Streptococcus mutans in atherosclerotic plaque: Molecular and immunohistochemical evaluations.

OBJECTIVES: To verify the presence of Streptococcus mutans (S. mutans) in atherosclerotic plaque (AP) using techniques with different sensitivities, correlating with histological changes in plaque and immunoexpression of inflammatory markers. MATERIALS AND METHODS: Thirteen AP samples were subjected to real-time polymerase chain reaction (qRT-PCR), histopathological analyses, histochemical analysis by Giemsa staining (GS), and immunohistochemical analysis for S. mutans, IL-1ß, and TNF-α (streptavidin-biotin-peroxidase method). Ten necropsy samples of healthy vessels were used as controls. RESULTS: All AP samples showed histopathological characteristics of severe atherosclerosis and were positive for S. mutans (100.0%) in qRT-PCR and immunohistochemical analyses. GS showed that Streptococcus sp. colonized the lipid-rich core regions and fibrous tissue, while the control group was negative for Streptococcus sp. IL-1ß and TNF-α were expressed in 100% and 92.3% of the AP tested, respectively. The control samples were positive for S. mutans in qRT-PCR analysis, but negative for S. mutans, IL-1ß, and TNF-α in immunohistochemical analyses. CONCLUSION: The detection of S. mutans in AP and the visualization of Streptococcus sp. suggested a possible association between S. mutans and atherosclerosis. The results obtained from the control samples suggested the presence of DNA fragments or innocuous bacteria that were not associated with tissue alteration. However, future studies are necessary to provide more information.

Relationship of Streptococcus mutans with valvar cardiac tissue: A molecular and immunohistochemical study.

BACKGROUND: The present study aimed to investigate the presence or absence of Streptococcus mutans in oral cavity and valvular samples associating with the histomorphologic alterations of calcified aortic stenosis. METHODOLOGY: Dental plaque and cardiac valve samples were collected from 10 patients with calcified aortic stenosis for molecular analysis of S mutans by real-time polymerase chain reaction (PCR). Healthy valve tissue was also collected from five young cadavers and analyzed for S mutans. Moreover, fragments of all valvar specimens were submitted for histomorphological analysis and immunohistochemistry (anti-S mutans and anti-CD61). RESULTS: Streptococcus mutans was present in 100% of the oral cavity samples from the patients with calcified aortic stenosis in the molecular analysis. The analysis by real-time PCR showed that S mutans presented the same proportion in healthy valves and those with calcified aortic stenosis (80%; P = 1.000). Conversely, the immunoexpression of S mutans was 37.40 (IC95% = 1.49-937.00) times superior in samples of patients with cardiac disease (P = .007). The immunoexpression analysis showed that CD61 was present in seven (70%) calcified aortic stenosis samples, all of which were also immunopositive for S mutans. CONCLUSIONS: Streptococcus mutans was found in the oral cavity, healthy valve tissue, and calcified aortic stenosis samples. However, the microorganism was visualized by immunohistochemistry only in the calcified aortic stenosis samples, which may suggest viability and an increased bacterial density in this condition. The association of the presence of S mutans and positive CD61 immunoexpression suggests a probable relationship with calcified aortic stenosis.

Effect of ancestry on interleukin-10 haplotypes in chronic periodontitis.

Chronic periodontitis is caused by an inflammatory reaction of the periodontal tissues and alveolar bone. This inflammation is caused by periodontopathic bacteria located in the subgingival biofilm, resulting in inflammatory reactions that may lead to loss of attachment. This tissue destruction is a consequence of host immune and inflammatory responses to specific periodontal pathogens and their metabolic products. Cytokines modulate the immune response, altering its efficiency in the competition against pathogens and increasing periodontal susceptibility. This study investigated genetic polymorphisms in Interleukin 10 (A-1082G, C-819T and C-592A) in 205 individuals from an admixed Brazilian population. A significantly increased risk of developing chronic periodontitis was observed in individuals with low IL-10 production and Amerindian ancestry. These results suggest that the polymorphisms A-1082G, C-819T, and C-592A, which are associated with ancestry, are involved in the susceptibility to the development of chronic periodontitis in an admixed northern Brazilian population.