction. In modern humans, canine contacts between the mesial surfaces of the lowers and the distal surfaces of the uppers can thrust condyles posteriorly and laterally, where TMJ disorder patients most frequently show bruising.97-100 

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. Muscles generally benefit from more freedom of motion. In studies where jaw muscles are rehabilitated and occlusions are stabilized, the functional mandibular range of motion naturally widens.101-103 Steepening canine guidance narrows the mandibular range of motion, which can diminish masticatory efficiency by activating the posterior temporalis muscles earlier in the chewing cycle to pull the mandible away from the anterior stop, which can lead to overlapping firings of jaw opening and closing muscles.

When necessary, the forces used in nocturnal bruxism can be specifically targeted and significantly reduced by simply wearing a removeable oral appliance that prevents all posterior tooth contacts during sleep. Without the positive feedback provided by stable bilateral posterior occlusal contacts, the jaw muscles are unable to exert most of their strength. If the appliance eliminates all posterior tooth contacts by means of an anterior flat plate, it can also improve jaw muscle health by widening a restricted mandibular range of motion every night.

The canines provide important contributions to the anchorage of natural dentitions and mandibular support during antero-lateral excursions.  However they are not fundamentally different from the other teeth in their role in dental occlusion,104 and they are not specially designed to remove all horizontal forces from the posterior teeth.  


The canine guidance concept was extended to include the anterior teeth.  Natural dentitions have eventual (rather than immediate) anterior guidance anyway, and steepening it should help remove horizontal forces from the posterior teeth according to the same rationale that was being used to promote steeper canine guidance.  Insufficient anterior guidance is ICD 10 code M26.54.


Combining CR with steep anterior and canine guidance led to an occlusal philosophy known as mutual protection - the posterior teeth protect the anterior teeth by providing stable CR contacts that prevent the most powerful mandibular elevator forces from impacting the anterior teeth, and the anterior teeth protect the posterior teeth from laterally directed forces by separating them when the mandible moves away from CR. Mutual protection provides a conceptual framework that facilitates prosthodontic reconstruction of both anterior and posterior teeth.  Posterior occlusal surfaces just need to provide multiple simultaneous centric stops and do not also require precise cusp and fossa interdigitation during gliding contacts.  Anterior occlusal surfaces can focus on esthetics and do not also require enough stability to function as an incisal bracing platform. Mutual protection has been widely embraced by dentists and dental laboratories.


A few dentists extrapolated the concepts of canine and anterior guidance to their logical extreme, speculating that they should be steep enough to protect the posterior teeth from all lateral forces. They advocate for immediate disclusion - guidance that separates all the posterior teeth as soon as the mandible moves away from CR.105 They treat TMJ and myofascial pain disorders with Disclusion Time Reduction (DTR),106 and they promote an electronic bite pressure measuring device (T-scan), which happens to be the only device that can measure disclusion times. However, immediate disclusion is never found in natural dentitions, and there is no good evidence that short disclusion times are healthy or even any reason to think that they might be desireable.


Dr. Robert Lee extended these previous occlusal philosophies to create a new occlusal philosophy he called bioesthetics. He proposed that, in addition to CR and immediate disclusion, dentists should reconstruct the teeth to their original unworn shapes and also include CR contacts on the anterior teeth.  He claimed that occlusal wear and nocturnal bruxism are pathologies that result from the masticatory system being "out of balance", and they can be prevented by restoring balance to the occlusion. In practice his technique usually involves increasing the steepness of the anterior and canine guidance.  

However, Lee's hypothesis about the role of occlusion in nocturnal bruxism has no basis. Research has shown that nocturnal bruxism is a sleep behavior, usually associated with microarousals following increased sympathetic activity, and it reflects no particular occlusal condition. It cannot be caused by occlusal factors or eliminated by occlusal treatment.107-108  Bruxism is a physiological behavior that is common to nearly all mammalian species.

Lee's hypothesis that even small amounts of occlusal wear are pathological also has no basis. Researchers have found no significant correlation between occlusal wear, bruxism, or attrition, and TMJ disorders.109-113 In most mammals, bruxism is actually a tooth sharpening behavior that is necessary to keep the dentition functional.114 Most species do not even achieve effective mastication until occlusal wear has reduced the complex arrangement of cusps and fossae that cover the occlusal 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. In pre-industrial humans as well, occlusal attrition is a physiologic rather than a pathologic behavior.

Our unworn enamel covered occlusal contours were designed to align the dental arches and then provide a constant supply of working surface at the occlusal table - not to maintain a continuous layer of enamel on the occlusal surfaces or to determine the lifelong exercise template for the masticatory system.115 In designing our teeth, evolution took advantage of the differential wear rates between enamel and dentin by combining these materials in tooth shapes that get converted by occlusal wear into effective working surfaces. For example, the slower wearing vertical slopes of enamel that surround the cusp tips leave protruding ridges and rings that function like graters in the middle of the occlusal surfaces while sharp bucco-occlusal and linguo-occlusal line angles function like blades to cut food at the edges of the occlusal table.

The human masticatory system was designed to accommodate all different rates of wear. Depending on age, diet, techniques of food preparation and the extent to which the teeth are used as tools, the degree of wear can vary from barely perceptible to so extensive that little or nothing remains of the original crowns, and the molars and premolars function as separate roots, each with its own occlusal surface and interproximal contact areas with adjacent roots. In minimal wear, multiple small facets can also masticate effectively, whether or not they extend into dentin. However, even in the absence of wear, functional natural dentitions do not demonstrate CR contacts on anterior teeth.

Thus bioesthetic dentistry is not biologic - it is esthetic dentistry for people who want a youthful looking dentition. The continuous layer of enamel that covers the occlusal surfaces of newly erupting teeth does not necessarily need restoration if portions of it wear away.  Caries occurs where food gets trapped or plaque accumulates, whether the tooth surface there is covered by dentin or enamel.  Occlusal wear is only problematic when it occurs rapidly enough to cause pulpal sensitivity or prevent the teeth from lasting a lifetime.


The idea that posterior teeth should only receive forces that are directed straight axially is also not plausible biologically, because all joints, including the dento-alveolar (periodontal) joints, 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 metabolically hyperactive periodontal ligament (PDL) spaces 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 its PDL space and into venous circulation, then release of the compression allows new blood to flow back into the PDL space 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 requires sufficient variability to supply the whole joint space.  The PDL spaces were designed to benefit from a range of motion with a transverse component that includes some lateral forces on all teeth.  Interproximal facets in dentitions with significant interproximal wear show that each tooth's normal range of motion includes mesio-distal movements as well as bucco-lingual ones.


Group function, not anterior and canine guidance or CRO, is the natural state of the dental occlusion in almost all mammals, including humans.122 Until the industrialization of our diet in the last couple of centuries, anterior and canine guidance were only present temporarily in some newly erupted dentitions, but they never persisted for long. Their chief function was to provide enough early coupling between the diverse growth patterns in the maxilla and the mandible to approximate the dental arches in a sagittal plane. Once normal functional mandibular movement and facial growth patterns were established, the anterior and canine teeth did not restrict or "guide" mandibular movements but cooperated with the neighboring teeth to provide a stable bracing platform for the mandible when it moved anteriorly or antero-laterally. Omnidirectional group function gave the dentition longevity by evenly distributing occlusal wear. The teeth all worked together, and they all wore out together.

In most modern humans, group function is still present to some degree.123 While it is no longer commonly needed to ensure longevity of the dentition, it is still an effective way to evenly distribute the forces of nocturnal bruxism in a manner that protects individual teeth.

The trouble with group function is that it is difficult to produce prosthodontically. Even if a mandibular movement simulator could accurately recreate the complex functional micro-movements of the mandible on the occlusal table, it still could not take into account the independent movements of teeth within their sockets, the bending of the mandible, the compression and release of the circum-maxillary sutures, and other variables that can alter occlusal contacts. Therefore, creating good group function prosthodontically still requires dynamic bite registration techniques and intraoral occlusal adjustment.


While CR and anterior and canine guidance techniques almost always shift the mandibular bracing position posteriorly, "neuromuscular" techniques almost always shift the mandibular bracing position anteriorly. If the cause of most jaw muscle and TMJ disorders is the mandible being forced anteriorly by CR interferences, as still taught in most dental schools, neuromuscular dentistry should consistently exacerbate those disorders by creating CR interferences, but such problems only happen occasionally.   

Neuromuscular dentistry was an occlusal philosophy built around marketing a diagnostic package and TMJ disorder treatment based on those diagnostic findings. It began in 1969 when Dr. Barney Jankelson pointed out that, because CR is based solely on the mechanical fit between the mandible and the skull, it ignores any role for nerves or muscles.  He introduced a theory that placing a pulsing TENS (transcutaneous electrical nerve stimulation) source directly over the motor root of the trigeminal nerve fires all the mandibular elevator muscles evenly, keeping it there for a period of time can relax all the muscles and locate the ideal mandibular resting position (characterized by minimal resting EMG activity), and then increasing the amplitude of the TENS can close the mandible from the ideal mandibular resting position directly into the ideal mandibular bracing position - 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. When Dr. Jankelson was near the end of this life, the ADA awarded his equipment its seal of recognition and later its seal of acceptance.  

Soon afterwards, scientific research undermined all the assumptions on which neuromuscular dentistry was based.  Researchers showed that the mandibular posture that produces the lowest jaw muscle resting activity is located too far inferiorly to serve as a rest position.123  They also showed that small changes in the location of the EMG electrodes caused significant differences in the results – making any longitudinal monitoring useless.124-125 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.126-127 One study found that the myotronics diagnostic package was unable to even distinguish between TMJ disorder patients and "normals".128

TENS is used in medicine to provide pain relief, not muscle relaxation,129 and there is no good evidence that it actually relaxes jaw muscles.130-132  Any relaxation of the jaw muscles brought about by TENS treatment would be most likely a secondary effect of diminishing the pain, because anything that diminishes pain relaxes muscles. 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 many TMJ disorders are caused by longstanding retrusion of the mandible, not because TENS has some special ability to relax the jaw muscles.


The only attempt at deriving a technique from an occlusal philosophy was positioning the condyles in the radiographic centers of the glenoid fossae. Initial studies indicated, and many dentists expected, that many TMJ disorder patients have nonconcentric and especially posteriorly located condyle positions.133-140 Later Harold Gelb developed a formula for more accurately locating the ideal condyle position on a grid placed over transcranial TMJ X-rays. His 4/7 condylar position is probably very close to ideal in the average patient, however large studies of both patients and normals show that the position of the condyle in the fossa is much too variable to provide a formula for locating the ideal mandibular bracing position in any individual patient.141-142 Even in patients with unilateral disk disorders, condyles were often displaced in unexpected directions and distances.143-144

Actually the position of the condyles relative to the glenoid fossae has little significance, because the glenoid fossa is not an inert framework that can serve as a reference point. It too relocates in response to functional forces.145 Also the position of a condyle relative to the glenoid fossa has inherent stability due to the tissues that bind them together. As a result, attempts to change condylar position in the fossa using full mouth reconstruction, equilibration, or orthodontics usually relapse.146-148


For almost a century, we have managed occlusions by trying to precisely locate one ideal mandibular bracing position, stabilize it with as many simultaneous tooth contacts as possible, and then surround it with chosen angles of anterior and lateral guidance that force all mandibular closing and bracing into that one position. That concept never had anatomical, physiological, or orthopedic justification. It is not an anatomical situation seen in any mammals, it does not recognize any role for occlusion in jaw muscle exercise physiology, and it does not recognize the natural orthopedic function of the mandible. We need new perspectives on dental occlusion.


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.

  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. Wilkinson T. Disk and lateral pterygoid muscle in TMJ. J Pros Dent. 1988.

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

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

  71. 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.

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

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

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

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

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

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

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

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

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

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

  82. Brace CL. Occlusion to the anthropological eye. The biology of occlusal development. Monograph. 1977;7:179-209.

  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. 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.

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

  106. 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. 

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

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

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

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

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

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

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

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

  115. 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.

  116. 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.

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

  118. 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.  

  119. 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. 

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

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

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

  123. 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.

  124. 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.

  125. 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.

  126. 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.

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

  128. 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.

  129. 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.

  130. 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.

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

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

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

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

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

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

  137. 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.

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

  139. 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.

  140. 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.

  141. 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.

  142. 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.

  143. 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.

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

  145. 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.

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

  1. Bakke M, Moller E, Thorsen NM. Occlusal control of temporalis and masseter activity during mastication. J Dent Res. 1982;81:257.