“…C3a and sTCC were significantly higher in the SF from patients with early-stage knee OA (having symptoms less than 1 year) compared to healthy individuals [ 49 , 51 ] and complement transcripts and/or activation components C3/C3a, C4a, C4d, C3bBbP, factor B, and sTCC have been detected at high levels in the SF, synovial membrane and in the cartilage of patients with OA in the knee joint [ 36 , 47 , 48 , 49 , 53 ]. Recent evidence suggests that all three complement pathways are capable of being activated within the knee joint in both early and late knee OA and that the synovial membrane is the main source of complement activation rather than the articular cartilage tissue [ 50 ]. Patients with OA also exhibited high concentrations of lectin complement pathway components, including mannose bindin lectin (MBL), H-ficolin, M-ficolin, mannan-binding lectin serine protease- 2 (MASP-2), and MASP-3, which were higher in the plasma than the SF [ 54 ], and while the levels were significantly lower than patients with RA, this data suggests a possible role of the lectin pathway in promoting chronic disease in knee OA.…”