Bacteria behind dental gingivitis may cause cardiac scarring and trigger atrial fibrillation

A common gum disease caused by the bacteria Porphyromonas gingivalis (P. gingivalis) has been linked to the accumulation of scar tissue in the heart muscle and a heightened risk of developing atrial fibrillation (AF). A study from Hiroshima University (HU) has found that P. gingivalis can enter the bloodstream and damage heart muscle by causing scar tissue to buildup – fibrosis – which in turn can interfere with its electrical signalling to cause AF.

Worldwide, AF cases have nearly doubled in the past ten years, up from 33 million in 2010 to around 60 million by the end of the decade with gum disease seen as a potential contributing factor to that spike.

Research has previously suggested that inflammation was at cause with immune cells in the gums when fighting infection give an opportunity for chemical signalling in that inflammatory response to enter the bloodstream. Once there they could bring about a systemic response which damaged other organs, including the heart.

And in the clinic, healthcare professionals had been aware for some time that patients with periodontitis – a common form of gum disease – seem to be more prone to cardiovascular disease.

However, inflammation wasn’t the only threat from the periodontitis with research having found the DNA of oral bacteria present in heart muscle, valves and even arterial plaques. The bacteria P. gingivalis has been suspected to have a role in other systemic diseases, including Alzheimer’s, diabetes, and certain cancers, and now with cardiovascular disease. It has previously been detected in brain tissue, the liver and the placenta. 

The study by the HU team draws a link between P. gingivalis in the gums and its presence in the left atrium of the heart in both animal models and humans. This suggests a prospective pathway for the microbe which links periodontitis and AF.

“The causal relationship between periodontitis and AF remains unknown, but the spread of periodontal bacteria through the bloodstream may connect these conditions,” said Assistant Professor Shunsuke Miyauchi, at HU’s Graduate School of Biomedical and Health Sciences and the first author on the study.

“Among various periodontal bacteria, P. gingivalis is highly pathogenic to periodontitis and some systemic diseases outside the oral cavity. 

“In this study, we have addressed these two key questions: Does P. gingivalis translocate to the left atrium from the periodontitis lesion? And if so, does it induce the progression of atrial fibrosis and AF?”

The research team divided 13-week-old male mice into two groups, and in the first group introduced the aggressive W83 strain of the P. gingivalis into the tooth pulp, with in the second remaining uninfected. Each cohort was further divided into other groups to track the cardiovascular risks of prolonged exposure at 12 and 18 weeks.

At 12 weeks no difference was found in AF risk between infected and uninfected mice when the AF diagnostic technique of intracardiac stimulation was used. However, by week 18, the mice that had been exposed to P. gingivalis were found to be six times more likely to have AF induced at 30% compared to just 5% in the control group.

However, at 12 weeks post-infection, those mice exposed to P. gingivalis did already show more heart scarring than their uninfected counterparts. And at 18 weeks, the heart scarring in the infected group had climbed to 21.9% compared to 16.3% in the control group. This suggested that P. gingivalis may not just trigger early heart damage but also accelerate it.

The research team saw jaw lesions and found signs of periodontitis disease. Tooth pulp decay and micro abscesses caused by P. gingivalis were also detected. And, importantly, evidence of the bacteria was found in the left atrium of the mice’s hearts, with the tissue being fibrous and having stiffened. Loop-mediated isothermal amplification confirmed that the P. gingivalis W83 strain the team had introduced was present in the heart. By contrast, the control group had both healthy teeth and no trace of P. gingivalis in their heart tissue.

In a separate study in humans, researchers analysed left atrial tissue from 68 AF patients who underwent cardiac surgery. P. gingivalis was also found there and in greater amounts in people who had severe gum disease.

“P. gingivalis invades the circulatory system via the periodontal lesions and [can] translocate to the left atrium, where its bacterial load correlates with the clinical severity of periodontitis. 

“Once in the atrium, it exacerbates atrial fibrosis, which results in higher AF inducibility,” Miyauchi said. 

“Therefore, periodontal treatment, which can block the gateway of P. gingivalis translocation, may play an important role in AF prevention and treatment.”

“For the next step, we’re investigating the specific mechanisms by which P. gingivalis affects atrial cardiomyocytes,” Miyauchi added. 

“We’re also now focusing on establishing a collaborative medical and dental system in Hiroshima Prefecture to treat cardiovascular diseases, including atrial fibrillation. We aim to expand this initiative nationwide in the future,” he concluded.