Posttraumatic knee osteoarthritis following anterior cruciate ligament injury: Potential biochemical mediators of degenerative alteration and specific biochemical markers

As a common injury, anterior cruciate ligament (ACL) injury is unable to heal itself naturally, which possibly increases knee instability, accelerates the risk of joint degeneration and leads to knee osteoarthritis (OA) in the ACL-injured knee. Thus, ACL reconstruction using an autograft or allograft tendon is proposed to maintain the biomechanical stability of the knee joint. However, previous studies demonstrate that surgical management of ACL reconstruction failed to abrogate the development of OA completely, indicating that biochemical disturbance is responsible for the osteoarthritic changes observed following ACL injury. Inflammatory mediators are elevated subsequent to ACL injury or rupture, inducing matrix metalloproteinase production, proteoglycan degradation, collagen destruction, chondrocyte necrosis and lubricin loss. These potential biochemical mediators may aid in the development of effective biological management to reduce the onset of future posttraumatic OA. Furthermore, during the degenerative process of cartilage, there are a number of cartilage-specific biomarkers, which play a critical step in the loss of structural and functional integrity of cartilage. The present review illustrates several specific biomarkers in the ACL-injured knee joint, which may provide effective diagnostic and prognostic tools for investigating cartilage degenerative progression and future posttraumatic OA of ACL-injured patients.