Oscar, also known as osteoclast-associated receptor, is a regulator of osteoclast differentiation and provides a co-stimulatory pathway for osteoclastogenesis. It is involved in processes related to bone remodeling and repair, and its abnormal function may lead to excessive bone degradation in aging and bone diseases [2].

In osteoarthritis (OA), 5-aminosalicylic acid (5-ASA) can compete with extracellular-matrix collagen-II to bind to OSCAR on chondrocytes. Intra-articular 5-ASA injections ameliorate OA in male mice even when administered after OA onset. Mechanistically, 5-ASA reverses OSCAR-mediated transcriptional repression of PPARγ in articular chondrocytes, suppressing COX-2-related inflammation, improving chondrogenesis, down-regulating ECM catabolism, and promoting ECM anabolism [1]. Also, blocking OSCAR with a soluble OSCAR decoy receptor or anti-OSCAR monoclonal antibodies ameliorates OA in animal models, reducing cartilage destruction and other OA signs such as subchondral bone plate sclerosis and loss of hyaline cartilage [3].

In conclusion, Oscar plays a crucial role in osteoclastogenesis and is significantly involved in the pathogenesis of osteoarthritis. Studies using animal models, like those with OA-induced surgical methods, have revealed that targeting Oscar can be a promising strategy for treating osteoarthritis, providing new insights into the disease mechanism and potential treatment options.