Periodontitis as a systemic inflammatory driver

Abstract

Current scientific data demonstrate a radical revision of the concept of periodontitis as a localized inflammatory process in favor of its consideration as a powerful driver of systemic inflammation. The pathogenetic role of specific periodontal pathogens, especially Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, is realized through the activation of Toll-like receptors and NF-κB-dependent pathways, which leads to a massive release of proinflammatory cytokines and the formation of a stable systemic inflammatory response. Metastatic spread of bacteria and their toxins creates conditions for the development of distant pathological foci in the cardiovascular system, which is confirmed by the detection of periodontal pathogens in the myocardium, pericardial fluid and vascular intima. The key mechanism of systemic impact is the development of endothelial dysfunction through decreased NO synthase activity and activation of VCAM-1 and ICAM-1 adhesion molecules. Progression of the inflammatory process leads to structural changes in the myocardium through activation of fibrotic processes and creates prerequisites for the development of arrhythmias. Systematic analysis of long-term consequences has established an increased risk of developing cardiovascular diseases and the formation of multimorbid conditions in patients with periodontitis. The concept of periodontal pockets as a reservoir for systemic dissemination of pathogens substantiates the multifactorial nature of the systemic impact of periodontitis through microbiological, microcirculatory, immunological and metabolic mechanisms. The data obtained substantiate the need to revise clinical approaches to the diagnosis and treatment of periodontitis with the development of integrated therapeutic strategies aimed at correcting the local inflammatory process and its systemic manifestations.