Both CVD and periodontitis involve an inflammatory process and dysregulation of the immune system. Since periodontal diseases are initiated by bacteria, which leads to host immunologically mediated tissue destruction48,49 the influence of periodontitis on CVD may be two-fold: 1) the increase in local and systemic pro-inflammatory mediators and 2) the induction of systemic , which can then lead to an increase in a systemic inflammatory response.
Periodontal tissue breakdown occurs in response to bacterial stimuli as a result of the host inflammatory response. This tissue breakdown is mediated by pro-inflammatory cytokines and mediators such as interleukin-1ß (IL-1ß), interleukin-6 (IL-6), 79 Bacteria associated with periodontal diseases can colonize the atheromatous plaques.78 This colonization can cause damage by elevating local inflammation levels, leading to atheroma formation, maturation, and rupture. At the same time, a low-grade systemic elevation of inflammatory markers could result from or elevated levels of circulating pro-inflammatory cytokines from periodontal pockets and this could induce atherogenesis or growth.80necrosis factor-α (TNF-α), prostaglandin E2 (PGE2), receptor activator of nuclear factor kapp B ligand (RANKL), and matrix metalloproteinases (MMPs). These pro-inflammatory mediators interact with bacteria and the surrounding tissues and can influence disease susceptibility and severity.
Inflammation is central to the pathophysiology of both periodontitis and CVD. The role of inflammatory mediators in the interaction of these disease is thought to be critical. A summary of some of the potential key mechanisms are shown in Figure 3.