Dental plaque has been considered a natural occurrence in the human body in response to bacterial invasion of the oral cavity. It is an indication of the extent to which autoimmune mechanisms have been activated in controlling the effects of harmful bacteria upon other organ systems. Studies have shown where heart disease and plaque formation may have an interrelationship. This study seeks to explore this relationship in more depth.
Health Care: Dental Plaque and Heart Disease
The oral cavity is predisposed to bacteria accumulation due to its anatomical structure and functions. A major feature is it inability to shed surfaces as in any other tissues such as the skin. Teeth do not have the capacity to engage in this physiology. Linking heart disease with plaque formation is a pathophysiology, which scientist have found very difficult to explain because there may be many other associating factors influencing the condition besides plaques in the teeth (Kreth, Merritt & Qi, 2009).
One explanation, however, has been that since organisms grow between the teeth creating plaque formation in the same way they can enter the blood stream, especially when gums begin to bleed. Scientists contend that gum bleeding is an inevitable symptom of gum disease. Once this occurs organisms can escape by attaching themselves to pre-existing fatty deposits in coronary arteries. These are the essential arteries, which carry blood supply to the heart. Inflammation can occur resulting in blood clots, which can be released, decreasing blood flow to the heart and developing into a heart attack (Kreth et.al, 2009).
While this sounds plausible the contention still lays in whether coronary heart disease is exclusively caused by teeth plaque formation or it may occur in conjunction with other health conditions such as diabetes and hypertension. Researchers have not able to agree on this issue. As such, this investigation seeks to explore the extent to which plaque formation influences heart disease.
A study conducted by Ohki, Itabashi, Kohno, Yoshizawa, Nishikubo,Watanabe,Yamane and, Ishihara (2012) isolated periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction. These researchers studies 81 myocardial infarction patients who had primary percutaneous coronary intervention (PCI). Thrombus was removed from and samples taken for detection of the presence of periodontal bacteria. 25% of these specimens contained significant amounts of three types of periodontal bacteria. Conclusions were that there is a possibility of these bacteria being latent in plaques which may play a role in plaque inflammation and instability (Ohki, Itabashi, Kohno, Yoshizawa, Nishikubo,Watanabe,Yamane & Ishihara, 2012)
Similar studies have been conducted by de Toledo, Nagata, Yoshida and Oho (2012) which revealed that streptococcus oralis coaggregation receptor polysaccharides induce inflammatory responses in human aortic endothelial cells. These organisms can be found in dental plaques. These researchers examined the capacity of these organisms to induce inflammatory responses in endocardia tissue. All the organisms tested had stimulatory effects on producing inflammatory reactions. Hence, it was concluded that they may have an impact on heart disease (de Toledo, Nagata, Yoshida & Oho, 2012).
Zoellner (2011) discussed incidences in, a literature review, of dental infection and vascular disease confirming that ‘periodontitis is a chronic inflammatory response to bacterial plaque’ (Zoellner, 2011). Consequently, the bone anchoring teeth to soft tissue are destroyed. This involves the spread of infection from dentine to vascular dentine tissue into the circulatory system. Obvious complications are cardiovascular, cerebrovascular, and peripheral artery disease, which has been identified clinically through, angiography, ultrasonography, and reduced flow-mediated dilation. The researcher contends that there are numerous cross-sectional studies confirming the association of periodontitis with heart disease (Zoellner, 2011).
The three studies cited in this investigation while inconclusive regarding the role of dental plaques in inducing heart disease inferences point towards a relationship between the two variables. For example, when Ohki (2012) and counterparts isolated periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction there is indication that the underlying organism came from plaque formation activity (Ohki et.al, 2012).
Importantly, plaque formation is an indication of the extent to which autoimmune mechanisms have been activated in controlling the effects of harmful bacteria upon other organ systems. Consequently, de Toledo (2012) and his group found that streptococcus oralis coaggregation receptor polysaccharides induce inflammatory responses in human aortic endothelial cells. Again this suggests that there is a relationship between plaque formation and heart disease.
Researchers have not been able to identify the direct relationship between the pathophysiology of dental plaque creation in relation to heart disease. However, the progression can be traced to complications of untreated dental plaques resulting in periodontitis as advanced by Zoellner (2011) it establishes the extent to which plaque formation influences heart disease (Zoellner, 2011)
de Toledo A, Nagata E, Yoshida Y, Oho T. (2012). Streptococcus oralis coaggregation receptor polysaccharides induce inflammatory responses in human aortic endothelial cells. Mol Oral Microbiol. 27(4), 295-307.
Kreth, J. Merritt, J., & Qi, F. (2009). Bacterial and Host Interactions of Oral Streptococci. DNA and Cell Biology, 28 (8), 397–403.
Ohki T, Itabashi Y, Kohno T, Yoshizawa A, Nishikubo S, Watanabe S, Yamane G, Ishihara K.(2012). Detection of periodontal bacteria in thrombi of patients with acute myocardial infarction by polymerase chain reaction. Am Heart J, 163(2), 164-7
Zoellner, H. (2011). Dental infection and vascular disease. Semin Thromb Hemost. 37(3), 181-92