One of these mechanisms is based on the potential effects of the inflammatory phenomenon of periodontitis on the systemic dissemination of the locally produced mediators such as C-reactive protein (CRP), interleukins-1 beta (IL-1β) and -6 (IL-6), and tumor necrosis factor-alpha (TNF-α;).[2] Periodontitis creates a burden of bacterial pathogens, antigens, endotoxins, and inflammatory cytokines that contribute to the process of atherogenesis and thromboembolic events. Here, IL1B is linked to periodontitis.