Role for periodontal bacteria in cardiovascular diseases.
BACKGROUND
Several epidemiological studies as well as a recent animal model approach have suggested a role for periodontal diseases in the development of cardiovascular disease (CVD). This relationship could be mediated by inflammatory responses induced by periodontal pathogens as well as direct interaction of these organisms with cardiac tissue.


METHODS
In order to explore these possibilities, the effects of the periodontal pathogen Porphyromonas gingivalis on cellular events proposed to play a role in CVD were investigated.


RESULTS
P. gingivalis, as well as its outer membrane vesicles (OMV), was able to induce foam cell formation (an important characteristic of CVD) in the murine macrophage cell line J774 A.1. This property appears to be mediated by the lipopolysaccharide (LPS) fraction of the cells. Several other oral bacteria were also able to induce foam cell formation. Furthermore, since the rupture of the fibrous cap of plaque appears to be an important factor in acute coronary syndrome, it was demonstrated that P. gingivalis 381 degraded fibrous caps isolated from autopsy samples. In addition, it was observed that strain 381 strongly induced matrix metalloproteinase (MMP)-9 protease activity, implicated in plaque rupture, from the J774 A.1 macrophages. Finally, strain 381 was able to enhance monocyte chemoattractant protein-1 (MCP-1) and NADH oxidase expression from endothelial cells.


CONCLUSIONS
Therefore, P. gingivalis exhibits several properties which could play a role in CVD as mediators of LDL oxidation, foam cell formation, and rupture of atherosclerotic plaque.
Kuramitsu
H K
HK
Department of Oral Biology, University at Buffalo, Buffalo, New York, USA.
Qi
M
M
Kang
I C
IC
Chen
W
W
D000818:Animals; D001161:Arteriosclerosis / Q000378:metabolism; D016866:Bacteroidaceae Infections / Q000150:complications*; D002318:Cardiovascular Diseases / Q000382:microbiology*; D002460:Cell Line; D002462:Cell Membrane / Q000502:physiology; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis; D008078:Cholesterol, LDL / Q000378:metabolism; D004730:Endothelium, Vascular / Q000201:enzymology; D004790:Enzyme Induction; D005487:Foam Cells / Q000473:pathology; D006801:Humans; D008264:Macrophages / Q000201:enzymology; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis; D051379:Mice; D009097:Multienzyme Complexes / Q000096:biosynthesis; D009247:NADH, NADPH Oxidoreductases / Q000096:biosynthesis; D010084:Oxidation-Reduction; D010510:Periodontal Diseases / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000201:enzymology / Q000378:metabolism / Q000502:physiology*; D014617:Vacuoles / Q000502:physiology
D018932:Chemokine CCL2; D008078:Cholesterol, LDL; D009097:Multienzyme Complexes; C023107:NADH oxidase; D009247:NADH, NADPH Oxidoreductases; D020780:Matrix Metalloproteinase 9