Need for Procedural Details in Detection of Periodontopathic Bacterial DNA in the Atheromatous Plaque by PCR

We read with interest the recent paper published by Ishihara and colleagues (1) in which the authors detected the presence of DNA from periodontopathic bacteria in stenotic artery plaques and in samples obtained from periodontal pockets. This group has already published a report describing the detection of Treponema denticola in atherosclerotic lesions by using both PCR and polyclonal serum-based immunofluorescence assay techniques (2).

We agree with the conclusion of Ishihara et al. that these results, taken together with the large amount of already-published epidemiological, microbiological, and clinical data, give support to the hypothesis that periodontopathic bacteria could, in some way, play a role in the pathogenesis of the atheromatous plaque. Anyway, we feel that some additional details could add value to the data presented in this paper.

At first, the title of the paper refers to “carotid coronary artery plaque,” whereas in the text the authors wrote that “… we sought to detect…DNA from stenotic coronary artery plaques…,” and no mention is made anywhere to vascular samples obtained from the carotids. This is in our opinion a point that need to be clarified, since the presence of bacteria could be different in the two vascular segments, and if no specimens from the carotids were studied, there is no reason to include this word in the title of the paper. In addition, in case the authors have been using only vascular fragments obtained from the coronary artery, it could be very useful to describe which segment of these arteries was studied and what have been both the clinical diagnosis and surgical procedures for the patients studied, since it is quite uncommon for the stenotic segment of the coronary artery to be removed during a bypass procedure with a vascular graft. Moreover, the addition of some details about the well-known risk factors for atherosclerosis, like cholesterol plasmatic level and smoking, for the patients that gave the vascular fragments used could increase the significance of these results. Another point that in our opinion needs to be clarified is the real significance of the negative controls used in this study. In fact, 2 clinically unrelated negative vascular samples are quite a disproportionate number when correlated to the 51 specimens obtained from the atherosclerotic patients. In addition, one of these two negative control vascular samples gave a positive result for the presence of Actinobacillus actinomycetemcomitans and for Campylobacter rectus, with the results of the dental examination of these two patients being totally negative and with, as far as we know, the etiology of the Kawasaki syndrome not being strictly related to any bacterial infection. These findings, which demonstrated the presence in the coronary artery of DNA from periodontopathic bacteria in a nonatherosclerotic and periodontally healthy patient, could suggest that these microorganisms are unrelated to the presence of atheromatous plaque. A last point that should benefit from additional details is the statistical analysis performed to assess the correlation between the rates of detection for DNA in periodontal and vascular specimens. In fact, it is quite difficult to understand why the correlation was statistically significant only in the case of detection of Porphyromonas gingivalis and C. rectus DNA and not for other bacteria, such as, for instance, T. denticola, which was detected in a very high percentage of samples (67.7 and 29.4% in subgingival and artery specimens, respectively, in patients showing four or more periodontal lesions). Further clarification of the above points would allow the reader to consider more deeply the results and conclusions of this interesting study, which could improve knowledge of the various factors that may have a role in atherogenesis.