Author(s) year [Ref]

Study design

Outcomes

Conclusions

Hanatani, T., et al., 2012 [20]

Animal study.

8 male mouse injected Aa, 6 cases injected PBS. Experimental MI induced by permanent ligation of the left anterior descending coronary artery

Plasma level of anti-Aa antibody higher in Aa-infected mice than control mice. 7 days after myocardial ischemia, Aa-positive MI hearts showed larger infarct size and length than control mice. Aa-positive MI hearts showed more MOMA-2 positive myocardial infiltrating cells compared to negative MI.

Periodontal pathogen might deteriorate ventricular remodeling after MI through inflammatory cell infiltration

Iwai, T., 2009 [21]

Mini review.

The Medline and Tokyo Medical and Dental University databases were searched to identify the literature currently available on oral bacteria and vascular diseases.

Bacteria from mouth to the bloodstream and then to vein of venous angle near supraclavicular area. Periodontal bacteria, such as Pg, activate platelets and make them mass, including bacteria without phagocytosis. Animal study showed the formation of a small arterial thrombus after continuous intravenous infusion of Pg for 2 - 4 week.

Periodontal bacteria, may play an important role in the development of various vascular diseases, such as atherosclerosis and varicose veins, through bacteremia.

Haraszthy, V.I., et al., 2000 [22] .

Clinical study.

50 specimens obtained, examined Cp, HCMV, and bacterial 16S ribosomal RNA using PCR. 100 ng of chromosomal DNA extracted from specimen. PCR product generated with eubacterial primers transferred and probed with digoxigenin labeled synthetic oligonucleotides for Aa, Bf, Pg, and Pi.

80% of the specimens were positive in 1 or more of PCR assays. 38% were positive for HCMV and 18% positive for Cp. The presence of bacteria in 72% of surgical specimens. 44% of the 50 atheromas were positive for at least one of periodontal pathogens. 30% of surgical specimens were positive for Bf, 26% positive for Pg, 18% positive for Aa, and 14% positive for Pi. 13 (59%) of the 22 periodontal pathogen-positive surgical specimens were positive for 2 or more of the target species

Periodontal pathogens present in atherosclerotic

Plaques, such as Cp. They play a key role in the development of atherosclerosis leading to coronary vascular disease.

Kebschull, M., et al., 2010 [23]

Critical review.

(1) Observational studies; (2) interventional studies; (3) Potential mechanisms linking periodontal infections and atherosclerosis. (4) Periodontal pathogens in animal models of atherogenesis. (5) Available mechanistic studies.

Periodontal treatment resulted in favorable effects on subclinical markers of atherosclerosis. In vitro and in vivo studies established plausibility of a link between periodontal infections and atherogenesis. Utilized models are mostly mono-infections of host cells, and may not adequately portray human periodontitis as a polymicrobial, biofilm-mediated disease.

Periodontal therapy results in lower levels of systemic inflammation and favorable effects on subclinical markers of atherosclerosis.

Gaetti-Jardim, E., et al., 2009 [24]

Clinical study.

44 patients displaying CVD were submitted and endarterectomy of coronary arteries. 60 - 100 mg atherosclerotic tissue removed. Quantitative detection of periodontopathic bacteria using TaqMan probe. Aa, Fn, Pg, Pi, Pn and Tf determined by real-time PCR.

Total bacterial and periodontopathic bacterial DNA found in 94.9% and 92.3% respectively, of atheromatous plaques from periodontitis patients, and in 80.0% and 20.0%, of atherosclerotic tissues from periodontally healthy subjects. DNA represented 47.3% of total bacterial DNA obtained from periodontitis patients. Pg, Aa and Pi detected most often.

Periodontopathic bacteria in coronary lesions are not coincidental and that they may contribute to the development of vascular diseases.

Mattila, K., et al., 1989 [25]

Clinical study.

100 patients with acute MI and 102 controls selected from community at random. Serum total cholesterol, triglyceride, and high density lipoprotein cholesterol measured on admission and 4 weeks. Lipid values obtained during second visit. Dental scores measured. The index ranged from 0 to 10.

Smoking was more common among acute MI, and had lower concentrations of high density lipoprotein cholesterol and higher serum concentrations of triglycerides and C peptide than the controls. Hypertension was more common among patients than controls. Serum total cholesterol concentration was not associated with MI. Total dental index and the pantomography index highly correlated. Two indexes higher among patients than controls.

Dental health was significantly worse in patients with acute MI than in controls. Periodontal disease and dental caries is more common among patients with acute MI than controls