Abstract
Periodontitis is a chronic inflammatory condition initiated by dental plaque that progressively damages the structures supporting teeth. It involves complex interactions between bacterial pathogens, the host’s immune responses, and environmental factors such as smoking. Conventionally, periodontitis was attributed to poor oral hygiene, but recent decades have revealed that specific bacterial infections and individual susceptibility play crucial roles. This has shifted the focus toward identifying at-risk individuals and modifiable risk factors. The pathogenesis of periodontitis centers on the dental biofilm, which harbors Gram-negative anaerobic bacteria like Porphyromonas gingivalis. These bacteria trigger immune responses, leading to inflammation and tissue destruction. The disease progresses through acute episodes of tissue damage followed by remission periods. Diabetes mellitus significantly correlates with periodontitis, with evidence suggesting that treating periodontal disease can improve glycemic control in diabetic patients. Smoking is a major environmental risk factor, increasing the prevalence of periodontal pathogens and exacerbating disease outcomes. In addition, periodontitis is linked to myocardial infarction, endothelial dysfunction, peripheral artery disease (PAD), stroke, and heart failure through shared risk factors and inflammatory pathways. Periodontal treatment shows promise in mitigating systemic conditions such as endothelial dysfunction and PAD, although more research is needed to establish definitive links and therapeutic benefits. The ongoing investigation into these associations underscores the importance of periodontal health in overall well-being.
Published Version
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