New Delhi, May 17 People suffering from gum disease may be at an increased risk of developing heart rhythm disorder also known as atrial fibrillation, according to a study.
Researchers from Hiroshima University in Japan found that gum disease-causing bacterium Porphyromonas gingivalis (P. gingivalis) can slip into the bloodstream and infiltrate the heart.
Once in the heart, it quietly drives scar tissue buildup -- distorting the heart’s architecture, disrupting electrical signals, and raising the risk of atrial fibrillation (AFib) -- a potentially serious heart rhythm disorder that can lead to stroke, heart failure, and other life-threatening complications.
Globally, AFib cases nearly doubled in under a decade, rising from 33.5 million in 2010 to roughly 60 million by 2019. Growing evidence suggests that gum disease might be contributing to the surge.
The study, published in the journal Circulation, provides the first clear evidence that P. gingivalis in the gums can work its way into the left atrium in both animal models and humans, pointing to a potential microbial pathway linking periodontitis to AFib.
“The causal relationship between periodontitis and atrial fibrillation is still unknown, but the spread of periodontal bacteria through the bloodstream may connect these conditions,” said Shunsuke Miyauchi, Assistant Professor at the varsity’s Graduate School of Biomedical and Health Sciences.
For the study, the team created a mouse model using the bacterium’s aggressive W83 strain. They divided 13-week-old male mice into two groups: one had the strain introduced into the tooth pulp, and the other remained uninfected.
Each was further split into subgroups and observed for either 12 or 18 weeks to track the cardiovascular risks of prolonged exposure.
The results revealed no difference in AFib risk between infected and uninfected mice at 12 weeks.
But by week 18, tests showed that mice exposed to the bacterium were six times more likely to develop abnormal heart rhythms, with a 30 per cent AFib inducibility rate compared to just 5 per cent in the control group.
Further, the team also spotted P. gingivalis in the heart’s left atrium, where infected tissue had turned stiff and fibrous.
In contrast, the uninfected mice had healthy teeth and no trace of the bacterium in heart tissue samples.
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