Relação da patogênese de COVID-19 para pesquisa de medicina periodontal. Parte II: Medicina Periodontal
DOI:
https://doi.org/10.33448/rsd-v10i5.13731Palavras-chave:
Infecção por Coronavírus; Patogênese; Periodontia.Resumo
A resposta imunoinflamatória à infecção por SARS-CoV-2 leva à infiltração excessiva de monócitos, macrófagos e células T, anticorpo não neutralizante, tempestade de citocinas sistêmica, microtrombos mediados por fator de tecido e estresse oxidativo, contagem de plaquetas mais baixa, dímero D, aumentado proteína C reativa e anormalidades de coagulação, aumento da permeabilidade vascular, edema pulmonar, pneumonia, inflamação generalizada e danos a múltiplos órgãos. As doenças periodontais apresentam um perfil inflamatório crônico e multifatorial, de origem infecciosa, com interações sistêmicas vinculadas a mais de 50 condições sistêmicas. A resposta imunoinflamatória dos tecidos periodontais ao desafio microbiano, a resposta de proteção e a destruição local do periodonto influenciam e são influenciadas por condições sistêmicas. O sistema renina-angiotensina/inibidores da ECA também estão relacionados à patogênese do COVID-19 pelo SARS-CoV-2-ACE2 e à patogênese da periodontite, por meio da reabsorção óssea regulada pelo eixo ACE2/Ang (1-7) / MasR e IL1 - β, regulação positiva da via do receptor de quinina/B2 devido à inflamação do receptor Toll-like 2 e respostas Th1/Th17, expressão do receptor de angiotensina II tipo 1 em tecido gengival inflamado e modulação induzida por IL-1β 6 produção em fibroblastos gengivais humanos. É possível que a infecção por SARS-CoV-2 aumente os eventos inflamatórios locais no tecido periodontal, levando à destruição dos tecidos periodontais, provavelmente potencializado pelos efeitos sistêmicos da periodontite. Apesar das evidências científicas limitadas ou inexistentes sobre os efeitos do COVID-19 nas doenças periodontais e suas interações sistêmicas até o momento, é possível esperar seu impacto na pesquisa da medicina periodontal.
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