<p>Periodontitis and atherosclerosis are chronic inflammatory diseases which share some common risk factors including aberrant release of pro-inflammatory cytokines and an imbalance in the levels of reactive oxygen species (ROS). Several studies have suggested a potential link between the two diseases with supporting evidence of periodontal pathogens detected in atherosclerotic lesions. The proposed mechanism as reported in the literature involves the accumulation of periodontal pathogens entering into the bloodstream and thereby contributing to atherosclerotic plaque formation. However, the underlying factors contributing to this association remain largely underexplored. Hence, this review is crucial in addressing this gap in knowledge by emphasizing the roles of endothelial dysfunction, autophagy and mitophagy as key mechanisms linking periodontitis to an increased risk of future cardiovascular complications, particularly atherosclerosis. Exploring and understanding these cellular pathways would provide valuable insights into the predisposition of periodontitis to future cardiovascular events. Furthermore, this review also aims to bring awareness to the serious systemic complication of periodontitis and highlight the need for the development of targeted therapeutic strategies to control atherosclerosis in periodontitis patients and prevent future cardiovascular complications.</p>

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A narrative review on bridging the gap between periodontitis and cardiovascular disease: exploring the cellular and molecular mechanisms of periodontitis-driven atherosclerosis

  • Rithwik Kumar,
  • Anuradha Dhanasekaran,
  • Priyanka Venugopal

摘要

Periodontitis and atherosclerosis are chronic inflammatory diseases which share some common risk factors including aberrant release of pro-inflammatory cytokines and an imbalance in the levels of reactive oxygen species (ROS). Several studies have suggested a potential link between the two diseases with supporting evidence of periodontal pathogens detected in atherosclerotic lesions. The proposed mechanism as reported in the literature involves the accumulation of periodontal pathogens entering into the bloodstream and thereby contributing to atherosclerotic plaque formation. However, the underlying factors contributing to this association remain largely underexplored. Hence, this review is crucial in addressing this gap in knowledge by emphasizing the roles of endothelial dysfunction, autophagy and mitophagy as key mechanisms linking periodontitis to an increased risk of future cardiovascular complications, particularly atherosclerosis. Exploring and understanding these cellular pathways would provide valuable insights into the predisposition of periodontitis to future cardiovascular events. Furthermore, this review also aims to bring awareness to the serious systemic complication of periodontitis and highlight the need for the development of targeted therapeutic strategies to control atherosclerosis in periodontitis patients and prevent future cardiovascular complications.