Gum Disease Bacteria Linked to Hardening of Heart Valves, Study Suggests

By Boston Editorial Team
New research presented at the American Heart Association's Basic Cardiovascular Sciences Scientific Sessions 2026 indicates that the bacteria Porphyromonas gingivalis, which causes gum disease, may promote calcium buildup in the aortic valve, leading to calcific aortic valve stenosis, a common heart valve disease with no current drug treatments.
Gum Disease Bacteria Linked to Hardening of Heart Valves, Study Suggests

A new study presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions 2026 in Boston suggests that bacteria from gum disease may contribute to the hardening of heart valves, potentially opening a new avenue for prevention and treatment of a common heart condition. The research, conducted on mouse and human cardiac tissue, found a link between periodontitis and calcific aortic valve stenosis (CAVS), a condition where the aortic valve thickens and calcifies, restricting blood flow from the heart.

Currently, there is no medication available to prevent or slow the progression of CAVS, which can lead to fatigue, chest pain, shortness of breath, heart failure, and even premature death. Standard treatment for severe cases is valve replacement surgery. The study identifies a potential biological pathway connecting chronic oral gum disease and infection to CAVS, focusing on the bacterium Porphyromonas gingivalis (P. gingivalis), a key player in gum inflammation and tissue destruction.

Researchers measured bacterial levels in human cardiac valve tissue removed during valve replacement surgery and found that P. gingivalis was significantly more abundant in calcified aortic valves from people with CAVS compared to those with other valve diseases. In mouse experiments, repeated exposure to live P. gingivalis led to bacterial accumulation in aortic valves, increased valve calcification, and symptoms of aortic stenosis. Preventive antibiotic treatment reduced these effects.

The study also revealed that P. gingivalis activates interleukin-1 beta (IL-1b), an inflammation-spurring protein. When researchers genetically deleted IL-1b in mice, calcification and valve symptoms were significantly reduced even in the presence of P. gingivalis. This suggests that targeting this inflammatory pathway could be a potential therapeutic strategy.

“The key message is simple: take good care of your oral health,” said co-lead author Chenyang Li, M.D., a Ph.D. candidate at Fuwai Hospital in Beijing. “Good oral hygiene and treatment of periodontal disease are important for overall health and may also have benefits for cardiovascular health.”

Eduardo Sanchez, M.D., M.P.H., FAHA, chief medical officer for prevention for the American Heart Association, added, “This study adds to the growing evidence that oral health and heart health are closely connected.” The American Heart Association’s Healthy Smiles, Healthy Hearts™ initiative provides dental care teams with professional education highlighting this connection.

The study has limitations as its findings have not been confirmed in people, and the researchers have started a clinical study to further evaluate the link between gum disease and CAVS. The findings are considered preliminary until published in a peer-reviewed scientific journal.

Boston Editorial Team

Boston Editorial Team

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