|3049 NO Production in Mechanical-Stress-Induced OA Cartilage of the Rabbit TMJ|
T. FUJISAWA, T. KUBOKI, T. KASAI, W. SONOYAMA, S. KOJIMA, J. UEHARA, and H. YATANI, Okayama University Graduate School of Medicine and Dentistry, Japan|
Objective: We have already demonstrated that excessive mechanical stress applied to the cultured chondrocytes accelerates matrix degradation in vitro (Fujisawa et al., J Biochem, 1999). Furthermore, excessive mechanical stress induced by repetitive forced-mouth-opening produced osteoarthritis (OA) -like lesions in the rabbit temporomandibular joint (TMJ), and chondrocytes apoptosis seems to be one of the cartilage degradation mechanisms in vivo (Fujisawa et al., AADR, 2001). However, the induction mechanism of the chondrocytes apoptosis in the OA cartilage is not clear. Methods: In this study we further examined the anatomical relationship between apoptotic chondrocytes and nitric oxide (NO) production in the mechanical-stress-induced TMJ OA cartilage in vivo. TMJ OA was induced in six experimental rabbits (adult Japanese white rabbits) by a forced-mouth-opening protocol under general anesthesia, while control three rabbits received the same anesthetic protocol without forced opening as described before (Fujisawa et al., AADR, 2001). Mandibular condyles of the rabbits were harvested after fixation and the condyles were decalcified and embedded in paraffin. Existence of apoptotic cells was examined by a TUNEL staining (TREVIGEN, MD, USA), and NO production was immunohistochemically examined by using a rabbit anti-nitrotyrosine antibody (Upstate, NY, USA) Results: In the experimental OA joints, TUNEL positive cells were seen mainly in the hypertrophic chondrocytes in the regenerating articular cartilages (e.g., osteophyte formation sites) at 7 days after mechanical stress application. In the same area, high levels of NO production were concomitantly observed. Meanwhile, TUNEL positive chondrocytes and NO production were not observed in the control articular cartilages. Conclusions: These results suggest that NO production in the mechanical-stress-induced OA cartilage can be related to the chondrocyte apoptosis in vivo. This study was partially supported by a Grant-in-Aid (No.12557169) from the Japanese Ministry of Education, Sports, Science, Culture and Technology.
|Seq #275 - TMJ - Structure and Function II|
3:45 PM-5:00 PM, Friday, 8 March 2002 San Diego Convention Center Exhibit Hall C