Yemm R
Oral Sci Rev. 1976;7:31-53.
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.
人们尝试将临床思维与颞下颌关节功能障碍生理背景的现有实验证据联系起来。几乎没有证据表明该病症是由下颌髁突移位所致。认为肌肉活动过度是主要病因的观点得到了一些实验支持，但没有明确证据表明牙齿咬合不正通过反射机制导致肌肉持续活动过度。相反，越来越多的证据表明，闭口肌活动过度可能源于中枢神经系统。得出的结论是，这种由中枢引发的活动可能足以导致肌肉损伤，进而引起功能紊乱、局部疼痛和压痛以及牵涉至相邻结构的疼痛。
