Gum disease bacteria may spur calcium build-up in the heart’s aortic valve, leading to a common and serious heart valve disease, according to preliminary, independent research in China.
This study—presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions 2026—held in Boston, 13-16 July identifies a potential biological pathway linking chronic oral gum disease and infection to calcific aortic valve stenosis (CAVS).
“There 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,” co-lead author Dr Chenyang Li said.
The researchers focused on Porphyromonas gingivalis, measuring different bacterial levels in human cardiac valve tissue removed during valve replacement surgery. They studied samples from people with CAVS and from those with other valve diseases.
“We were surprised by how much P. gingivalis was present in the calcified aortic valves,” Dr Li said.
“Although 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.”
Using mice, researchers also explored how P. gingivalis might be linked to the development of CAVS. Researchers gave mice live and heat-inactivated P. gingivalis to see if the bacteria built up in the aortic valve, caused more calcification and led to symptoms of aortic stenosis. Some mice received antibiotics, while in others the IL-1β inflammatory pathway was genetically disabled or removed.
Researchers found that repeated exposure of mice to live P. gingivalis led to the accumulation of bacteria in aortic valves, increased valve calcification and symptoms of aortic stenosis, while preventive antibiotic treatment reduced these effects. In the mouse valve cells, P. gingivalis activated interleukin-1 beta (IL-1b), an inflammation-spurring protein made mainly by the body’s immune cells.
In further testing, when researchers genetically deleted IL-1b in the mice, calcification and valve symptoms were significantly reduced even in the presence of P. gingivalis.
“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,” Dr Li said.
