Substantial evidence has suggested that proinflammatory cytokines such as IL1β, TNFα, IL-6, IL-17, and others, derived from synovial fibroblasts in the inflamed joints, are the primary trigger for the local or systemic high expression of RANKL in RA [25, 26], which is the main explanation of inflammation-induced osteoclast activation and bone lose. Here, TNF is linked to rheumatoid arthritis.