Molecular biomarker approaches to prevention of post-traumatic osteoarthritis.

Up to 50% of individuals develop post-traumatic osteoarthritis (PTOA) within 10 years following knee-joint injuries such as anterior cruciate ligament rupture or acute meniscal tear. Lower-extremity PTOA prevalence is estimated to account for ≥12% of all symptomatic osteoarthritis (OA), or approximately 5.6 million cases in the USA. With knowledge of the inciting event, it might be possible to 'catch PTOA in the act' with sensitive imaging and soluble biomarkers and thereby prevent OA sequelae by early intervention. Existing biomarker data in the joint-injury literature can provide insights into the pathogenesis and early risk trajectory related to PTOA and can help to elucidate a research agenda for preventing or slowing the onset of PTOA. Non-traumatic OA and PTOA have many clinical, radiological and genetic similarities, and efforts to understand early risk trajectories in PTOA might therefore contribute to the identification and classification of early non-traumatic OA, which is the most prevalent form of OA. Early identification of osteoarthritis (OA) prior to the development of symptoms is challenging. Post-traumatic OA provides a model for the development of OA following a defined event. In this Review, the authors describe the existing knowledge relating to the biomarkers of post-traumatic OA, which might also be applicable to the identification of early non-traumatic OA. Key points: Molecular biomarkers have potential for monitoring of the post-traumatic osteoarthritis (PTOA) trajectory, as treatment targets for the prevention of PTOA, and as indicators of the efficacy of PTOA prevention strategies. The early inflammatory response to joint injury is acutely beneficial, but thereafter contributes to PTOA development; the optimal approach and timing of anti-inflammatory interventions are yet to be determined. Biomarker expression varies with time after injury; the optimal timing and choice of biomarkers for definitive identification of a PTOA trajectory are yet to be determined. Long-term elevation of elastase after injury could identify a group at a high risk of PTOA. The early appearance of collagen biomarkers after injury, portending irreversible joint damage, suggests the possible need for very early intervention to prevent PTOA. Haemarthrosis related to injury and surgery is a risk factor for cartilage degradation that deserves more widespread recognition and early amelioration in clinical practice to prevent PTOA. [ABSTRACT FROM AUTHOR]