Systemic inflammation emerges as a central mediator, with periodontitis inducing chronic low-grade inflammation marked by elevated levels of pro-inflammatory cytokines—namely interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6)—which exacerbate atherosclerosis and contribute to vascular dysfunction [9]. This evidence concerns the gene IL1B and periodontitis.