PURPOSE: Nitric oxide (NO) plays an important role as a regulator of inflammatory functions. Since NO is a short-lived, gaseous free radical produced by inducible NO synthase (iNOS), so iNOS is closely related to the pathophysiologic nature of the inflammatory articular diseases. A recent investigation shows that NO and iNOS have close relationship to the cartilage destruction in human temporomandibular joint (TMJ) arthritis. Apoptosis, known as programmed cell death plays diverse roles in various pathologic conditions. Recently, NO was proved to function as a modulator of apoptosis, and apoptosis caused by oxidative stress is involved in inflammatory articular diseases. In this study, we investigated the relationship between iNOS protein and apoptosis in mandibular condyle in antigen-induced arthritis of the rabbit TMJ. MATERIALS AND METHODS: Twenty adult male New Zealand White rabbits were used. Unilateral arthritis was induced with intra-articular injection of ovalbumin and the contralateral joint was sham induced with saline injection. The TMJs were retrieved en bloc at 1, 3, 7, 21 and 42 days after the induction of arthritis. Apoptosis of the mandibular condyle was examined by TUNEL method. The localization of iNOS was examined by immunohistochemically using antibodies against iNOS. RESULTS: Although little morphological changes of condylar cartilage was observed in the late acute phase arthritic joint, a larger number of TUNEL positive chondrocytes as well as iNOS positive chondrocytes were observed in the arthritic joint than in sham induced joint. In the chronic stage of arthritis, TUNEL positive cells seemed to be close to the area of cartilage degradation. The iNOS in the condyle immunoreactivity were detected in similar distribution of the TUNEL positive chondrocytes. CONCLUSION: These findings suggest that inflammatory oxidative stress and apoptosis in condylar cartilage are involved in the onset and progression of cartilage destruction in this TMJ arthritis model.

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