Gingivitis Bacteria Causes Harms in the Heart, Impairing Already Poor Recovery from Heart Attack

Inflammatory periodontal disease is caused by a specific bacterial species. The bacteria can use damaged gums to enter the bloodstream. It is thought that its ability to provoke inflammation can then contribute to cardiovascular disease and dementia, though the size of the effect is up for debate. Along these lines, researchers here show that periodontal bacteria can worsen the consequences of a heart attack, impairing the already limited ability of the heart to regenerate and restore function following injury.

Heart attacks occur when blood flow in the coronary arteries is blocked, resulting in an inadequate supply of nutrients and oxygen to the heart muscle, and ultimately death of cardiac myocytes. To prevent this, cardiac myocytes use a process known as autophagy to dispose of damaged cellular components, keeping them from causing cardiac dysfunction. Previous studies have shown that the periodontal pathogen Porphyromonas gingivalis, which has been detected at the site of occlusion in myocardial infarction, can exacerbate post-infarction myocardial fragility. However, the mechanisms underlying this effect remained unknown.

To investigate this, researchers created a version of P. gingivalis that does not express gingipain, its most potent virulence factor, which an earlier study showed can inhibit cells from undergoing programmed cell death in response to injury. They then used this bacterium to infect cardiac myocytes or mice. "The results were very clear. 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."

More detailed investigation of this effect showed that gingipain interferes with fusion of two cell components known as autophagosomes and lysosomes, a process that is crucial to autophagy. In mice, this resulted in an increase in the size of cardiac myocytes and accumulation of proteins that would normally be cleared out of the cells to protect the cardiac muscle. "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."