Abstract
Objectives. Interest in periodontitis as a potential risk factor for atherosclerosis and its complications resulted from the fact that the global prevalence of periodontal diseases is significant and periodontitis may induce a chronic inflammatory response. Many studies have analyzed the potential impact of the Porphyromonas gingivalis, major pathogen of periodontitis, on general health. The purpose of this study was to find the presence of the Porphyromonas gingivalis DNA in the atherosclerotic plaques of coronary and carotid arteries and in the periodontal pockets in patients with chronic periodontitis, who underwent surgery because of vascular diseases. Methods and Results. The study population consisted of 91 patients with coronary artery disease or scheduled for carotid endarterectomy. The presence of Porphyromonas gingivalis DNA in atheromatous plaques and in subgingival samples was determined by PCR. Bacterial DNA was found in 21 of 91 (23%) samples taken from vessels and in 47 of 63 (74.6%) samples from periodontal pockets. Conclusions. Porphyromonas gingivalis DNA is frequently found in atheromatous plaques of patients with periodontitis. That is why more research should be conducted to prove if this periopathogen may have an impact on endothelium of patients at risk of atherosclerosis.
Highlights
Research over the past two decades has suggested that, beyond the conventional risk factors leading to the development and progression of atherosclerotic plaques, the condition may result from microorganisms, increased levels of fibrinogen, the level of the white blood cell count, C-reactive proteins, and antibodies directed against heat shock proteins HSP 60
The DNA of Porphyromonas gingivalis was detected in 28 samples from periodontal pockets in group A patients (87.5%) and in 19 patients in group B (61.3%)
There was no statistically significant association between these findings. Comparison between these two test groups of patients showed a difference in the prevalence of Porphyromonas gingivalis DNA in samples taken from vessels
Summary
Research over the past two decades has suggested that, beyond the conventional risk factors leading to the development and progression of atherosclerotic plaques, the condition may result from microorganisms, increased levels of fibrinogen, the level of the white blood cell count, C-reactive proteins, and antibodies directed against heat shock proteins HSP 60. On this basis, the immunoinflammatory theory of atherosclerosis was established, according to which atherosclerosis is a chronic immunofibroproliferative inflammatory response to factors that damage vascular endothelial cells [1]. The presence of the DNA of several microorganisms in atherosclerotic plaques, for example, Chlamydia pneumoniae, Helicobacter pylori, Cytomegalovirus (CMV), and HSV, has been reported [2,3,4,5].
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