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Archives of cardiovascular diseases
Volume 104, n° 5
pages 352-358 (mai 2011)
Doi : 10.1016/j.acvd.2011.02.002
Received : 17 April 2010 ;  accepted : 25 February 2011
Evaluating periodontal risk for patients at risk of or suffering from atherosclerosis: Recent biological hypotheses and therapeutic consequences
Évaluer le risque parodontal chez les patients à risque ou présentant une pathologie athéromateuse : hypothèses biologiques actuelles et conséquences thérapeutiques
 

Figure 1




Figure 1 : 

Clinical views of periodontitis. Major clinical signs are gingival inflammation (a), calculus (b) and gingival retraction (c).


Figure 2




Figure 2 : 

Bacterial theory: periodontal bacteria such as P.  gingivalis promote the development of atheromatous plaque via virulence factors. The effects of bacteria on the atheromatous plaque are dependent on the presence of other cardiovascular risk factors.


Figure 3




Figure 3 : 

Process of atherogenesis and role of direct and indirect periodontal factors.

Periodontal pathogens may directly and indirectly affect blood cells and blood vessels, resulting in foam-cell formation. CRP: C-reactive protein; Hsp: heat shock protein; IL-1b: interleukin-1b; MCP-1: monocyte attractant protein-1; M-CSF: macrophage colony-stimulating factor; oxLDL: oxidized low-density lipoprotein; PGE2: prostaglandin E2; ROI: rate of infection; TNF-a: tumour necrosis factor-a; VCAM: vascular cell adhesion molecule [39].


Figure 4




Figure 4 : 

Inflammatory theory: infection of epithelial cells by periodontal bacteria promotes the production of proinflammatory cytokines. These cytokines (TNF-⍺, IL-1β, PGE-2) enter the blood circulation and affect cells in atheromatous plaques, leading to the development of atherosclerosis in the presence of other risk factors.


Figure 5




Figure 5 : 

Immune theory: the host’s immune system will react in response to the presence of bacteria. With the monocytic hyperinflammation phenotype, the host reaction will lead to the production of cytokines, which are deleterious for host cells. Cross-reactivity between anti-Hsp will induce destruction of host cells and the development of atherosclerosis.

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