Abstract

Purpose: Following anterior cruciate ligament reconstruction (ACLR), patients are at an increased risk of developing post-traumatic osteoarthritis (PTOA). Pathogenesis of PTOA is multifactorial and although the mechanisms that lead to PTOA remain unclear, it is theorized that an altered joint environment due to the release of inflammatory and catabolic cytokines may contribute as these cytokines promote the breakdown of type II breakdown. Increased expression of inflammatory (e.g. MMP-3) and type 2 collagen turnover (e.g.

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