“Undisclosed Danger Inside Your Mouth: Researchers Uncover a Connection Between a Common Oral Pathogen and Increased Heart Attack Damage”

A recent study conducted by Tokyo Medical and Dental University has shed light on a concerning link between the oral pathogen Porphyromonas gingivalis and impaired heart muscle repair following a heart attack. This discovery implies that addressing oral infections could potentially play a pivotal role in preventing fatal heart attacks.

The research conducted by scientists at Tokyo Medical and Dental University has revealed that Porphyromonas gingivalis, a bacterium responsible for gum disease, can disrupt the fusion of autophagosomes and lysosomes. This interference exacerbates the process of heart tissue regeneration and heightens the risk of heart rupture following a heart attack.

Regular dental hygiene practices, such as brushing and flossing, not only contribute to maintaining a radiant smile but also hold the potential to safeguard your heart. Recent findings from Japan emphasize that an infected oral cavity might lead to cardiac complications.

Published in the International Journal of Oral Science and conducted by Tokyo Medical and Dental University, the study highlights how a common oral pathogen can impede the self-repair mechanisms of cardiac myocytes following a heart attack triggered by coronary heart disease.

In the context of heart attacks, coronary arteries become obstructed, resulting in an insufficient supply of nutrients and oxygen to the heart muscle, ultimately leading to the death of cardiac myocytes. To counteract this process, cardiac myocytes employ autophagy, a cellular mechanism that eliminates damaged components, thereby preventing cardiac dysfunction.

The bacterium P. gingivalis, through the release of gingipain, disrupts autophagy by inhibiting the fusion of autophagosomes and lysosomes, which consequently leads to cardiac dysfunction. This inhibition hinders the normal clearance of cellular proteins, causing an increase in the size of cardiac myocytes and an accumulation of proteins within the cells, posing a threat to cardiac muscle health.

Lead author Yuka Shiheido-Watanabe comments, “Previous studies had already established that the periodontal pathogen Porphyromonas gingivalis, often found at the site of occlusion in myocardial infarction, could worsen post-infarction myocardial fragility. However, the underlying mechanisms remained elusive.”

To unravel this mystery, the researchers engineered a variant of P. gingivalis that does not produce gingipain, its most potent virulence factor, known to inhibit programmed cell death in response to injury. Subsequently, they used this modified bacterium to infect cardiac myocytes and mice.

The results were unequivocal. Cells infected with the gingipain-deficient mutant bacterium exhibited significantly higher viability compared to cells infected with the wild-type P. gingivalis. Moreover, mice infected with the wild-type P. gingivalis experienced significantly more severe effects from myocardial infarction than those infected with the gingipain-deficient mutant.

A deeper investigation into this phenomenon unveiled that gingipain disrupts the fusion of autophagosomes and lysosomes, a critical step in autophagy. In mice, this disruption led to an enlargement of cardiac myocytes and the accumulation of proteins that would typically be eliminated to safeguard cardiac muscle function.

Shiheido-Watanabe concludes, “Our findings indicate that infection with P. gingivalis, particularly the strain producing gingipain, results in an excessive buildup of autophagosomes, leading to cellular dysfunction, cell death, and ultimately, cardiac rupture.”

Given the substantial impact of P. gingivalis on the cardiac muscle’s ability to regenerate after a heart attack, addressing this common oral infection could potentially reduce the risk of fatal heart attacks.

This groundbreaking research was made possible through funding from the Ministry of Education and the MSD Life Science Foundation.

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• Tokyo Medical and Dental University
• International Journal of Oral Science
• Ministry of Education
• MSD Life Science Foundation