The pathogenesis of periodontitis is a result of complex interactions between the periodontal pathogens and immune response.5 Some studies have reported the activity of periodontal pathogens and the presence of inflammatory cytokines [interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α), and others] in systemic inflammatory diseases.6 Cardiovascular diseases, such as atherosclerosis, showed associations with periodontitis through inflammatory markers; immune markers also presented in rheumatoid arthritis (RA),6 especially C-reactive protein and IL-1β. This evidence concerns the gene CRP and rheumatoid arthritis.