Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine

The dysfunctional immunoinflammatory response to SARS-CoV-2 infection leads excessive infiltration of monocytes, macrophages and T cells, non-neutralizing antibody, systemic cytokine storm, microthrombi mediated by tissue factor oxidative stress, lower platelet counts, increased D-dimer, C-reactive protein coagulation abnormalities, vascular permeability, pulmonary edema pneumonia, widespread inflammation multi-organ damage. Periodontal diseases have a chronic multifactorial inflammatory profile, infectious origin, with bidirectional interactions linked over 50 conditions/diseases. Immunoinflammatory periodontal tissues the microbial challenge, protective/repair local destruction periodontium influence are influenced Renin-angiotensin system/ACE inhibitors also related pathogenesis COVID-19 SARS-CoV-2-ACE2 periodontitis, through bone resorption regulated ACE2/Ang-(1-7)/MasR axis IL1-b, positive regulation kinin/receptor pathway B2 due Toll-like receptor 2 Th1/Th17 responses, expression type 1 angiotensin II in inflamed gingival tissue, modulating IL-1β-induced IL-6 production human fibroblasts. It is possible that increases events leading tissues, probably enhanced effects periodontitis. Despite limited or non-existent scientific evidence on their date, it expect its impact medicine research from natural history relationship conditions treatment, as an environmental acquired risk factor.