The role of subchondral bone damage in post-traumatic osteoarthritis.

Abstract

Osteoarthritis (OA), the most common musculoskeletal disease in the United States, is characterized by cartilage breakdown, pain, and restricted movement. Post-traumatic OA (PTOA) occurs subsequent to traumatic joint injury, such as anterior cruciate ligament (ACL) rupture, and makes up 12% of the overall disease burden, with healthcare costs of approximately $3 billion/year. The current paradigm for PTOA is based on the observation that joint injury affects multiple tissues, all of which may contribute to subsequent joint failure. Subchondral bone plays a significant role in PTOA, as shown by magnetic resonance imaging evidence that subchondral bone marrow lesions (BMLs) are present in 80% of ACL rupture cases immediately after joint injury. The presence of BMLs indicates an acute consequence of injury, specifically in subchondral bone, which could be targeted with preventative therapy. BMLs may be a direct representation of physical damage to bone tissue. Interestingly, microdamage is known to induce osteoclast-mediated remodeling in bone. Furthermore, the contiguous link between subchondral bone and articular cartilage may allow transport of small molecules, resulting from these remodeling processes, to cross the osteochondral junction and contribute to PTOA development. Targeting subchondral bone by inhibiting subchondral remodeling, particularly in the early phase postinjury, may be a potential approach for preventing PTOA.