Inflammation is common in OA ST and characterized by immune cell infiltration and cytokine secretion. This inflammation seems quantitatively and qualitatively different from inflammation in RA. Further research is needed to clarify the role of inflammation, immune cells and their cytokines in the pathogenesis of OA.

These data are consistent with the hypothesis that the IPFP is an osteoarthritic joint tissue capable of modulating inflammatory and destructive responses in knee-OA.

Objective. In osteoarthritis (OA), changes occur in both cartilage and subchondral bone. The subchondral bone plate facilitates normal cross-talk between articular cartilage and trabecular subchondral bone, and adaptive changes in the plate due to OA may therefore disturb cross-talk homeostasis. To investigate these changes over time, we examined the cartilagesubchondral bone interface using a combined approach of histologic analysis and in vivo microfocal computed tomography.Methods. Sixteen-week-old male C57BL/6 mice (n ‫؍‬ 32) received intraarticular injections of collagenase in 1 joint to induce instability-related OA and received saline injections in the contralateral knee joint (control joint). At 2, 4, 6, 10, and 14 weeks after injection, changes in the tibial subchondral bone plate and subchondral trabeculae were analyzed.Results. Two weeks after injection, collagenaseinjected joints had significantly more cartilage damage and osteophytosis than did control joints. Osteoclast activity directly underneath the subchondral bone plate was significantly elevated in collagenase-injected joints compared to control joints (mean ؎ SEM osteoclast surface/bone surface 11.07 ؎ 0.79% versus 7.60 ؎ 0.81%), causing the plate to become thinner and creating a large increase in subchondral bone plate porosity In osteoarthritis (OA), changes in bone are thought to accompany cartilage deterioration, although it remains unclear which process is responsible for the initial homeostatic disturbance. Located directly underneath the articular cartilage, the subchondral bone plate provides structural support and acts as a portal for biochemical interactions between the cartilage layer and bone marrow and/or subchondral trabecular bone (1-5). Therefore, any changes in its structure may well have an effect on the overlying cartilage as well as on the underlying subchondral bone. In OA, subchondral bone is hypomineralized and of inferior quality as a consequence of abnormally high turnover (6-10). The exact cause of this increased bone turnover is as yet unknown, but the involvement of changes in the overlying articular cartilage is proposed as the principal cause (11-13). In contrast, other studies have shown that the OA process starts with an increase in subchondral bone turnover, which in turn, initiates cartilage damage (12-15). Whichever theory is true, extensive interaction between carti-

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Background: This study evaluates changes in peri-articular bone in two canine models for osteoarthritis: the groove model and the anterior cruciate ligament transection (ACLT) model.