Subchondral bone sclerosis in osteoarthritis: not just an innocent bystander

Abstract  Osteoarthritis (OA) is considered to be a complex illness in which the tissues of the joint play a significant role in the initiation and/or progression of the pathophysiology. We still do not completely understand what initiates the degradation and loss of cartilage. However, it has been suggested that increased catabolism due to elevated cytokines and growth factors in OA joints plays a significant role. Recent evidence suggests a key role for the subchondral bone tissue in the progression and/or initiation of OA. Indeed, the subchondral bone tissue produces a number of similar proinflammatory cytokines, and growth factors are involved in cartilage tissue remodeling. Interestingly, studies have shown the presence of clefts or channels in the tidemark that appears early in OA, indicating a possible way to traffic cytokines and growth factors from the subchondral compartment to the overlying cartilage. Therefore, it is possible that certain bone-derived products drive cartilage metabolism. Potential candidates include insulin-like growth factor-1 (IGF-1), transforming growth factor-β (TGF-β) interleukin 1β (IL-1β), and interleukin-6 (IL-6). Demonstrating that the subchondral bone plays a role in the initiation of OA would greatly contribute to furthering our knowledge of this pathology and provide new insights for therapeutic approaches.