This literature review discusses the findings of more recent studies investigating the relationship between chronic inflammatory periodontal disease and risk for cardiovascular disease and stroke. The intensity of inflammation in moderate and severe chronic periodontitis is clearly sufficient to induce a systemic response. The systemic response is commonly expressed by elevated serum levels of inflammatory mediators and acute-phase reactants like C-reactive protein (CRP), interleukin- 6 (IL- 6), interleukin- 8 (IL- 8), tumor necrosis factor-alpha (TNF-α), serum amyloid A, fibrinogen, and haptoglobin. The presence of chronic oral inflammation may enhance atherosclerotic pathogenesis through one or more mechanisms, such as stimulation of humoral and cell-mediated inflammatory pathways, bacteremia leading to direct interaction of periodontal pathogenic microbes with the arterial wall, and increases in circulating mediators of inflammation.
There are many clinical studies and investigations using animal models that, when collectively considered, indicate a significant association of periodontitis with cardiovascular and cerebrovascular diseases. Although a direct causal relationship remains to be demonstrated, it appears that at the very least, periodontitis represents a systemic inflammatory burden that facilitates atheroma formation, which may lead to a cardiovascular or cerebrovascular event.
Citation: Gapski R, Cobb CM. Chronic inflammatory periodontal disease: A risk factor for cardiovascular disease and ischemic stroke? Grand Rounds in Oral-Sys Med. 2006;1:14-22.
Hujoel and colleagues1 have calculated that among individuals with chronic periodontitis, the surface area of the dentogingival epithelium exposed to potential bacterial invasion and/or infiltration of antigenic microbial components ranges between 8 cm2 and 20 cm2. Thus, it is not surprising that a breach of this epithelial barrier is a common occurrence in chronic and aggressive periodontitis, and is likely to result in systemic dissemination of microbes, antigens, and mediators of inflammation.
Locally, bacteria and their byproducts of metabolism stimulate a cellular immune response represented by a dense infiltration of neutrophils, macrophages, and various lymphoid cells. These cells and the host connective tissue cells associated with the inflammatory lesion are stimulated to synthesize and release proinflammatory cytokines and prostanoids — interleukin-1 (IL-1), interleukin- 6 (IL- 6), interleukin- 8 (IL- 8), tumor necrosis factor-alpha (TNF-α), prostaglandin E (PGE ), and various matrix metalloproteinases (MMPs) — which play a role in the destruction of
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