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Bacterial Link Between Gum Disease and Heart Disease

Bacterial Link Between Gum Disease and Heart Disease

While gum disease and heart disease have long been known to be associated by a bacterial infection common to both illnesses, a new study out of Orebro University in Sweden has clarified the link. The results of the study were published in the journal Infection and Immunity.

The bacterial strain common to both conditions – Porphyromonas gingivalis – is a well-characterized pathogen responsible for the development of periodontitis in infected individuals. Periodontitis is an invasive infection which attacks the soft tissue around the teeth, and eventually degrades the underlying bone.

Torbjörn Bengtsson, a professor in the department of clinical medicine at Orebro University and his team, found that P. gingivalis bacteria were capable of altering the expression of genes involved in the promotion of inflammation and atherosclerosis in the coronary arteries. Atherosclerosis is a condition that results in the accumulation of cholesterol and other fats in the artery walls. As these plaques can eventually break-up – triggering formation of a blood clot – and the coronary arteries supply blood to the heart, atherosclerosis can be a very dangerous condition.

Using animal models, P. gingivalis has previously been implicated in the initiation and hastening of plaque formation in the aorta, as well as the coronary arteries. Though earlier research had identified P. gingivalis within coronary artery plaques in those who have suffered a heart attack, the molecular mechanisms of the bacteria’s involvement in the condition, were not understood.

Bengtsson and his colleagues infected cultured human aortic smooth muscle cells with P. gingivalis bacteria, in order to study their effect. This cell type is used as a model to study disease processes such as atherosclerosis, because changes to this cell type can greatly impact the regular functioning of the heart and associated arteries. Smooth muscle cells are found in the wall of the aorta and are responsible for contracting the artery following each pump of the heart.

The researchers found that following infection, the P. gingivalis bacteria produced gingipains – enzymes that alter the ratio of two angiopoietins involved in inflammation – which increase arterial inflammation, potentially leading to the development of atherosclerosis. The excreted gigipains reduced the expressions of the anti-inflammatory protein angiopoietin 1 (Angpt1), and enhanced the expression of the pro-inflammatory protein angiopoietin 2 (Angpt2).

“Our research clarifies the mechanism behind the association of periodontitis and cardiovascular disease. Our aim is to find biomarkers that can help us diagnose and treat both diseases,” said Boxi Zhang, a PhD student in Prof. Bengtsson’s lab, and first author on the paper. Currently, periodontitis is treated using antibiotics.

Though a cell-signaling protein called tumor necrosis factor (TNF) can also promote atherosclerosis through the inhibition and enhancement of Angpt1 and Angpt2, respectively, the researchers say that gingipains influence the two proteins independently from TNF.