Abstract
Cell invasion mediated by angiotensin-converting enzyme 2 (ACE2) ectoenzyme and cellular proteases, such as trypsin-like proteases, cathepsins, transmembrane serine protease 2 and furin, target different tissues and organs as lung, gut, colon, ileum, kidney, gallbladder, heart muscle, epididymis, breast, ovary, stomach, bile duct, liver, oral cavity, lung, thyroid, esophagus, bladder, breast, uterus, prostate, pancreas, cerebellum, as well as calyx secreting cells in the nasal and sinus tissue. Loss of homeostasis of the renin-angiotensin system deregulates different axes compromising metabolic, cardiorespiratory, renal and hepatic control. SARS-CoV-2 infected cell undergoes pyroptosis and releases molecular patterns associated with damage: pro-inflammatory interleukin (IL) -1b, IL-6, IL-8, IL-10, IL-17, induced protein-10, interferon gamma, interferon gamma-induced protein-10, granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, macrophage inflammatory protein 1α and 1β, monocyte chemotherapy activating protein 1, inflammatory macrophage protein 1a, tumor necrosis-α, and mediators of immune-mediated inflammatory diseases. Cytokine storm and non-neutralizing antibodies produced by B cells circulate, cause/exacerbate damage to various organs. During viral replication and low oxygen saturation, loss of HIF-mediated cell homeostasis can lead to cell death/lysis and tissue damage, related to the hyperinflammatory response. The SARS-CoV-2-ACE2 can increase permeability, inflammation and microbial transmission by bacteremia or endotoxemia, in addition to dysbiosis. Thrombotic potential and the immunoinflammatory imbalance compromise function or lead to injuries and multiple organ failure. Infection by SARS-CoV-2 has the potential to modify the natural history of diseases, the relationships or interactions between the different systems and pathologies and the effects of their treatments, as in periodontal medicine approach.
Highlights
SARS-CoV-2 infection appears to directly affect tissues and organs by exposure and presence of the angiotensinconverting enzyme 2 (ACE2) ectoenzyme and cellular proteases (Bertram et al, 2011, Glowacka et al, 2011, Raj et al, 2013, Wang et al, 2013, Gheblawi et al, 2020, Gralinski & Menachery, 2020, Hoffmann et al, 2020, Wan, Shang, Graham, Baric &Li, 2020, Zhou et al, 2020)
New coronavirus SARS-CoV-2 and host cell infection The first cases of COVID-19 were reported to the World Health Organization (WHO) on December 31, 2019, where 27 individuals suffered pneumonia with no known cause and all were related to a wholesale market for wet animals in the city of Wuhan, China
All available evidence for COVID-19 suggests that SARS-CoV-2 has a zoonotic source
Summary
SARS-CoV-2 infection appears to directly affect tissues and organs by exposure and presence of the angiotensinconverting enzyme 2 (ACE2) ectoenzyme and cellular proteases (Bertram et al, 2011, Glowacka et al, 2011, Raj et al, 2013, Wang et al, 2013, Gheblawi et al, 2020, Gralinski & Menachery, 2020, Hoffmann et al, 2020, Wan, Shang, Graham, Baric &Li, 2020, Zhou et al, 2020). The pathogenesis of COVID-19 and its systemic impacts are associated with intense pro-inflammatory events and loss of homeostasis, associated with a hyperinflammatory state, secondary bacterial infections, bacteremia, endotoxemia, loss of function and multiple organ failure The systemic impacts of the COVID-19 have the potential to influence the relationships and interactions between periodontal diseases and systemic conditions/diseases, previously reported in the literature. The aim of this study was to review the literature and propose a conceptual hypothesis on the subject, based on the interception between the pathogenesis of COVID-19 and its main systemic repercussions, and periodontal medicine
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