In most diseases, the goal of treatment is to identify the cause of the symptoms and remove it.  In the small number of TMJ disorders which have one distinct cause, that technique can work.  However, most TMJ disorders do not have a one distinct cause.  They may have begun with a single triggering event, but over time they have become chronic conditions in which the generation of symptoms is no longer dependent on the original triggering event.  The symptoms are generated by a vicious cycle that includes muscle tension, bite strain, central nervous system stress, postural strain, and facial growth.  Thus relieving the symptoms does not require identifying the original cause, - it requires correcting the dysfunctional state that is generating the symptoms.


Often the symptoms are preceded by an event such as a blow to the head or face, whiplash, a long dental appointment, a high filling, a period of excessive central nervous system stress, extensive dental work, a difficult chewing episode, or hormonally mediated joint laxity (childbirth or menstrual cycle).  Assuming that the event immediately preceding the onset of symptoms is the cause of the symptoms has led some researchers to conclude that the cause of TMJ disorders must be multifactorial, with dozens of factors involved.  In addition to presumed microtraumatic incidents, joint laxity, and psychosocial factors; they include predisposing factors, initiating factors, and perpetuating factors.  A few clinics try to provide multifactorial treatment by addressing all of these potential causes, but that approach can be very costly.


Nocturnal bruxism (clenching or grinding the teeth during sleep), may aggravate the nightly bruising of a TMJ with a dislocated disk, but it cannot be considered the cause of most TMJ disorders.  Nocturnal bruxism is part of normal sleep.  It becomes more frequent and severe in the presence of stress, but it affects everybody to some extent, and it is not found more frequently in TMJ disorder patients than in other people.  


The vast majority of TMJ disorders begin with a dislocation of the articular disk from one or both of the TMJs.  Joints are designed to hold a cushion (in this case a flexible fibrous articular disk) between two opposing bones so those bones do not rub directly together.  After that articular disk has become dislocated from its proper position between the jawbones, the affected TMJ functions like a door off its hinges. Damage can occur to the door (the lower jawbone), the door frame (the upper jawbone), or its hinges (the TMJs).


Whiplash is one common cause of disk dislocation.  A sudden blow that drives the head forward can also drive the condyles backward in the TMJs and cause them to strike the joint edges like the clanger in a bell, especially when the blow came without any warning.  People who see the accident coming automatically clench their teeth, which makes the teeth more prone to damage but less likely to injure the TMJs. 


Jaw muscle tightness certainly plays a role in TMJ disorders, but it is rarely the primary cause.  Muscles are responding organs.  They rarely start problems, but they automatically respond to joint conditions by tightening up to proect the joints.  In the presence of TMJ inflammation, the jaw muscles automatically tighten up much like your leg muscles would tighten up if you tried to walk on an inflamed ankle.  The resulting increase in background tension can cause pain in the jaw muscles by impairing their resting circulation.

After the jaw muscles have remained tight for months, they anatomically shorten.  Subsequently, your jaw will not hang very far open when you are at rest, like when you fall asleep in a chair.  The teeth may even rest in light contact, and they may go into a clench whenever tension in the jaw muscles increases further. Tooth contact can then trigger reflex clenching, causing a cycle that maintains the jaw muscle tension. 

Until MRI showed that the vast majority of TMJ disorder patients have a dislocated disk in at least one TMJ, dentists simply managed all TMJ disorders by treating the jaw muscles using physical therapy, medications, simple bite raising oral appliances, or occlusal equilibration (drilling away high spots on back teeth).  These muscle treatments often provided short term relief.  However, the role of the jaw muscles was secondary, not primary, in most of the patients.  As a result, their symptoms usually returned - prompting dental authorities to advise dentists to warn TMJ disorder patients that their condition can be managed but not cured.  

Damage from either TMJ tightens up the jaw muscles on both sides, because the two TMJs are connected to the same bone and therefore are wired as if they were both part of the same joint.  All signals from the brain to the jaw muscles pass through a central connector.  As a result, TMJ damage on one side often causes jaw muscle symptoms on the opposite side.


Another cause of jaw muscle tension may be bite strain.  If the jaw muscles lack a stable comfortable bite table on which they can rest the lower jawbone, they cannot fully relax. They automatically hold themselves tightly, much like they do in response to TMJ inflammation. 


Increased central nervous system stress can trigger or sustain symptoms by increasing muscle tightness in all of the body's muscles.  When jaw muscles are already at borderline resting circulation due to reflex tightening caused by TMJ tissue damage or bite strain, any further increase in central nervous system stress can lower resting jaw muscle circulation below a threshold level that results in pain.

While stress can worsen any muscle related condition, it has an especially powerful effect on TMJ disorders because of the imbalance between jaw opening and jaw closing muscles.  In most parts of the body, bones rest in position between equally sized muscles pulling in opposite directions; therefore increasing resting tension in the muscles does not move the bones, - it just holds them more tightly.  However, in the jaw system, the closing muscles dwarf the opening muscles.  As a result, when stress increases resting tensions, it further closes the jaw. 


Jaw muscle tightness can then become a link in the chain of events that perpetuates a TMJ disorder.  Since the jaw muscles are oriented vertically, jaw muscle tightness increases the pressure between the bones at the TMJs.  When a TMJ has lost its disk and thereby also much of its shock absorbing capacity, such pressure can cause tissue damage, which triggers more jaw muscle tightness, which causes more tissue damage -resulting in a vicious cycle that can maintain the symptoms long after the injury that triggered them has resolved.  

In these situations, anything that breaks the cycle, even an injury or a treatment for a different problem, can provide quick relief.  The speed of the relief can convince people that whatever interrupted the cycle has addressed the original cause of the problem.  That thinking has led to much confusion regarding the cause of TMJ problems.


Because adaptation is such an important factor in the production and relief of symptoms, anything that diminishes adaptive capacity, such as increased stress or an unrelated injury, can also function as a trigger that seems like a cause.  Frequently a strained bite exists without causing symptoms for many years before a failure to adapt to the strain permits tissue damage and clinical symptoms.  Conversely, anything that enhances adaptive capacity (such as nutritional support, relaxation, meditation, aerobic exercise, or feeling loved) can eliminate symptoms and thereby seem like a cure.


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.  Central sensitization occurs when chronic pain leads to changes in pain circuitry by lowering activation thresholds of sensory nerves on that pathway, and synaptic plasticity in the spinal cord responds 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.