Periodontal disease (PD) is generated by microorganisms. These microbes can enter the general circulation causing a bacteraemia. The result can be adverse systemic effects, which could promote conditions such as cardiovascular disease. Level A evidence supports that PD is independently associated with arterial disease. PD is a common chronic condition affecting the majority of Americans 30 years of age and older. Atherosclerosis remains the largest cause of death and disability. Studies indicate that the adverse cardiovascular effects from PD are due to a few putative or high-risk bacteria: Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola or Fusobacterium nucleatum. There are three accepted essential elements in the pathogenesis of atherosclerosis: lipoprotein serum concentration, endothelial permeability and binding of lipoproteins in the arterial intima. There is scientific evidence that PD caused by the high-risk pathogens can influence the pathogenesis triad in an adverse manner. With this appreciation, it is reasonable to state PD, due to high-risk pathogens, is a contributory cause of atherosclerosis. Distinguishing this type of PD as causal provides a significant opportunity to reduce arterial disease.
Bacteraemia with germs from the oral cavity was well documented in a publication in 1954. The landmark study indicated systemic spread of oral microbes occurs frequently. The per cent incidence found was 40% with periodontal cleaning, 35% with dental extractions, 24% with brushing and up to 17% with mastication.1 The spread of these oral bacteria throughout the body happens quickly. This results in acute and chronic inflammation, which can be pathological. High-risk periodontal pathogens include Aggregatibacter actinomycetemcomitans (Aa), Porphyromonas gingivalis (Pg), Tannerella forsythia (Tf), Treponema denticola (Td) and Fusobacterium nucleatum (Fn). They are prevalent in periodontitis. These germs enter the systemic circulation directly, and they also produce endotoxins such as lipopolysaccharides (LPS). These endotoxins generate inflammatory cytokines, upregulate endothelial adhesion molecules and induce a prothrombotic environment. These actions can favour the formation of arterial disease and can enhance the risk of an atherothrombotic event.2 Using DNA to identify putative oral bacteria, several studies have documented their presence within atheroma. In 2009, 44 patients underwent coronary endarterectomies. Thirty-nine of the subjects had periodontal disease (PD). Thirty-six of the specimens from patients with PD were positive for oral pathogens.
The most common were Pg and Aa. Sixty-four per cent of those atheromas had two or more pathogens. Only one of the atheroma from a patient without PD demonstrated any oral pathogens.3 In 2011, 42 carotid endarterectomy specimens were analysed for oral pathogen DNA. Every atheroma had at least one pathogen, and many had multiple pathogens. Again, the most common bacteria were Pg and Aa. 4 Oral pathogens create bacteraemia, and those bacteria, especially the high-risk microbes, are frequently associated with atherosclerotic lesions. The American Heart Association (AHA) stated after an extensive review of the literature that PD was independently associated with arteriosclerotic vascular disease (ASVD). This relationship was demonstrated with level A evidence. They discussed in their statement several plausible mechanisms by which PD could be associated with arterial disease. One explanation involves systemic inflammation, which can occur with periodontitis.
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