A review of the literature reveals three common points regarding the etiology of temporomandibular disorders (TMD):

    1. There is no universal etiology.
    2. MD is recognized as a nonspecific term representing a wide variety of painful and/or dysfunctional jaw conditions.(1)
    3. There is no single cause that accounts for all signs and symptoms.

Unfortunately, beyond these three points, there is little congruity and much controversy surrounding this topic. Even the name "TMD" is not used universally.

One explanation of how TMD’s arise, formulated by Okeson, seems to be most applicable to other author’s approaches. The basic formula can be written as:
 
 

NORMAL FUNCTION + AN EVENT > PHYSIOLOGIC TOLERANCE à TMD

Okeson’s use of "physiologic tolerance" in the formula can be justified by the logical fact that people with compromised masticatory systems cannot tolerate events as well as people with healthy, normal ones. Okeson goes on to state that physiologic tolerance is influenced by anatomic form, previous trauma, local tissue conditions, and occlusal features. It is apparent that the inconsistencies in the etiology of TMD lie in the classification and definition of "an event" which triggers the onset of symptoms. Okeson identifies two types of events, local and systemic. Local events include trauma, such as an impact injury; abnormal functional habits such as teeth grinding (bruxism), and changes in sensory or proprioreceptive input such as the use of a dental or orthodontic device. A systemic event encompasses all types of emotional distress that may contribute to the development of TMD symptoms.(4)
 
 

McNeill categorizes the primary etiologic factors of TMD as traumatic, anatomic, pathophysiologic, or psychosociologic. Traumatic factors include a blow or impact injury, dental procedures, exaggerated mouth opening, and parafunctional habits such as excessive teeth clenching or grinding. Anatomic factors are primarily concerned with occlusal features. Pathophysiologic factors include degenerative, endocrine, neoplastic, infectious, metabolic, and rheumatologic involvement. McNeill’s psychosocial factors equate to Okeson’s definition of systemic events in that anxiety and emotional distress are involved.(2,4)

In the classification of an event, Okeson and McNeill also consider whether the factors involved are predisposing, initiating, perpetuating, or combinations of the three. This aids in pairing a specific etiology to a specific case.(3,4)

Shankland foregoes classification and categorization and simply states that the etiology of TMD centers on internal joint derangement. He then identifies factors contributing to such a derangement including trauma, malocclusion, ligament laxity, stress, systemic disease, and a few others.(5)

A perfect example of the inconsistency regarding the etiology of TMD can be seen in a comparison of studies as reported by Okeson. In 7 different studies performed by numerous authors investigating the presence of signs and symptoms of TMD across given sample sizes, results ranged from 11 percent to 76 percent of the subjects showing signs or symptoms of TMD. Keeping in mind that the subjects were chosen randomly, the variability is indicative of the multifactorial nature of TMD and the difficulty in differentiating potential etiologies.(4)

The information cited here does not nearly encompass the range and scope of etiologies offered. Despite an overwhelming overlap of etiological factors between scholars and physicians reporting on the cause of TMD, there is no universal etiology. Furthermore, in some cases subjectivity weighs heavily on the etiology offered by a physician. In light of this, "diagnosis and initial treatment often depend on the practitioner’s experience and philosophy, rather than scientific evidence." (2). It is imperative to realize that TMD is a term that may encompass many causal factors. Thus, the etiology of TMD will depend on the specific case at hand and be revealed only after systemic evaluation and subsequent elimination of other possible etiologic factors.
 
 

Trauma- Due to impact injury or abnormal or excessive force applied to the joint and/or surrounding structures. Frequently results in a dislocated disc and bruising, directly or indirectly causing altered mechanics of the TMJ.

Bruxism- Diurnal or nocturnal parafunctional activity including clenching, bracing, gnashing, and grinding of the teeth.(3)

Malocclusion-Basically, a bad bite. Malocclusion may be caused by poor development of the jaws, or a displaced TMJ disc. It can result from bruxism.(5)

Stress-Sum of the biologic reactions to any adverse stimulus. These reactions may include the production of certain chemicals in the blood (catecholamines) which start a chain of events eventually leading to muscle tightness and pain.(3,5)
 
 

References

 1 Goldstein, BH. Temporomandibular Disorders, A Review of Current Understanding. Oral Surgery, Oral Medicine, Oral Pathology. 1999;88(4): 379-385.

 2 Management of Temporomandibular Disorders. NIH Technology Statement Online. (No date) Available: http://text.nlm.nih.gov/nih/ta/www/018txt.html

 3 McNeill, C., ed.. Temporomandibular Disorders, Guidelines for Classification, Assessment, and Management. Chicago, IL: Quintessence Publishing Co., 1993.

 4 Okeson, JP., Management of Temporomandibular Disorders and Occlusion. St. Louis, MO: Mosby Publishing Co., 1998.

 5 Shankland, WS., TMJ: Its Many Faces. Diagnosis of TMJ and Related Disorders. Columbus, OH: Anadem Publishing Co., 1998.