Periodontitis and RA exhibit several common features, including shared pathogenetic processes, cytokine profiles, inflammatory markers and genetic associations, such as HLA-DRB1.67 Both conditions are linked to polymorphisms in IL-1β and TNF-α, as well as the presence of citrullinated proteins and RF.67 Furthermore, these diseases share a pathobiology characterised by elevated pro-inflammatory cytokines, reduced tissue inhibitors of metalloproteinases, increased MMPs and prostaglandin E2 (PGE2), all of which contribute to the tissue destruction observed in periodontitis and RA.68 This evidence concerns the gene TNF and rheumatoid arthritis.