Abstract
Purpose: Both animal and human studies indicate that changes of subchondral bone play an important pathogenic role in the initiation development and progression of osteoarthritis (OA). Transforming Growth Factor β1 (TGFβ1) is abundant in bone where it has multiple essential roles in development, homeostasis and repair, maintaining both bone volume and bone quality. Further, it has been shown that over-activity of TGFβ1 in subchondral bone has a direct causal role in rodent knee OA, which can be blocked by TGFβ1 neutralization.
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