This study evaluates the progression of osteoarthritis (OA) in the adult New Zealand white rabbit temporomandibular joint following unilateral disc perforation. Thirty-seven animals were divided into five groups: control (n = 8), 6-week sham (n = 5), and experimental 6-, 12-, and 24-weeks (n = 8 each). Quantitative data was examined with two-way analysis of variance, and followed by Scheffe pair-wise comparisons. Transmission electron microscopy, acid phosphatase [AcP] activity, uronic acid content, and gross morphologic analysis indicated that disc perforation induced remodeling activity and degenerative changes in the condylar cartilage and bone as early as 6 weeks postoperatively. AcP activity of homogenized cartilage samples was significantly increased in experimental joints versus the side that did not undergo surgery at 6 and 12 weeks (P < .05). Uronic acid content was significantly greater in experimental joints versus the side that did not undergo surgery at 6 weeks (P < .05). Heightened cellular activity was present in the deep zone of osteoarthritic fibrocartilage of the 6- and 12-week experimental groups. Degenerating chondrocytes appeared to contain greater proportions of intracytoplasmic filaments and lysosome-like bodies. Disc perforation provided the impetus for degenerative or remodeling changes in the condylar cartilage of experimental joints, and is consistent with secondary OA. These dynamic events were most significant in the deep zone of articular fibrocartilage.