The link between oral ill health and cardiovascular problems has been known for some time. Previous research has shown that bacteria from the mouth can enter the bloodstream and cling to damaged areas, resulting in inflammation, which may lead to atherosclerosis. Now, new preliminary research has suggested a possible connection between gum disease and calcific aortic valve stenosis (CAVS), further reinforcing the mouth-heart relationship.
The findings were presented at the American Heart Association’s Basic Cardiovascular Sciences Scientific Sessions 2026, held in Boston, US, this month. The researchers presented data showing a possible link between the bacteria that cause gum disease and the build-up of calcium in the heart’s aortic valve, potentially leading to CAVS.
Specifically, the researchers looked at Porphyromonas gingivalis (P gingivalis), which is a bacterium known to play a significant role in gum disease by causing gum inflammation and the degradation of gum tissue. P gingivalis has also been associated with systemic inflammation.
In this research, the team measured bacterial levels in heart valve tissue in patients who had undergone valve replacement surgery. This was compared to valve tissue from patients who had other heart conditions.
Dr Chenyang Li, Department of Cardiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital’s National Centre for Cardiovascular Diseases, the Chinese Academy of Medical Sciences, and Peking Union Medical College, Beijing, commented: “We were surprised by how much P gingivalis was present in the calcified aortic valves. 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.”
And investigate they did, using mouse models. Either live or heat-inactivated P gingivalis were administered to the mice to establish what the bacteria were doing in the aortic valve and some of the mice were given preventive antibiotics. Others had the IL-1b inflammatory pathway genetically removed.
In short, they found that repeated exposure to the bacteria resulted in an accumulation in the aortic valves, calcification, and symptoms consistent with aortic stenosis. They also showed that genetically deleting IL-1b significantly reduced valve calcification and disease symptoms, even when P gingivalis was present.
“There are currently no medications proven to prevent or slow the progression of CAVS,” said Dr Li. He expressed hope that the findings would stimulate further research into new preventive and therapeutic approaches for the condition.
“…. Good 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.”
If these findings are confirmed in human studies, they would add to the growing body of evidence linking oral health and cardiovascular disease. That is a message that deserves to be widely shared – not only with the public, but also among dental professionals and other healthcare providers.
In a separate study, researchers from the University of Minnesota (UM), US, published work that suggests it’s possible to nullify the bacteria that cause gum disease without obliterating the ‘good’ bacteria in the mouth.
They discovered that dental plaque bacteria use chemical signals to co-ordinate growth and ‘talk’ to each other. Blocking those signals encouraged healthier bacteria to thrive, while hampering the microbes implicated in gum disease. This cross-talk process, known as ‘quorum sensing’, helps the approximately 700 bacterial species that inhabit our mouths to exchange chemical messages. Targeting the right bacteria and interrupting those signals can stop gum disease in its tracks, they postulated in npj Biofilms and Microbiomes.
Speaking upon the study’s publication in late 2025, Prof Mikael Elias, Associate Professor in the College of Biological Sciences at UM and senior author of the study, commented: “Dental plaque develops in a sequence, much like a forest ecosystem. Pioneer species like Streptococcus and Actinomyces are the initial settlers in simple communities – they’re generally harmless and associated with good oral health.
“Increasingly diverse late colonisers include the ‘red complex’ bacteria like Porphyromonas gingivalis, which are strongly linked to periodontal disease. By disrupting the chemical signals bacteria use to communicate, one could manipulate the plaque community to remain or return to its health-associated stage.”
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