Defective Signal Transduction in Osteoarthritic Chondrocytes and Synovial Fibroblasts Should Become a Target for Drug Intervention

ry cytokines are an essential driver of synovial joint inflammation in osteoarthritis (OA), drugs [e.g. Anakinra, Tocilizumab, Tofacitinib, Adalibumab] that target the signal transduction pathways activated by these cytokines including, Interleukin-1β (IL-1β), IL-6 and tumor necrosis Factor-α (TNF-α) are routinely employed in the medical therapy of rheumatoid arthritis (RA) [1], but NOT OA. Why is that? Several possible explanations arise from a perusal of the relevant medical literature in the PubMed database. For example, it is well known that genetic and mechanical stressors are integral to the development and progression of OA pathology but the type of inflammation inherent in cartilage destruction in OA was originally classified as “non-classical.” [1]. But is this the case? I think not.