Oral Pathogen Linked to Cardiac Health, New Study Reveals

JAPAN: A recent study conducted by researchers at Tokyo Medical and Dental University (TMDU) in Japan suggest that a common oral pathogen could have detrimental effects on the heart, potentially worsening cardiac conditions, particularly after a heart attack.

Impact of Coronary Heart Disease

Heart attacks, caused by coronary heart disease, occur when blood flow in the coronary arteries is obstructed. This leads to an inadequate supply of oxygen and nutrients to the heart muscle, causing damage to cardiac myocytes and, in severe cases, cardiac rupture. To prevent such damage, cardiac myocytes rely on a cellular process called autophagy to eliminate damaged cellular components, safeguarding the heart from dysfunction.

The research team focused on a periodontal pathogen known as Porphyromonas gingivalis, which has previously been detected at the site of occlusion in myocardial infarction, a severe heart condition. The exact mechanisms behind the impact of this pathogen were not fully understood until now.

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Key Discovery

Yuka Shiheido-Watanabe, the lead author of the study, explained, “Previous studies have shown that the periodontal pathogen Porphyromonas gingivalis can exacerbate post-infarction myocardial fragility. However, the mechanisms underlying this effect remained unknown.”

The researchers took a significant step by creating a mutated version of P. gingivalis, one that doesn’t express its most potent virulence factor called gingipain. Earlier research had suggested that gingipain inhibited cells from undergoing programmed cell death in response to injury. With this new bacterium, the research team infected cardiac myocytes and mice to investigate the consequences.

Yasuhiro Maejima, the corresponding author of the study, clarified the results. “The viability of cells infected with the mutant bacterium lacking gingipain was much higher than that of cells infected with the wild-type bacterium. In addition, the effects of myocardial infarction were significantly more severe in mice infected with wild-type P. gingivalis than in those infected with the mutant P. gingivalis lacking gingipain.”

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Mechanism at Play

Detailed investigations uncovered a critical mechanism. Gingipain was found to interfere with the fusion of autophagosomes and lysosomes, two essential cell components crucial for autophagy. In mice, this interference resulted in larger cardiac myocytes and the accumulation of proteins that would typically be cleared from the cells to protect the cardiac muscle.

Yuka Shiheido-Watanabe explained, “Our findings suggest that infection with P. gingivalis producing gingipain results in excessive autophagosome accumulation, which can lead to cellular dysfunction, cell death, and ultimately cardiac rupture.”

Implications for Heart Health

The study’s findings emphasize the potential impact of P. gingivalis on the cardiac muscle’s ability to repair itself after a heart attack. By treating this common oral infection, it may be possible to reduce the risk of fatal heart attacks and protect cardiac health.

For further information, please refer to the original research published in the International Journal of Oral Science, titled “Porphyromonas gingivalis, a periodontal pathogen, impairs post-infarcted myocardium by inhibiting autophagosome–lysosome fusion.”

Source: Tokyo Medical and Dental University