Patients with Parodont Diseases Have Disorders of Vascular Endothelial Function

Abstract

Endothelin (ET), a key regulatory peptide, plays a crucial role in various physiological and pathological processes, including the progression of periodontal diseases. This study examines the multifaceted involvement of ET in the intricate interactions between periodontal pathogens, host defense mechanisms, and the immune system. Pathogenic bacteria such as Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans release virulence factors that induce immune activation and tissue destruction. In response, innate and adaptive immune cells produce pro-inflammatory cytokines (IL-1, TNF-α, IL-8) and matrix metalloproteinases, which, while protecting against infection, can also contribute to tissue damage. ET further amplifies inflammation by promoting cytokine and chemokine production, attracting additional immune cells to the affected site. Moreover, its role in impairing microcirculation leads to hypoxia and tissue degeneration, exacerbating periodontal inflammation. These findings highlight ET as a potential therapeutic target for modulating inflammation and preventing periodontal tissue destruction.