The release of degradation fragments of COMP into the joint cavity may activate complement in the synovial fluid and further exacerbate the destruction of articular cartilage; whereas the failure to detect COMP-C3b complexes in the sera of patients with OA suggests that the degradation fragments produced by COMP may be different in the 2 types of arthritis, and that binding to complement may require some specific amino acid sequences or antigenic epitopes to be realized (93). The gene discussed is COMP; the disease is Arthritis.