Bacteria in Dental Plaque and Atheroma Plaque

Overview

Periodontitis is considered a focus of infection where oral bacteria, bacterial by-products or inflammatory mediators can interact with other parts of the organism via the blood. Periodontal pathogen components such as DNA, RNA or specific antigens of P. gingivalis, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Treponema denticola (T. denticola), Fusobacterium nucleatum (F. nucleatum) or Campylobacter rectus have been isolated from different tissues such as atheroma plaques, placenta, amniotic sac and respiratory tract. It has been reported that periodontitis may contribute to endothelial dysfunction leading to the formation of atherosclerosis.

Periodontitis is considered a focus of infection where oral bacteria, bacterial by-products or inflammatory mediators can interact with other parts of the organism via the blood. Periodontal pathogen components such as DNA, RNA or specific antigens of P. gingivalis, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Treponema denticola (T. denticola), Fusobacterium nucleatum (F. nucleatum) or Campylobacter rectus have been isolated from different tissues such as atheroma plaques, placenta, amniotic sac and respiratory tract. It has been reported that periodontitis may contribute to endothelial dysfunction leading to the formation of atherosclerosis. Severe chronic generalized periodontitis may result in systemic inflammation and endothelial dysfunction. Periodontal bacteria produce endotoxins in the form of lipopolysaccharide (LPS). Circulating LPS causes an early systemic inflammatory response in the intima. The aim of this study is to assess the relationship between bacteria in atheroma plaque, and dental plaque in patients grouped using the new periodontal classification. In addition, the relationship between demographic findings and bacterial count and frequency will be evaluated.

Conditions