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Dental Infection and Vascular Diseases

  1. Cultivation of Enterobacter Hormaechei from Human Atherosclerotic Tissue. [Aim: To determine whether culturable bacterial strains are present in human atheromatous tissue and to investigate their properties using culture, quantitative PCR, metagenomic screening, genomic and biochemical methods. Methods: We analyzed femoral atherosclerotic plaque and five pairs of diseased and healthy arterial tissue for the presence of culturable bacteria using cell cultures and genomic analysis. Results: Gram negative aerobic bacilli were cultivated from the plaque tissue. Ribosomal 16S DNA amplification and sequencing identified the isolates as Enterobacter hormaechei. The isolate was resistant to ampicillin, cefazolin, and erythromycin. A circular 10kb plasmid was isolated from the strain. Antibiotic protection assays of the isolate demonstrated invasive ability in a human monocytic cell line. To extend the study, five matched pairs of diseased and healthy aortic tissue were analyzed via quantitative PCR. Eubacterial 16S rDNA was detected in all specimens, however, E. hormaechei DNA was detected in surprisingly high numbers in two of the diseased tissues only. Conclusions: While it is well documented that inflammation is an important risk factor for vascular pathophysiology, the association of bacteria with atherosclerosis has not been clearly established, in large part due to the inability to isolate live bacteria from atheromatous tissue. This is the first study providing direct evidence of Enterobacter spp. associated with atheromatous tissues. The data suggest that chronic infection with bacteria may be an under-reported etiologic factor in vascular pathogenesis. Importantly, characterization of the clinical isolate supports a model of atherogenesis where systemic dissemination of bacteria to atherosclerotic sites may occur via internalization in phagocytic cells.] Rafferty B, Dolgilevich S, et al. Journal of Atherosclerosis and Thrombosis,Advanced Publication, Sept 2010.  http://www.jstage.jst.go.jp/article/jat/advpub/0/advpub_1010190295/_article
  2. Dental Disease, Coronary Heart Disease and Stroke, and Inflammatory Markers. [In addition to "classical" risk factors for coronary heart disease (CHD) and stroke, "emerging" risk predictors (which may also play roles in pathogenesis) include measures of chronic infections and of chronic, low-grade activation of inflammation and of hemostasis. As all dental healthcare professionals know (butprobably fewer medical practitioners and their patients), the oral cavity is a major site of chronic infection and inflammation, particularly periodontal disease. In recent years there has been increasing interest in the "periodontal-systemic connection" between dental health parameters and the risks of cardiovascular disease, respiratory disease, diabetes mellitus, osteoporosis, and adverse pregnancy outcomes.] Lowe G, Circulation 2004;109:1076-1078.http://circ.ahajournals.org/cgi/content/full/109/9/1076 .
  3. Dental disease, fibrinogen and white cell count; links with myocardial infarction? [Inflammatory dental disease may be a determinant of fibrinogen level and white cell count in the general population, and that fibrinogen and white cell count may be two mediators of the link between dental disease and myocardial infarction.] Kweider M, Lowe GD, et. al, Scott med J. 1993 Jun;38(3):73-4. Department of Oral Surgery, Dental Hospital & School, Glasgow. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8356427&dopt=Abstract.
  4. Dental infection and vascular disease. [Periodontitis is a chronic inflammatory response to bacterial plaque in which the anchoring bone and soft tissues supporting teeth are destroyed, resulting in tooth mobility and loss. Dental caries involves the spread of infection from the dentine to the vascular dental pulp and periapical bony tissues, before involvement of adjacent soft tissues and spreading sepsis. Several case-controlled, cross-sectional, and cohort studies report correlation between periodontitis and increased cardiovascular, cerebrovascular, and peripheral artery disease, as determined by clinical disease, angiography, ultrasonography, and reduced flow-mediated dilation. Some studies report a similar relationship of atherosclerosis with periapical infection and potentially also with coronal caries, and this review identifies the need to investigate these associations further. Smoking and cadmium exposure are epidemiologically confounding environmental risk factors shared by atherosclerosis and periodontitis. Further complicating epidemiological studies are the risk factors for both atherosclerosis and periodontitis, with which periodontitis appears to have separate positive feedback relationships. These include diabetes, increased plasma lipid levels, hypertension, and white blood cell count. Animal and human intervention studies provide some direct support of a causal role for periodontitis in atherosclerosis, and possible mechanisms include bacterial invasion of arteries, specific atherogenic properties of oral bacteria, the acute phase response, and cytokine polymorphisms.] Zoellner H. Semin Thromb Hemost. 2011 Apr;37(3):181-92. Epub 2011 Mar 31.http://www.ncbi.nlm.nih.gov/pubmed/21455852