It sometimes seems like TMJ disorders can have many causes.  Often the symptoms are preceded by an event such as a blow to the head or face, whiplash, extreme mouth opening, a strenuous or traumatic chewing event, a long dental appointment, a period of excessive central nervous system stress, or hormonally mediated joint laxity.  Assuming that the event immediately preceding the onset of symptoms is the cause of the symptoms has led researchers to conclude that the cause of TMJ disorders must be multifactorial, and there are dozens of factors involved.  In addition to presumed microtraumatic incidents, joint laxity, and psychosocial factors; they include predisposing factors, initiating factors, and perpetuating factors.   

Actually, most of these factors are just triggers.  They may initiate symptoms, but they are not the underlying cause. Removing the trigger will not reverse the injury, because the overall cause of the symptoms is dysharmony among the components of the masticatory system.  In the history of medicine, multifactorial etiology theories have usually meant simply that we do not yet understand the underlying or ultimate cause.


In most TMJ disorders, the triggering event acts as the straw that broke the camel's back.  The ultimate cause of the dysharmony is a strained facial growth pattern that continues in adulthood to create mechanical strains between teeth, jawbones, and TMJs that fail to develop the goodness of fit normally found in other joints.  The role of facial growth in the genesis of TMJ disorders is explained extensively in chapters 3 and 4 of ETIOLOGY, and the role of adaptation is explained in chapter 5.

Fortunately, effective treatment of TMJ disorders usually rarely requires intervening to alter facial growth patterns (other than providing a stable occlusion which promotes healthy jaw muscle exercise), it just requires restoring harmony by eliminating the blend of triggering events, sustaining factors, and vicious self-perpetuating cycles that has been generating the symptoms.  The most common of these immediate causes and their roles in producing symptoms are described below: 


The vast majority of TMJ disorders begin with dislocation of the articular disk (also called disk displacement or internal derangement) in at least one TMJ and the subsequent bruising of the vascular retrodiskal tissues which were pulled into the joint space following the disk.  The loss of the disk from the articular zone deprives the involved TMJ of cushioning and lubrication, making it susceptible to damage by triggering events such as a minor trauma, a period of increased central nervous system stress, a long dental appointment, or destabilization of the bite.  When the disk is dislocated, even normal jaw function can damage the vulnerable retrodiskal tissues. Eventually these vulnerable retrodiskal tissues fibrose to create a pseudo-disk that can restore functional capacity, and the soft tissues of the articular eminence thicken to provide cushioning; but the internally deranged TMJ remains more vulnerable to injury than a normal TMJ.

The role of disk dislocation has been controversial, and opinions have swung like a pendulum, as they often do after new information is uncovered.  The new information was Farrar's discovery that most of the clicking and popping sounds heard in the TMJs of patients who suffer from TMJ disorder symptoms are due to dislocated articular disks, unlike the clicking sounds commonly heard in other joints.  Within the next decade, many dentists tried to recapture dislocated disks without understanding how to establish the necessary therapeutic occlusion, and consequently most of their attempts failed.  In addition, many of those dentists trying to recapture dislocated disks did not understand the self-limiting nature of TMJ disorders and were therefore overtreating patients who had little pain and an excellent prognosis even without treatment.  About a decade later, the pendulum swung back the other way.  Some dental authorities warned that dislocated disks could never be recaptured.  Others claimed that, because TMJ disk dislocation occurs in about 30% of the general population, it should not be considered pathological but simply a variation of normal.   

Dislocation of the articular disk is the initial event in the vast majority of TMJ disorders.  It can produce severe symptoms in some people, but it produces little or no symptoms in others. In many patients seeking treatment, it does not need to be directly addressed, because the retrodiskal tissues have already fully adapted to the disk dislocation and are no longer inflamed.      


Nocturnal bruxism certainly applies large forces to the masticatory system, and a TMJ with a displaced disk is more susceptible to damage from nocturnal bruxism than a normal TMJ.  However there is no evidence that nocturnal bruxism is the cause of most or even many TMJ disorders.  It does not occur more frequently or forcefully in TMJ disorder patients than in normals.  In addition, its prevalence decreases while the prevalence of TMJ disorders increases during the second through fourth decades of life. 


The jaw muscles are always involved in TMJ disorders, because muscles are responding organs.  They rarely start problems, but they respond rapidly to conditions in nearby joints.  A common misconception is that the jaw muscles in TMJ disorders go into spasm, which is a sustained maximal or submaximal contraction.  Actually, in response to a TMJ injury such as a dislocated disk, the muscles go into a state of protective bracing.

Reflex protective bracing changes jaw muscle behavior in three ways.  1) It causes increased resting tension, because the muscles hold themselves constantly on guard as if they were applying continuous low level tension to stabilize the joint.  2)  It causes decreased functional tensions, because the muscles fire weakly during function as if they are afraid of damaging the articular structures.  3)  It causes overlap of firing activity (co-contraction) of jaw opening and closing muscles, because the muscles work against each other in order to more tightly control mandibular movements.  

The increased resting tension of jaw muscles that results from protective bracing can also be exacerbated by jaw muscle tightening from other sources, because sources of jaw muscle tension are cumulative.  Those sources can include periodontal disease, occlusal instability, increased central nervous system stress, or noxious sensory input from almost any area of the face.  

Jaw muscle tightness can also be a by-product of overall postural muscle tightness.  The jaw muscles are integral components of the head posture mechanism, as explained in OCCLUSION AND POSTURE.  As a result, when the postural muscles tighten, the jaw muscles also tighten, especially the temporal muscles, which are the primary postural muscles for the mandible.

If maintained over time, jaw muscle tightness can cause pathologic changes, such as contracture, that may be difficult to reverse.  Even after the cause of the tightness has been eliminated, the jaw muscles may not return to a normal relaxed resting state on their own.  They may need to be stretched along with their tightly attached sheets of fascia.

Fortunately, many physical therapists, chiropractors, and massage therapists are well trained to treat tight muscles and fascia.  Their work alone often provides short term relief of muscle symptoms, and the relief may last if the TMJs are already in full adaptation. 


Because stress increases the tonus of all the skeletal muscles, it can exacerbate almost any muscular condition; and it has an especially potent influence in TMJ disorders because of the imbalance between the antagonistic muscles controlling the position of the mandible. In other parts of the body, the bones are held at rest between generally equal masses of muscles pulling in opposite directions.  Therefore increasing the tonus in the muscles does not move the bones, it just holds them more tightly.  In the masticatory system, on the other hand, the jaw closing muscles dwarf the jaw opening muscles. Consequently, increasing the tonus in the muscles does not just hold the mandible more tightly, it brings the mandible further closed, diminishes the freeway space, and increases resting intrajoint pressure in the TMJs.   


Because the symptoms are caused by progressive growth strains to which the system is continually trying to adapt; loss of overall adaptive capacity can produce symptoms.   Many people have a dislocated disk for years until a loss of adaptive capacity due to stress, injury, or some unrelated disease condition makes it symptomatic.   Subsequently the problem can often be returned to a subclinical state by enhancing adaptive capacity with relaxation, exercise, stretching, nutritional support, postural work, accupuncture, or a wide variety of muscle treatments and even placebo treatments.  If any of these techniques eliminates the symptoms, it can feel like a cure.  


The standard medical treatment for an acute injury is rest of the affected part.  For that reason, many doctors and dentists advise TMJ disorder patients to adopt a soft food diet.  Such limitation of use can provide short term relief in acute TMJ conditions, like those caused by a recent trauma; however most TMJ disorders are not acute injuries - they are chronic conditions sustained by self-perpetuating features that must be addressed if the condition is to be eliminated in a lasting way.  Chronic conditions require rehabilitation and restoration of healthy function rather than rest of the affected part.


In some chronic TMJ disorder patients, the pain has become centralized, and treatment that is solely directed at the periphery (muscles, joints, and teeth) can only provide limited relief unless it is combined with more centrally operating treatment modalities that alter brain chemistry.  Chronic pain leads to changes in pain circuitry by lowering activation thresholds of sensory nerves.  In central sensitization, synaptic plasticity in the spinal cord has responded to chronic noxious inputs in a pain pathway by sprouting sensory receptors at both ends of the pathway - the brain and the area of injury.  Eventually the amplification or gain of neural signaling within the pain pathway can be increased so much that it can be activated by normally innocuous inputs, and the perceptual responses to all inputs become exaggerated and prolonged.   Central sensitization is often associated with endocrine abnormalities, persistent elevation of sympathetic tone, fibromyalgia, chronic headache, idiopathic dental pain, and neuropathic pain.