Abstract

Myogenous pain associated with temporomandibular disorders (TMDs) has traditionally been linked to hyperactivity or abnormal contraction of masticatory muscles. The evidence in the literature for a reinforcing vicious cycle between muscle hyperactivity and pain has, however, been critically reviewed and cannot confirm all previous beliefs. In the absence of identifiable tissue pathology, another common idea has been that myogenous pain is a psychological or psychosomatic disorder, but research results may now be able to explain TMD pain from a more neurobiologic perspective. Based on present knowledge, new appealing hypotheses regarding pathophysiologic reactions in acute and chronic myogenous TMD pain can be formulated. Facing the many controversies in the TMD literature, the challenge of this article is to provide a short status of suggested pain mechanisms. It will be argued that different subtypes of myogenous TMDs have distinct pathophysiologic characteristics with increasing levels of complexity as the pain persists: acute TMD pain is the result of primarily peripheral problems, whereas chronic TMD pain is a central problem with plastic neural changes at the trigeminal level and impairment of endogenous pain regulatory systems.

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