Several studies [27–29] have demonstrated that TNF-α inhibitors and some synthetic DMARDs (such as MTX and sulfasalazine) inhibit the expression of RANKL in RA synoviocytes while augmenting the secretion of OPG in synoviocyte supernatants, and they all inhibited osteoclast formation in vitro. Here, TNF is linked to rheumatoid arthritis.