Reactive species of oxygen, oxidative stress and its relationship with tissular destruction in periodontitis/Especies reactivas de oxigeno, estrés oxidativo y su relación con la destrucción tisular en periodontitis/Especies reativas de oxigenio, estresse oxidativo e sua relacao com destruicao tecidual na periodontite

During periodontitis inflammatory mediators and reactive oxygen species (ROS) are released, when they increase they produce oxidative stress. This review article describes the role played by ROS and oxidative stress in the development and evolution of inflammation and tissue injury during periodonti...

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Published inCES odontología Vol. 33; no. 2; p. 112
Main Authors Menaca-Guerrero, Lorena, Suarez-Causado, Amileth, Diaz-Caballero, Antonio Jose
Format Journal Article
LanguageEnglish
Published Universidad del CES 01.07.2020
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Summary:During periodontitis inflammatory mediators and reactive oxygen species (ROS) are released, when they increase they produce oxidative stress. This review article describes the role played by ROS and oxidative stress in the development and evolution of inflammation and tissue injury during periodontitis. For this, a review of the literature was carried out in databases such as PubMed, ScienceDirect, Wiley Online Library, Springer, Plos one, Nature, Sage journals, Hindawi and Taylor & Francis Online, showing the following results: ROS produce direct damage and indirect to periodontal tissues. Direct damages include lipid peroxidation, protein and DNA oxidation. Indirect damage involves the regulation of signaling pathways of the nuclear transcription factor kappa B (NF-[kappa]B), the c-Jun N-terminal kinase pathway (JNK), the pathways of inflammasome and autophagy causing tissue destruction and creation of a pro-inflammatory state in periodontitis. Keywords: Reactive oxygen species; Oxidative stress; Periodontitis Durante la periodontitis se liberan mediadores inflamatorios y especies reactivas de oxigeno (ROS), cuando se incrementan producen estres oxidativo. Este articulo de revision describe el papel que desempenan las ROS y el estres oxidativo en el desarrollo y evolucion de la inflamacion y lesion tisular durante la periodontitis. Para ello, se realizo una revision de la literatura en bases de datos como PubMed, ScienceDirect, Wiley Online Library, Springer, Plos one, Nature, Sage journals, Hindawi y Taylor & Francis Online, mostrando los siguientes resultados: las ROS producen dano directo e indirecto a los tejidos periodontales. Los danos directos incluyen peroxidacion de lipidos, oxidacion de proteinas y del ADN. Los danos indirectos involucran la regulacion de las vias de senalizacion del factor de transcripcion nuclear kappa B (NF-[kappa]B), la via de la quinasa c-Jun N-terminal (JNK), las vias del inflamasoma y autofagia provocando la destruccion tisular y creacion de un estado proinflamatorio en la periodontitis. Palabras clave: Especies reactivas de oxigeno; Estres oxidativo; Periodontitis. Durante a periodontite, sao liberados mediadores inflamatorios e especies reativas de oxigenio (EROs), no momento em que eles incrementam produzem estresse oxidativo. Este artigo de revisao descreve o papel que desempenham as EROS e o estresse oxidativo no desenvolvimento e na evolucao da inflamacao e lesao tecidual durante a periodontite. Por isso, uma revisao da literatura foi realizada em bancos de dados como PubMed, ScienceDirect, Wiley Online Library, Springer, Plos one, Nature, Sage, Hindawi e Taylor & Francis Online, mostrando os seguintes resultados: as EROS produzem dano direto e indireto para os tecidos periodontais. O dano direto inclui peroxidacao lipidica, oxidacao de proteinas e DNA. O dano indireto involucra a regulacao das vias de sinalizacao do fator de transcricao nuclear kappa B (NF-[kappa]B), da via c-Jun N-terminal kinase (JNK), das vias inflamassoma e autofagia, causando destruicao tecidual e criacao de um estado pro-inflamatorio na periodontite. Palavras-chave: Especies reativas de oxigenio; Estresse oxidativo; Periodontite.
ISSN:0120-971X
DOI:10.21615/cesodon.33.2.10