Toothbrush protects the cardiovascular system

Kirill Stasevich, "Science and Life"

Among the many factors that increase the risk of atherosclerosis, along with habitual stress, smoking, poor nutrition, etc., there are also problems with teeth and gums – although, it would seem, how can the condition of the oral cavity affect the health of blood vessels? Nevertheless, according to medical statistics, people with periodontal diseases (the so-called complex of tissues connecting the tooth to the bone) are more likely to suffer from diseases of the cardiovascular system. Research by Maria Febbraio from the University of Alberta and her colleagues from the Cleveland Hospital (Researcher finds link between heart, gum disease) helps to understand why this happens. 

Many probably guessed that it's not without bacteria, because they cause the lion's share of diseases of the teeth and oral mucosa. If we talk about gum inflammation, then one of the most "popular" pathogen microbes is Porphyromonas gingivalis. When mice genetically predisposed to atherosclerosis were infected with it, characteristic changes in the walls of blood vessels began to actively appear in the animals, which then give rise to atheromatous plaques. 

Plaques are formed with the active participation of immune cells, while signaling molecules involved in triggering an inflammatory reaction are involved. The researchers were able to find the CD36 cellular receptor with which the bacterium P.gingivalis interacts. The CD36 protein sends a signal to toll-like receptors – they are responsible for innate immunity and are among the first to be triggered in response to infection. Toll-like receptors stimulate the synthesis of interleukin-1beta (IL1B), which triggers inflammation. The full results of the experiments are published in PLoS ONE (Brown et al., CD36/SR-B2-TLR2 Dependent Pathways Enhance Porphyromonas gingivalis Mediated Atherosclerosis in the Ldlr KO Mouse Model). 

It was previously known that both interleukin IL1B and toll-like receptors are involved in the development of both atherosclerosis and gum disease. However, not all molecular "players" were known, and the description of CD36 is very complementary to the picture. Bacteria sitting in the mouth irritate the receptor, forcing the cells to emit inflammatory signals that are carried through the blood vessels. Of course, P.gingivalis alone is unlikely to be able to provoke atherosclerosis, but if a person also eats incorrectly, or smokes, or is simply genetically predisposed, like those experimental mice, then why not? 

For doctors, the new results mean that they have another potential target for suppressing bad inflammation. The more we know about the molecular chain involved in a particular pathogenic process, the more specific, the more accurately we can act on it. In the case of such a multifactorial disease as atherosclerosis, this is especially important. 

Here it is worth remembering another bacterium called Streptococcus mutans – it also lives in the mouth, and it is to it that we owe the appearance of plaque. Releasing acids, streptococcus destroys tooth enamel, and usually its violent activity in the oral cavity ends with a visit to the dentist. But it happens that S.mutans is not limited exclusively to the mouth. If a microbe gets into the blood, it can easily get to the heart, and that's where more serious troubles begin than plaque. Streptococcus multiplies intensively in the heart, preferring heart valves, which leads to endocarditis (inflammation of the inner lining of the heart), fraught with death. So regular brushing of teeth can protect you not only from caries, but also from serious problems with the cardiovascular system. 

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02.07.2015