A new study from Hiroshima University (HU) has found that the gum bacterium Porphyromonas gingivalis(P. gingivalis) can enter the bloodstream and infect the heart. There, unnoticed, it promotes the formation of scar tissue – known as fibrosis – which deforms the heart structure, disrupts electrical signals and increases the risk of atrial fibrillation (AFib).
Bacteria Can Enter the Heart and Trigger a Serious Cardiac Arrhythmia
Doctors have long observed that people with periodontitis, a common form of gum disease, appear to be more susceptible to cardiovascular problems. A recent meta-analysis has found a link with a 30% higher risk of atrial fibrillation, a potentially serious heart rhythm disorder that can lead to stroke, heart failure and other life-threatening complications. Worldwide, cases of atrial fibrillation have almost doubled in less than a decade, from 33.5 million in 2010 to around 60 million in 2019. Now there is growing scientific curiosity about how gum disease could be contributing to this increase.
Previous research has identified inflammation as a likely cause. When immune cells in the gums mobilize to fight infection, the chemical signals they release can inadvertently enter the bloodstream, triggering systemic inflammation that can damage organs far from the mouth. However, inflammation is not the only danger posed by inflamed gums. Researchers have discovered DNA from harmful oral bacteria in heart muscle, heart valves and even fatty arterial plaques. Among these bacteria, P. gingivalis is particularly in the spotlight as it is suspected of playing a role in a growing number of systemic diseases, including Alzheimer’s, diabetes and certain cancers. It has previously been detected in the brain, liver and placenta. However, how it manages to establish itself in the heart was previously unclear. This study, published in Circulation, provides the first clear evidence that P. gingivalis can invade the left atrium from the gums in both animal models and humans, suggesting a possible microbial pathway linking periodontitis to atrial fibrillation.
“The causal relationship between periodontitis and atrial fibrillation is still unknown, but the spread of periodontitis bacteria through the bloodstream could link these diseases,” said the study’s first author, Shunsuke Miyauchi, assistant professor at HU’s Graduate School of Biomedical and Health Sciences. Among the various periodontal bacteria, P. gingivalis is highly pathogenic for periodontitis and some systemic diseases outside the oral cavity. In this study, the researchers investigated two central questions: Does P. gingivalis migrate from the periodontitis lesion to the left atrium? And if so, does it induce the progression of atrial fibrosis and atrial fibrillation?
Link Between Gum Disease and Atrial Fibrillation
To simulate how P. gingivalis might escape from the mouth and cause damage elsewhere, the researchers developed a mouse model using the aggressive W83 strain of the bacterium. They divided 13-week-old male mice into two groups: In one group, the strain was introduced into the dental pulp, while the other remained uninfected. Each group was further divided into subgroups and observed for 12 and 18 weeks to track the cardiovascular risks of prolonged exposure.
Intracardiac pacing – a diagnostic technique for cardiac arrhythmias – showed no difference in AFib risk between infected and uninfected mice at 12 weeks. However, at week 18, tests showed that mice exposed to the bacterium were six times more likely to develop arrhythmias, with an AFib inducibility rate of 30% compared to only 5% in the control group.
To test whether their model accurately replicated periodontitis, the researchers examined jaw lesions and found clear signs of it. They found dental pulp decay and microabscesses caused by P. gingivalis. But that was not all. They also discovered the bacteria in the left atrium of the heart, where the infected tissue had become stiff and fibrotic. Using loop-mediated isothermal amplification to detect specific genetic signatures, the team confirmed that the P. gingivalis strain they had introduced was present in the heart. In contrast, the uninfected mice had healthy teeth and no traces of the bacteria in the heart tissue samples.
Twelve weeks after infection, mice exposed to P. gingivalis already showed more heart scarring than their uninfected counterparts. After 18 weeks, scarring had increased to 21.9% in the infected mice, compared to the likely age-related 16.3% in the control group. This suggests that P. gingivalis not only triggers early heart damage, but also accelerates it over time. And this disturbing correlation was not only observed in mice. In a separate study in humans, researchers analyzed the tissue of the left ventricle of 68 atrial fibrillation patients who had undergone heart surgery. P. gingivalis was also found there, and in larger quantities in people with severe gum disease.
Improving Cardiovascular Care
Previous studies have shown that P. gingivalis can invade host cells and evade destruction by autophagosomes, the cellular garbage collectors. This ability to hide in cells suggests that it can sneak past immune defenses and trigger just enough inflammation to cause damage without being excreted. Infected mice showed an increase in galectin-3, a biomarker for fibrosis, and higher expression of Tgfb1, a gene associated with inflammation and scarring. The findings suggest that brushing, flossing and regular dental visits could not only promote oral hygiene but also help protect the heart. Healthy gums could block the way for infection with P. gingivalis.
The team is now working to strengthen interdisciplinary collaboration between medical and dental professionals in Hiroshima Prefecture to improve cardiovascular care. “Our next step is to investigate the specific mechanisms by which P. gingivalis affects atrial cardiomyocytes,” says Miyauchi. The researchers are also currently focusing on establishing a cooperative medical and dental system in Hiroshima Prefecture for the treatment of cardiovascular diseases, including atrial fibrillation, and plan to expand this initiative throughout Japan in the future.