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

Detalhes bibliográficos
Autor(a) principal: Barbirato, Davi da Silva
Data de Publicação: 2021
Outros Autores: Fogacci, Mariana Fampa, Azevedo, Pamella Oliveira de, Sansone, Carmelo, Carneiro, João Régis Ivar, Barros, Maria Cynésia Medeiros de
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Research, Society and Development
DOI: 10.33448/rsd-v10i5.13731
Texto Completo: https://rsdjournal.org/index.php/rsd/article/view/13731
Resumo: 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.
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spelling Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal MedicineRelación de la patogénesis de COVID-19 para la investigación en medicina periodontal. Parte II: Medicina Periodontal Relação da patogênese de COVID-19 para pesquisa de medicina periodontal. Parte II: Medicina Periodontal Coronavirus infectionsPathogenesisPeriodontics.Infecciones por CoronavirusPathogenesisPeriodoncia.Infecção por CoronavírusPatogênesePeriodontia.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.La respuesta inmunoinflamatoria a la infección por SARS-CoV-2 conduce a una infiltración excesiva de monocitos, macrófagos y células T, anticuerpos no neutralizantes, tormenta de citocinas sistémicas, menor recuento de plaquetas, aumento del dímero D, Proteína C reactiva y anomalías en la coagulación, aumento de la permeabilidad vascular, edema pulmonar, inflamación generalizada y daño multiorgánico. Las enfermedades periodontales tienen un perfil inflamatorio crónico, de origen infeccioso, con interacciones sistémicas vinculadas a más de 50 afecciones sistémicas. La respuesta inmunoinflamatoria de los tejidos periodontales al desafío microbiano, la respuesta protectora y la destrucción local de la influencia del periodonto están influenciadas por condiciones sistémicas. Los inhibidores del sistema renina-angiotensina/ECA también están relacionados con la patogenia de COVID-19 por SARS-CoV-2-ACE2 y con la patogénesis de la periodontitis, a través de la resorción ósea regulada por el eje ACE2/Ang- (1-7)/MasR e IL1 - β, regulación positiva de la vía cinina / receptor B2 debido a la inflamación del receptor 2 tipo Toll y respuestas Th1/Th17, la expresión del receptor de angiotensina II tipo 1 en el tejido gingival inflamado y la modulación de IL-1β inducida por IL- 6 producción en fibroblastos gingivales humanos. Es posible que la infección por SARS-CoV-2 aumente los eventos inflamatorios locales en el tejido periodontal que conducen a la destrucción de los tejidos periodontales. Apesar de la evidencia científica limitada o inexistente sobre los efectos del COVID-19 en las enfermedades periodontales y sus interacciones sistémicas hasta la fecha, es posible esperar su impacto en la investigación de la medicina periodontal.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.Research, Society and Development2021-04-25info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://rsdjournal.org/index.php/rsd/article/view/1373110.33448/rsd-v10i5.13731Research, Society and Development; Vol. 10 No. 5; e2010513731Research, Society and Development; Vol. 10 Núm. 5; e2010513731Research, Society and Development; v. 10 n. 5; e20105137312525-3409reponame:Research, Society and Developmentinstname:Universidade Federal de Itajubá (UNIFEI)instacron:UNIFEIenghttps://rsdjournal.org/index.php/rsd/article/view/13731/13074Copyright (c) 2021 Davi da Silva Barbirato; Mariana Fampa Fogacci; Pamella Oliveira de Azevedo; Carmelo Sansone; João Régis Ivar Carneiro; Maria Cynésia Medeiros de Barroshttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessBarbirato, Davi da Silva Fogacci, Mariana Fampa Azevedo, Pamella Oliveira de Sansone, Carmelo Carneiro, João Régis Ivar Barros, Maria Cynésia Medeiros de 2021-05-17T18:20:49Zoai:ojs.pkp.sfu.ca:article/13731Revistahttps://rsdjournal.org/index.php/rsd/indexPUBhttps://rsdjournal.org/index.php/rsd/oairsd.articles@gmail.com2525-34092525-3409opendoar:2024-01-17T09:35:00.655917Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)false
dc.title.none.fl_str_mv Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
Relación de la patogénesis de COVID-19 para la investigación en medicina periodontal. Parte II: Medicina Periodontal
Relação da patogênese de COVID-19 para pesquisa de medicina periodontal. Parte II: Medicina Periodontal
title Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
spellingShingle Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
Barbirato, Davi da Silva
Coronavirus infections
Pathogenesis
Periodontics.
Infecciones por Coronavirus
Pathogenesis
Periodoncia.
Infecção por Coronavírus
Patogênese
Periodontia.
Barbirato, Davi da Silva
Coronavirus infections
Pathogenesis
Periodontics.
Infecciones por Coronavirus
Pathogenesis
Periodoncia.
Infecção por Coronavírus
Patogênese
Periodontia.
title_short Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
title_full Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
title_fullStr Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
title_full_unstemmed Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
title_sort Relationship of COVID-19 pathogenesis for periodontal medicine research. Part II: Periodontal Medicine
author Barbirato, Davi da Silva
author_facet Barbirato, Davi da Silva
Barbirato, Davi da Silva
Fogacci, Mariana Fampa
Azevedo, Pamella Oliveira de
Sansone, Carmelo
Carneiro, João Régis Ivar
Barros, Maria Cynésia Medeiros de
Fogacci, Mariana Fampa
Azevedo, Pamella Oliveira de
Sansone, Carmelo
Carneiro, João Régis Ivar
Barros, Maria Cynésia Medeiros de
author_role author
author2 Fogacci, Mariana Fampa
Azevedo, Pamella Oliveira de
Sansone, Carmelo
Carneiro, João Régis Ivar
Barros, Maria Cynésia Medeiros de
author2_role author
author
author
author
author
dc.contributor.author.fl_str_mv Barbirato, Davi da Silva
Fogacci, Mariana Fampa
Azevedo, Pamella Oliveira de
Sansone, Carmelo
Carneiro, João Régis Ivar
Barros, Maria Cynésia Medeiros de
dc.subject.por.fl_str_mv Coronavirus infections
Pathogenesis
Periodontics.
Infecciones por Coronavirus
Pathogenesis
Periodoncia.
Infecção por Coronavírus
Patogênese
Periodontia.
topic Coronavirus infections
Pathogenesis
Periodontics.
Infecciones por Coronavirus
Pathogenesis
Periodoncia.
Infecção por Coronavírus
Patogênese
Periodontia.
description 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.
publishDate 2021
dc.date.none.fl_str_mv 2021-04-25
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://rsdjournal.org/index.php/rsd/article/view/13731
10.33448/rsd-v10i5.13731
url https://rsdjournal.org/index.php/rsd/article/view/13731
identifier_str_mv 10.33448/rsd-v10i5.13731
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://rsdjournal.org/index.php/rsd/article/view/13731/13074
dc.rights.driver.fl_str_mv https://creativecommons.org/licenses/by/4.0
info:eu-repo/semantics/openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by/4.0
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Research, Society and Development
publisher.none.fl_str_mv Research, Society and Development
dc.source.none.fl_str_mv Research, Society and Development; Vol. 10 No. 5; e2010513731
Research, Society and Development; Vol. 10 Núm. 5; e2010513731
Research, Society and Development; v. 10 n. 5; e2010513731
2525-3409
reponame:Research, Society and Development
instname:Universidade Federal de Itajubá (UNIFEI)
instacron:UNIFEI
instname_str Universidade Federal de Itajubá (UNIFEI)
instacron_str UNIFEI
institution UNIFEI
reponame_str Research, Society and Development
collection Research, Society and Development
repository.name.fl_str_mv Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)
repository.mail.fl_str_mv rsd.articles@gmail.com
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dc.identifier.doi.none.fl_str_mv 10.33448/rsd-v10i5.13731