PMID- 11887470
OWN - NLM
STAT- MEDLINE
DCOM- 20020612
LR  - 20161021
IS  - 1553-0841 (Print)
IS  - 1553-0841 (Linking)
VI  - 6
IP  - 1
DP  - 2001 Dec
TI  - Role for periodontal bacteria in cardiovascular diseases.
PG  - 41-7
AB  - 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.
FAU - Kuramitsu, H K
AU  - Kuramitsu HK
AD  - Department of Oral Biology, University at Buffalo, Buffalo, New York, USA.
FAU - Qi, M
AU  - Qi M
FAU - Kang, I C
AU  - Kang IC
FAU - Chen, W
AU  - Chen W
LA  - eng
GR  - DE08293/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Ann Periodontol
JT  - Annals of periodontology
JID - 9702874
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cholesterol, LDL)
RN  - 0 (Multienzyme Complexes)
RN  - EC 1.6.- (NADH oxidase)
RN  - EC 1.6.- (NADH, NADPH Oxidoreductases)
RN  - EC 3.4.24.35 (Matrix Metalloproteinase 9)
MH  - Animals
MH  - Arteriosclerosis/metabolism
MH  - Bacteroidaceae Infections/*complications
MH  - Cardiovascular Diseases/*microbiology
MH  - Cell Line
MH  - Cell Membrane/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Cholesterol, LDL/metabolism
MH  - Endothelium, Vascular/enzymology
MH  - Enzyme Induction
MH  - Foam Cells/pathology
MH  - Humans
MH  - Macrophages/enzymology
MH  - Matrix Metalloproteinase 9/biosynthesis
MH  - Mice
MH  - Multienzyme Complexes/biosynthesis
MH  - NADH, NADPH Oxidoreductases/biosynthesis
MH  - Oxidation-Reduction
MH  - Periodontal Diseases/*microbiology
MH  - Porphyromonas gingivalis/enzymology/metabolism/*physiology
MH  - Vacuoles/physiology
EDAT- 2002/03/13 10:00
MHDA- 2002/06/13 10:01
CRDT- 2002/03/13 10:00
PHST- 2002/03/13 10:00 [pubmed]
PHST- 2002/06/13 10:01 [medline]
PHST- 2002/03/13 10:00 [entrez]
AID - 10.1902/annals.2001.6.1.41 [doi]
PST - ppublish
SO  - Ann Periodontol. 2001 Dec;6(1):41-7. doi: 10.1902/annals.2001.6.1.41.