Parallel Distribution of Bcl-2 and Bax in Hypertrophied Chondrocytes of the Mandibular Condylar Cartilage from the Senescence-accelerated Mouse (SAMP3)

To demonstrate the distribution of apoptotic cell death in the temporomandibular joint of SAMP3 mice, showing degenerative joint disease resulting in overt deformation of the mandibular condyle, immunohistochemical localization of Bcl-2 and Bax in the condylar cartilage of the animals was examined. Histological changes revealed an apparent deformity of the condyles at around 6 months of age, and thereafter showed severe degeneration in accordance with advancing age until 13 months. The apoptotic changes by the Bcl-2 and Bax expressions were observed in the hypertrophied chondrocytes abutting on the endochondral ossification site, as well as in the synovial membrane, throughout all ages examined. The expression of both of these molecules remained to localize in these sites and increased with advancing age, in which proceeding matrix degradation and chondroid bone formation took place. In addition, the nidus of metaplastic cartilage that protruded into the joint space of the aged animals also demonstrated positive immunoreactivities. The radical production and parallel distribution of Bcl-2 and Bax in the hypertrophied chondrocytes in the affected condyles might indicate that hypertrophic cells may undergo apoptosis, and some others, survive, to regulate the cartilage degradation occurring in the mandibular condyles of SAMP3 mice.