Neurophysiologic studies of temporomandibular joint dysfunction.
An attempt has been made to relate clinical thinking to available experimental evidence of the physiological background to temporomandibular joint dysfunction. There is little or no evidence that the condition results from displacement of the mandibular condyles. The contention that muscle hyperactivity is a primary cause receives some experimental support, but there is no clear evidence that malocclusion of the teeth leads, through reflex mechanisms, to maintained hyperactivity. Instead there is an increasing weight of evidence that hyperactivity of jaw closing muscles may originate in the central nervous system. It is concluded that such centrally induced activity may be sufficient to cause muscle damage, which leads to disturbed function, local pain and tenderness and to pain referred to adjacent structures.
D000818:Animals; D004576:Electromyography; D005152:Facial Muscles / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008310:Malocclusion / Q000503:physiopathology; D008410:Masticatory Muscles / Q000294:innervation / Q000473:pathology / Q000503:physiopathology; D008465:Mechanoreceptors / Q000503:physiopathology; D009135:Muscular Diseases / Q000473:pathology; D009482:Neurophysiology; D010519:Periodontium / Q000294:innervation; D013035:Spasm / Q000473:pathology; D013312:Stress, Physiological / Q000503:physiopathology; D013315:Stress, Psychological; D013706:Temporomandibular Joint Dysfunction Syndrome / Q000503:physiopathology*