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The connection between mouth bacteria and inflammation in heart disease

Cell Press

Oral infections are the most common diseases of mankind and are also a key risk factor for heart disease, which is the leading cause of death worldwide. In a review article published in Trends in Endocrinology and Metabolism on April 16, researchers summarize the latest clinical evidence supporting a link between oral infections, which are caused by the bacteria in our mouth, and heart disease, and they emphasize the important role of inflammation in both of these conditions.

"Given the high prevalence of oral infections, any risk they contribute to future cardiovascular disease is important to public health," says senior author Thomas Van Dyke of the Forsyth Institute. "Unravelling the role of the oral microbiome and inflammation in cardiovascular disease will likely lead to new preventive and treatment approaches." The (oral) microbiome refers to the totality of microorganisms in a body part-in this case the mouth--that we all co-exist with.

The most common oral infections are cavities and periodontal diseases such as gingivitis and periodontitis, which are chronic inflammatory diseases that slowly and steadily destroy the supporting structures of multiple teeth. Significant epidemiological evidence supports an association between oral infections, particularly periodontitis, and stroke, especially among men and younger individuals.

Inflammation plays a major role both in oral infections such as periodontitis and in cardiovascular disease. However, over-the-counter nonsteroidal anti-inflammatory drugs such as ibuprofen can produce significant cardiovascular side effects, which means it is crucial that we consider alternative therapies. A high dose of a commonly prescribed cholesterol-lowering medication, atorvastatin, which boosts blood levels of anti-inflammatory molecules called lipoxins and resolvins, prevents both periodontal and cardiovascular inflammation and reverses existing disease in humans. This is exciting and promising because lipoxins and resolvins also have the advantage of naturally controlling inflammation without suppressing the immune system.

"New discoveries of natural pathways that resolve inflammation have offered many opportunities for revealing insights into disease pathogenesis and for developing new pharmacologic targets for the treatment of both oral infections and cardiovascular disease," Van Dyke says.

In future studies, it will be important to compare the effectiveness of these inflammation-reducing molecules, which we produce naturally, and other interventions that could potentially prevent or reverse periodontitis and cardiovascular disease. Another open question is whether there is a reverse relationship between these conditions: what if the onset of cardiovascular disease influences the presence or progression of periodontal disease? Or what are some of the common genetic mechanisms underlying periodontitis and cardiovascular disease?

In the meantime, Van Dyke recommends that people take better care of their teeth to potentially lower their risk of cardiovascular disease and other health problems. "The majority of diseases and conditions of aging, including obesity and type 2 diabetes, have a major inflammatory component that can be made worse by the presence of periodontitis," he says. "Periodontitis is not just a dental disease, and it should not be ignored, as it is a modifiable risk factor."

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Trends in Endocrinology & Metabolism, Kholy et al.:"Oral infections and cardiovascular disease" http://dx.doi.org/10.1016/j.tem.2015.03.001

Trends in Endocrinology & Metabolism (TEM), published by Cell Press, is a monthly review journal that publishes polished, concise, highly read and cited articles of topics at the cutting edge of metabolic diseases covering both clinical and research aspects of the field; from state-of-the-art treatments of endocrine diseases to new developments in molecular biology. For more information, please visit http://www.cell.com/trends/endocrinology-metabolism. To receive media alerts for TEM or other Cell Press journals, please contact press@cell.com.

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