Impact of Periodontitis on Endothelial Risk Dysfunction and Oxidative Stress Improvement in Patients with Cardiovascular Disease.

Abstract

Periodontitis is a multifactorial chronic inflammatory disease that affects the periodontium and overall oral health and is primarily caused by a dysbiotic gingival biofilm, which includes, among others, Gram-negative bacteria such as Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, and Tannerella forsythensis that colonize gingival tissues and that can lead, if not properly treated, to periodontal tissue destruction and tooth loss. In the last few decades, several large-scale epidemiological studies have evidenced that mild and severe forms of periodontitis are strictly bilaterally associated with several cardiovascular diseases (CVDs), stroke, and endothelial dysfunction. Specifically, it is hypothesized that patients with severe periodontitis would have compromised endothelial function, a crucial step in the pathophysiology of atherosclerosis and several CVD forms. In this regard, it was postulated that periodontal treatment would ameliorate endothelial dysfunction, hence bolstering the notion that therapeutic approaches targeted at diminishing cardiovascular risk factors and different forms of periodontal treatment could improve several CVD biomarker outcomes in the short- and long-term in CVD patients. The aim of this review is to update and analyze the link between periodontitis and CVD, focusing on the inflammatory nature of periodontitis and its correlation with CVD, the effects of periodontal therapy on endothelial dysfunction and oxidative stress, and the impact of such therapy on CVD biomarkers and outcomes. The article also discusses future research directions in this field.