Quantitative Detection of Periodontopathogenic Bacteria in Atherosclerotic Plaques from Coronary Arteries by Real-Time PCR
Nava Naghibi1, *, Naser Sargolzaie2, Amin Khajavi2, Amir Moeintaghavi3, Mohammad Abbasi Tashnizi4, Kiarash Ghazvini5, Farid Shiezadeh3
Epidemiologic studies have suggested periodontitis as a risk factor for coronary artery disease (CAD). Detection of periopathogens in atheromatous plaque provides some evidence for the causal relationship between these two conditions. The aim of this study was to determine the presence and quantity of periopathogens in coronary atherosclerotic plaques in patients undergoing coronary artery bypass graft (CABG) surgery.
20 patients who were candidates for endarterectomy were enrolled in this study for the periodontal examination. Subgingival and coronary atherosclerotic plaque samples were then collected. Thereafter, quantitative detection of Aggregatibacter actinomycetemcomitans (A.a), Porphyromonas gingivali (P.g), and all bacteria detected by Real-Time PCR (RT-PCR) were measured. The correlation analysis was also used to evaluate the relationship between quantities of periopathogens in atherosclerotic and subgingival plaque samples.
A.a was detected in 13 patients (68.4%) with subgingival plaques and 4 patients (20%) with atherosclerotic plaques. In addition, P.g was found in 15 patients (78.9%) with subgingival and 10 patients (50%) with atherosclerotic plaques. A.a represented means of 2.7% and 10.04% of detected bacteria in both atherosclerotic and subgingival plaque samples, respectively. The mean of quantity of P.g was 10.85% and 12.87% of the detected bacteria obtained from atherosclerotic and subginigival samples, respectively. Correlation analysis showed a significant correlation between the quantities of A.a in the atherosclerotic and subgingival plaques, but such a significant relationship was not found for P.g.
This study confirmed the detection of A.a and P.g in atheromatous plaque. The quantitative data suggested that periopathogens comprise a significant proportion of atherosclerotic plaque microbiome, which may consequently contribute to the development of CAD.
* Address correspondence to this author at Department of Periodontology, Mashhad University of Medical Sciences, Mashhad, Iran; E-mail: firstname.lastname@example.org