A study, published in Infection and Immunity, has clarified the mechanism behind a known link between gum disease and heart disease. Periodontitis, which results in an infection that damages the soft-tissue surrounding teeth and the bone supporting the teeth, is commonly caused by Porphyromonas gingivalis. P. gingivalis is a Gram-negative anaerobe that colonizes mouth tissues for lengthy periods of time after initial infection. It is commonly found within the arterial plaques common to heart disease patients.
The study authors discovered that the bacteria alters the gene expression of pro-inflammatory proteins that also promote coronary artery atherosclerosis. This was discovered by infecting cultured human aortic smooth muscle cells with P. gingivalis. Aortic smooth muscle cells were used because they contract the aorta after the pumping of the heart stretches it out.
After P. gingivalis was injected into the cells, the bacteria released gingipains. Gingipains are enzymes that change the ratio between different angiopoietins (inflammatory proteins) in such a way that inflammation is increased. The pro-inflammatory angiopoietin 2 had its expression increased by the gingipains, whereas the anti-inflammatory angiopoietin 1 had its expression reduced. P gingivalis was found to affect the levels of these proteins independent of tumor necrosis factor (TNF).
The study is significant because it helps to pinpoint the relationship between periodontitis and heart disease. Further research can help clarify potential targets for treatment of atherosclerosis.
- Periodontitis and heart disease share a common pathogen, P. gingivitis.
- A study found that P. gingivitis alters gene expression to increase production of the pro-inflammatory protein angiopoietin 2 and decreases presence of the anti-inflammatory protein angiopoietin 1. This results in increased atherosclerosis.
- The study further clarifies the cardiovascular risk of poor oral health and hygiene.
Paddock C. Scientists uncover bacterial mechanism that links gum disease to heart disease. published in the journal Infection and Immunity. September 14, 2015.