COMP as a significant non‐collagenous component of cartilage ECM, plays an essential role in matrix assembly by the interaction with several ECM proteins.53 Increased levels of COMP and its degradative fragments have been detected in the serum and synovial fluid of OA and RA patients, and have been described as biomarkers of joint damage and disease progression.2, 26, 53, 54 Our results indicate a time‐course degradation of COMP from cartilage explants because of the action of OA‐SF, supporting the contribution of SF to COMP degradation. This evidence concerns the gene COMP and rheumatoid arthritis.