Central to RA’s pathology is the persistent activation of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β), which not only perpetuate joint destruction but also compromise mucosal immunity and tissue integrity in the oral cavity [12]. These cytokines promote the recruitment of neutrophils and monocytes into periodontal and periapical tissues, exacerbating local inflammation and increasing the risk of deep-seated infections [13]. This evidence concerns the gene IL6 and rheumatoid arthritis.