Introdução: O indivíduo obeso apresenta um estado hiper-inflamatório e anormalidades metabólicas relacionadas com o metabolismo glicêmico e funções hepáticas que suportam as hipóteses de maior susceptibilidade e gravidade da periodontite nesses pacientes. Entretanto, a plausibilidade biológica para essa condição ainda não foi estabelecida. Objetivo: Descrever os principais eventos biológicos envolvidos na relação da obesidade com a periodontite. Material e métodos: Ensaio teórico a partir de uma revisão sistematizada de artigos científicos indexados nas bases de dados PubMed|MEDLINE, Scopus, Embase, Web of Science, Cochrane Library, e bvs|LILACS. Resultados e Discussão: Citocinas pró-inflamatórias como IL-1b, IL-6 e TNF-a, perda da homeostasia entre os níveis séricos de leptina e adiponectina, bem como o aumento dos níveis de ácidos graxos livres e de espécies reativas de oxigênio parecem exercer um feedback positivo entre os efeitos deletérios da obesidade e periodontite, com participação importante do fígado e da resistência insulínica nesse processo, potencializando cada vez mais esse sistema. O acúmulo de AGEs, aumento da colagenólise e complicações vasculares decorrentes da hiperglicemia relacionam-se de forma direta com a gravidade da periodontite e a destruição tecidual. O estresse oxidativo participa desse processo não apenas nos tecidos periodontais mas também no fígado, onde o comprometimento funcional desse órgão é acompanhado por aumento dos níveis séricos de proteína C reativa e angiotensinogênio, estimulados também pela endotoxemia, bacteremia e aumento dos níveis séricos de citocinas pró-inflamatórias a partir das bolsas periodontais. Conclusão: Os efeitos da obesidade sobre a periodontite parecem estar relacionados, principalmente, com o estado hiperinflamatório e o comprometimento do metabolismo da glicose.
The dysfunctional immunoinflammatory response to SARS-CoV-2 infection leads to excessive infiltration of monocytes, macrophages and T cells, non-neutralizing antibody, systemic cytokine storm, microthrombi mediated by tissue factor and oxidative stress, lower platelet counts, increased D-dimer, C-reactive protein and coagulation abnormalities, increased vascular permeability, pulmonary edema and pneumonia, and widespread inflammation and multi-organ damage. Periodontal diseases have a chronic and multifactorial inflammatory profile, of infectious origin, with bidirectional systemic interactions linked to over 50 systemic conditions/diseases. Immunoinflammatory response of periodontal tissues to the microbial challenge, protective/repair response and the local destruction of periodontium influence and are influenced by systemic conditions/diseases. Renin-angiotensin system/ACE inhibitors are also related to pathogenesis of COVID-19 by SARS-CoV-2-ACE2 and to pathogenesis of periodontitis, through bone resorption regulated by the ACE2/Ang-(1-7)/MasR axis and IL1-b, positive regulation of the kinin/receptor pathway B2 due to Toll-like receptor 2 inflammation and Th1/Th17 responses, the expression of the type 1 angiotensin II receptor in the inflamed gingival tissue, and modulating IL-1β-induced IL-6 production in human gingival fibroblasts. It is possible that SARS-CoV-2 infection increases local inflammatory events in periodontal tissue leading to destruction of periodontal tissues, probably enhanced by the systemic effects of periodontitis. Despite limited or non-existent scientific evidence on the effects of COVID-19 on periodontal diseases and their systemic interactions to date, it is possible to expect its impact on periodontal medicine research from the natural history of periodontal diseases to their pathogenesis and relationship with systemic conditions and response to treatment, as an environmental and acquired risk factor.
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.
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