{"id":769160,"date":"2026-07-17T23:07:21","date_gmt":"2026-07-17T23:07:21","guid":{"rendered":"https:\/\/www.newsbeep.com\/us\/769160\/"},"modified":"2026-07-17T23:07:21","modified_gmt":"2026-07-17T23:07:21","slug":"common-mouth-bacteria-may-trigger-dangerous-calcium-buildup-in-the-heart","status":"publish","type":"post","link":"https:\/\/www.newsbeep.com\/us\/769160\/","title":{"rendered":"Common Mouth Bacteria May Trigger Dangerous Calcium Buildup in the Heart"},"content":{"rendered":"

\"Human<\/a>Human Chest Cavity illustration: Right lung, left lung, heart. Credit: American Heart Association<\/p>\n

A gum disease bacterium may contribute to aortic valve calcification through inflammation, according to preliminary human tissue and mouse research.<\/p>\n

A bacterium best known for damaging gums may also be involved in the hardening of the heart\u2019s aortic valve. Preliminary research presented at the American Heart Association\u2019s Basic Cardiovascular Sciences Scientific Sessions 2026 points to a possible biological connection between chronic periodontal disease and a serious heart valve disorder.<\/p>\n

The condition, called calcific aortic valve stenosis (CAVS), develops when calcium accumulates in the aortic valve, causing it to thicken and narrow. Because this valve controls blood leaving the heart, the narrowing can restrict circulation throughout the body.<\/p>\n

CAVS may cause no noticeable problems at first. As it advances, however, patients can develop fatigue, chest pain, shortness of breath, fainting, heart failure, and premature death. Severe cases are generally treated by replacing the damaged valve<\/a> because no medication has been proven to stop or slow the disease.<\/p>\n

The researchers identified a possible pathway through which long-term gum infection could contribute to valve calcification.<\/p>\n

\"Heart<\/a>4 chambers of the heart: right atrium, right ventricle, left atrium, left ventricle. Credit: American Heart Association<\/p>\n

\u201cThere are currently no medications proven to prevent or slow the progression of CAVS. We hope our findings demonstrating the link between periodontal disease and CAVS will stimulate further research into new preventive and therapeutic approaches for this condition,\u201d said co-lead author of the study, Chenyang Li, M.D., a Ph.D. candidate in the department of cardiology at the State Key Laboratory of Cardiovascular Disease of Fuwai Hospital\u2019s National Center for Cardiovascular Diseases, the Chinese Academy of Medical Sciences and Peking Union Medical College all in Beijing.<\/p>\n

A gum bacterium emerges as a suspect<\/p>\n

The investigation centered on Porphyromonas gingivalis (P. gingivalis), a bacterium that plays an unusually influential role in gum inflammation and the breakdown of tissue supporting the teeth.<\/p>\n

\"Chenyang<\/a>Chenyang Li, M.D., a Ph.D. candidate in the department of cardiology at the State Key Laboratory of Cardiovascular Disease of Fuwai Hospital\u2019s National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College in Beijing. Credit: Chenyang Li<\/p>\n

Previous research has also connected P. gingivalis with inflammation beyond the mouth and with cardiovascular problems, including plaque buildup inside arteries and coronary artery disease. That history made it a plausible candidate for examining the possible link between periodontal disease and damaged heart valves.<\/p>\n

Diseased valves contained more bacteria<\/p>\n

The researchers first turned to human tissue for evidence. They measured bacterial levels in heart valves removed during replacement surgery, comparing samples from patients with CAVS with samples from people who had other valve disorders.<\/p>\n

The goal was to determine whether particular microbes appeared more often in calcified valves. P. gingivalis was not the most common bacterium detected, but its presence differed sharply between valves affected by CAVS and those without the condition.<\/p>\n

\u201cWe were surprised by how much P. gingivalis was present in the calcified aortic valves,\u201d Li said. \u201cAlthough it was not one of the most abundant bacteria overall, it showed one of the largest differences between valves with CAVS and valves without CAVS. This unexpected finding led us to investigate its potential role in the development of CAVS.\u201d<\/p>\n

The human tissue findings could show an association, but they could not establish whether the bacterium contributed to calcification. To explore that question more directly, the researchers moved to experiments in mice.<\/p>\n

Inflammation drove calcification in mice<\/p>\n

The researchers exposed mice to either live P. gingivalis or bacteria that had been inactivated by heat. They then examined whether the microbe accumulated in the aortic valve, increased calcium deposits, and produced signs resembling aortic stenosis.<\/p>\n

Some animals received antibiotics to test whether reducing the bacteria would change the outcome. In another group, the researchers genetically removed or disabled the inflammatory pathway involving interleukin-1 beta (IL-1\u03b2).<\/p>\n

Interleukin-1 beta is a signaling protein produced mainly by immune cells. It helps trigger inflammation, the body\u2019s response to infection or injury, but excessive or persistent activity can also damage tissues.<\/p>\n

Repeated exposure to live P. gingivalis caused the bacterium to build up in the aortic valves of the mice. The animals also developed more valve calcification and stronger signs of aortic stenosis. Preventive antibiotic treatment reduced those effects.<\/p>\n

Inside mouse valve cells, P. gingivalis activated interleukin 1 beta (IL-1b), providing a possible explanation for how infection could encourage calcium buildup.<\/p>\n

The researchers then removed IL-1b genetically. Even when P. gingivalis remained present, the mice developed substantially less valve calcification and fewer symptoms, suggesting that the inflammatory pathway played an important role in the damage.<\/p>\n

The human link still needs testing<\/p>\n

The results do not yet show that P. gingivalis causes CAVS in people. The human tissue analysis identified an association, while the experiments demonstrating a possible mechanism were performed in mice.<\/p>\n

\u201cThe key message is simple: take good care of your oral health,\u201d Li said. \u201dGood oral hygiene and treatment of periodontal disease are important for overall health and may also have benefits for cardiovascular health. While it is still too early to recommend specific treatments for preventing CAVS, our findings suggest that periodontal health could be an important piece of the puzzle.\u201d<\/p>\n

\u201cThis study adds to the growing evidence that oral health and heart health are closely connected,\u201d said Eduardo Sanchez, M.D., M.P.H., FAHA, chief medical officer for prevention for the American Heart Association. \u201cFor many people, regular visits to the dentist are their only connection to the healthcare system. That makes dental professionals important partners in spotting health conditions, including periodontal disease early \u2014 which can lead to quicker healthcare referrals and results, better health and lives saved.\u201d<\/p>\n

Because the findings have not been confirmed in people, they remain preliminary. The researchers have begun a clinical study to investigate whether gum disease and P. gingivalis are linked to CAVS in human patients.<\/p>\n

Meeting: AHA Basic Cardiovascular Sciences Scientific Sessions 2026<\/p>\n

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