The molecular events that underlie degenerative temporomandibular joint diseases are poorly understood. Recent studies have provided evidence that a variety of molecular species, including cytokines, matrix degrading enzymes, neuropeptides, and arachidonic acid catabolites may be involved. This paper advances the theory that mechanical stresses lead to the accumulation of damaging free radicals in affected articular tissues of susceptible individuals. This condition is called oxidative stress. The authors postulate mechanisms that may be involved in the production of free radicals in the temporomandibular joint and in the subsequent induction of molecular events that may amplify damage of articular tissues initiated by free radicals. If the proposed model is correct, then future therapeutic strategies directed at the control of oxidative stress could be effective in the management of degenerative temporomandibular joint diseases.