Fig. 1.

There are 2 main hypotheses to explain the link between periodontitis and cardiovascular disease. A, Bacteria or their by-products (primarily lipopolysaccharides or antigens) can disseminate from the oral cavity into blood vessels and, there, a host response can lead to damage and atherosclerotic plaque formation. B, Alternatively, localized inflammation from periodontitis enhances ongoing chronic inflammation due to atherosclerosis. Periodontal disease–derived reactive oxygen species contribute to systemic oxidative stress and inflammatory mediators, including various interleukins, chemokines, cytokines (IL-X), immunoglobulins, and inflammatory cells (lymphocytes, macrophages, neutrophils), contribute to a destructive immune response at areas in the vessel wall prone to atherosclerosis.