Thinking of skipping the floss? Your heart might thank you if you don’t. A new Hiroshima University (HU) study finds that the gum disease-causing bacterium Porphyromonas gingivalis (P. gingivalis) can enter the bloodstream and invade the heart. There, it quietly promotes a buildup of scar tissue (called fibrosis) that distorts the heart’s structure, interferes with electrical signaling, and increases the risk of atrial fibrillation (AFib).
Clinicians have long noticed that people with periodontitis, a common gum disease, appear to be more susceptible to cardiovascular problems. A recent meta-analysis shows that periodontitis is associated with a 30% higher risk of developing AFib, a potentially serious heart rhythm disorder that can lead to stroke, heart failure, and other life-threatening complications.
Globally, cases of atrial fibrillation (AFib) have nearly doubled in less than a decade, from 33.5 million cases in 2010 to about 60 million cases in 2019. Now, there’s a growing scientific curiosity about how gum disease might be contributing to this surge.
Past research has suggested that inflammation might be to blame. When immune cells in the gums band together to fight off infection, the chemical signals they release can inadvertently leak into the bloodstream, triggering systemic inflammation that can damage organs far from the mouth.
But inflammation isn’t the only threat that escapes the inflamed gums. Researchers have found DNA from harmful oral bacteria in heart muscle, valves, and even fatty arterial plaques. Among them, Porphyromonas gingivalis has received special attention for its role in a growing number of systemic diseases, including Alzheimer’s disease, diabetes, and certain cancers.
It has previously been detected in the brain, liver, and placenta. But how it takes root in the heart has been unclear. The study, published in the journal Circulation, provides the first clear evidence that Porphyromonas gingivalis in the gums can enter the left atrium in animal models and humans, pointing to a potential microbial pathway linking periodontitis to atrial fibrillation.
Among the many periodontal bacteria, Porphyromonas gingivalis has a high pathogenicity for periodontitis and some systemic diseases outside the oral cavity. In this study, we explored two key questions: Does P. gingivalis migrate from periodontitis lesions to the left atrium? If so, does it induce the progression of atrial fibrosis and atrial fibrillation?
To mimic how P. gingivalis escapes the oral cavity and wreaks havoc elsewhere, the researchers created a mouse model using the invasive W83 strain of the bacterium. They divided 13-week-old male mice into two groups: one group had the strain introduced into the dental pulp and the other remained uninfected. Each group was further subdivided into subgroups and observed for 12 or 18 weeks to track cardiovascular risks of long-term exposure.
Intracardiac stimulation, a diagnostic technique for arrhythmias, showed no difference in AFib risk between infected and uninfected mice at 12 weeks. But by 18 weeks, tests showed that mice exposed to the bacteria were six times more likely to develop arrhythmias, with 30 percent of mice inducing AFib, compared with just 5 percent of controls. To determine if their model accurately replicated periodontitis, the researchers examined jaw bone lesions and found telltale signs of it.
They detected dental pulp caries and microabscesses caused by P. gingivalis. But the damage didn’t stop there. They also found the bacteria in the heart’s left atrium, where infected tissue had become stiff and fibrotic. Using loop-mediated isothermal amplification to detect specific genetic signatures, the team confirmed that the strain of P. gingivalis they had introduced was present in the heart.
In contrast, uninfected mice had healthy teeth, and heart tissue samples showed no trace of the bacteria. Twelve weeks after infection, mice exposed to P. gingivalis already had more heart scarring than uninfected mice. At 18 weeks, scarring in infected mice had climbed to 21.9 percent, compared with just 16.3 percent in controls, which may be related to aging, suggesting that P. gingivalis may not only trigger early heart damage but also accelerate its progression over time.
And this troubling link isn’t just seen in mice. In another human study, researchers analyzed tissue from the left atria of 68 AFib patients who underwent heart surgery. P. gingivalis was found there, too, and in greater numbers in people with severe gum disease.
Past studies have shown that P. gingivalis is able to invade host cells and evade destruction by autophagosomes, the cell’s garbage disposal machines. This ability to lurk inside cells suggests it could bypass immune defenses, trigger mild inflammation, and cause damage without being cleared.
Infected mice showed a surge in levels of galectin-3, a biomarker for fibrosis, and increased expression of the transforming growth factor 1 (Tgfb1) gene, a gene associated with inflammation and scarring. These findings suggest that brushing, flossing, and regular dental checkups may not only promote oral hygiene but also protect the heart.