Anterior cruciate ligament (ACL) injuries are common, severe knee injuries that result in a high risk of developing knee osteoarthritis (OA) in the affected individuals. As proof of high impact forces applied to cartilage and bone at the time of injury, traumatic bone marrow lesions and osteochondral fractures, located predominantly in the lateral tibiofemoral compartment, are commonly associated with an ACL injury. The subsequent risk of OA may be closely associated with the knee injury mechanism and the panorama of injuries in the knee sustained at the onset of injury. The purpose of this work was to acquire a better understanding of how the initial impact, related to the trauma mechanism of acute knee injuries, may influence acute and chronic knee pathology.
In this work it was found that subjects with post-traumatic OA secondary to an ACL injury have more joint space narrowing and more osteophytes in the lateral compartment than in the medial compartment, compared with subjects with non-traumatic OA. Furthermore, it was found that an acute knee injury is associated with instant and sustained synovial fluid biochemical alterations within the first month of knee injury, suggestive of increased cartilage turnover and severe joint inflammation. Those subjects who sustained an osteochondral fracture with disrupted cortical bone in association with the soft tissue knee injury had increased joint inflammation. In an in vitro bovine cartilage study, mechanical injury to cartilage increased the matrix metalloproteinase-induced cleavage of cartilage aggrecan. Moreover, findings from this model suggest that the aggrecan degradation may differ between cytokine-stimulated cartilage explants compared with cartilage explants mechanically injured and (or) co-incubated with joint capsule.
Conclusively, the findings in this work underline the fact that the initial impact associated with an ACL appears to be important in terms of the risk of developing post-traumatic OA. In addition, this work emphasizes how the acute biological response to injury could be involved in cartilage degradation. A greater understanding of these processes could lead to the improved management of knee-injured patients and possibly delay, or even prevent, OA development