Chondrocyte death, induced by impact injury (necrosis) and/or apoptotic inducers such as cytokines, and high level of nitric oxide, is important for the development of post-traumatic arthritis (PTA) [1–3]. The upregulation of pro-inflammatory cytokines, such as interleukin −1 (IL-1) and Tumor necrosis factor (TNF) α, is known to mediate cartilage degradation in inflammatory diseases and after trauma injury [1,2, 6–9]. IL-1 induces the degradation of proteoglycan (PG) in cartilage through NF-κB and Mitogen-activated protein kinases (MAPK: p38, ERK and JNK) pathways [1,2,6]. IL-1 is highly upregulated in synovial joint after impact injury, but the role of IL-1 induced chondrocyte death and matrix/PG degradation in injured cartilage is not completely clear.

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