Abstract
Temporomandibular joint disorders (TMD) pose a significant challenge to the practice of oral and maxillofacial surgery. When painful, TMD are generally associated with hyperthermia of the overlying skin. It is hypothesized that this skin hyperthermia, caused by regional vasodilation, is induced by nitric oxide (NO) produced in the extravascular space of the joint. Extravascular NO can be produced by osteoblasts, chondrocytes and macrophages, or by stimulated neurons. It is suggested that this kind of pain is associated with NO-enhanced sensitivity of the peripheral nociceptors. Verification and clinical implications of the proposed mechanism are discussed.
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