Scientists have long linked severe gum disease to inflammation throughout the body and a higher risk of heart problems, including coronary artery disease, which can raise the risk of heart attack. Studies have also found that treating gum disease can improve blood-vessel health.
Dr. Elena Aikawa, a professor of medicine at Harvard Medical School who was not involved in the study, said the findings "fit well with our current understanding of calcific aortic valve disease as an active, inflammation-driven disease rather than simply wear and tear of the valve."
How mouth bacteria harm the heart
CAVD affects millions of people worldwide, and there are no approved drugs that slow or stop its progression. As the disease worsens, people may develop fatigue, shortness of breath and chest pain, and in severe cases, they often require valve-replacement surgery.
In CAVD, calcium builds up in the aortic valve, which connects the left side of the heart to the large artery that carries oxygen-rich blood to the body. (Image credit: Noctiluxx via Getty Images)
P. gingivalis is known to be particularly destructive to gum tissue, causing lots of inflammation, and it's been tied to cardiovascular disease in the past. To see if the bacterium might be directly impacting heart health, researchers at Fuwai Hospital in Beijing looked for P. gingivalis in aortic valve tissue removed during valve-replacement surgery. They compared this diseased tissue to valves that weren't calcified.
To test whether the bacteria might directly contribute to valve damage, Li and colleagues injected live P. gingivalis into the bloodstreams of healthy lab mice. The bacteria reached the animals' aortic valves, triggering inflammation, calcium buildup and narrowing of the valve.
A comparison group of mice was given antibiotics before the injection and had less bacteria in their aortic valves and slower disease progression. Meanwhile, mice injected with dead P. gingivalis bacteria did not show any changes in their aortic valves.
Related storiesThe researchers traced the changes in the mice's hearts to interleukin-1 beta, a signalling molecule that normally helps the body fight infections. Exposure to P. gingivalis ramped up the production of this molecule, and in turn, the immune signal switched on genes that pushed healthy valve cells to behave more like bone-building cells, which is a hallmark of CAVD. This switch causes the cells to lay down calcium in the surrounding valve tissue.
That said, the team also saw the same pattern in human valve cells grown in the lab. Exposure to P. gingivalis increased inflammation and calcium buildup among the cells, while blocking interleukin-1 beta blunted those effects.
This article is for informational purposes only and is not meant to offer medical advice.
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