Painful and inflamed joints result from joint trauma involving disruption of the cartilage [1]. The pathogenesis of post-traumatic osteoarthritis is not well understood but is most likely multifactorial. Other factors, such as inflammation, may be a critical precursor for post-traumatic arthritis. Transient acute synovitis and inflammation following a traumatic event can persist for months and may be representative of a serious joint injury [2]. Joint effusion aspirates from patients in the acute phase of injury have a higher level of activated leukocytes and an increased rate of reactive oxygen species (ROS) production relative to autologous peripheral blood [3]. In an in vitro study, the presence of inflammatory leukocytes caused more chondrocyte death isolated from traumatized matrix region relative to impacted cartilage alone [4]. Our previous study showed that severe trauma may not be a good predictor for the development of post-traumatic arthritis since chondrocyte death and matrix loss was minimal up to seven days post-trauma [5].

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