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Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle

Periodontitis is a chronic inflammatory immune disease associated with a dysbiotic state, influenced by keystone bacterial species responsible for disrupting the periodontal tissue homeostasis. Furthermore, the severity of periodontitis is determined by the interaction between the immune cell respon...

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Autores principales: Bendek, María José, Canedo-Marroquín, Gisela, Realini, Ornella, Retamal, Ignacio N., Hernández, Marcela, Hoare, Anilei, Busso, Dolores, Monteiro, Lara J., Illanes, Sebastián E., Chaparro, Alejandra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
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Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8584134/
https://www.ncbi.nlm.nih.gov/pubmed/34769262
http://dx.doi.org/10.3390/ijms222111831
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author Bendek, María José
Canedo-Marroquín, Gisela
Realini, Ornella
Retamal, Ignacio N.
Hernández, Marcela
Hoare, Anilei
Busso, Dolores
Monteiro, Lara J.
Illanes, Sebastián E.
Chaparro, Alejandra
author_facet Bendek, María José
Canedo-Marroquín, Gisela
Realini, Ornella
Retamal, Ignacio N.
Hernández, Marcela
Hoare, Anilei
Busso, Dolores
Monteiro, Lara J.
Illanes, Sebastián E.
Chaparro, Alejandra
author_sort Bendek, María José
collection PubMed
description Periodontitis is a chronic inflammatory immune disease associated with a dysbiotic state, influenced by keystone bacterial species responsible for disrupting the periodontal tissue homeostasis. Furthermore, the severity of periodontitis is determined by the interaction between the immune cell response in front of periodontitis-associated species, which leads to the destruction of supporting periodontal tissues and tooth loss in a susceptible host. The persistent bacterial challenge induces modifications in the permeability and ulceration of the sulcular epithelium, which facilitates the systemic translocation of periodontitis-associated bacteria into distant tissues and organs. This stimulates the secretion of pro-inflammatory molecules and a chronic activation of immune cells, contributing to a systemic pro-inflammatory status that has been linked with a higher risk of several systemic diseases, such as type 2 diabetes mellitus (T2DM) and gestational diabetes mellitus (GDM). Although periodontitis and GDM share the common feature of systemic inflammation, the molecular mechanistic link of this association has not been completely clarified. This review aims to examine the potential biological mechanisms involved in the association between periodontitis and GDM, highlighting the contribution of both diseases to systemic inflammation and the role of new molecular participants, such as extracellular vesicles and non-coding RNAs, which could act as novel molecular intercellular linkers between periodontal and placental tissues.
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spelling pubmed-85841342021-11-12 Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle Bendek, María José Canedo-Marroquín, Gisela Realini, Ornella Retamal, Ignacio N. Hernández, Marcela Hoare, Anilei Busso, Dolores Monteiro, Lara J. Illanes, Sebastián E. Chaparro, Alejandra Int J Mol Sci Review Periodontitis is a chronic inflammatory immune disease associated with a dysbiotic state, influenced by keystone bacterial species responsible for disrupting the periodontal tissue homeostasis. Furthermore, the severity of periodontitis is determined by the interaction between the immune cell response in front of periodontitis-associated species, which leads to the destruction of supporting periodontal tissues and tooth loss in a susceptible host. The persistent bacterial challenge induces modifications in the permeability and ulceration of the sulcular epithelium, which facilitates the systemic translocation of periodontitis-associated bacteria into distant tissues and organs. This stimulates the secretion of pro-inflammatory molecules and a chronic activation of immune cells, contributing to a systemic pro-inflammatory status that has been linked with a higher risk of several systemic diseases, such as type 2 diabetes mellitus (T2DM) and gestational diabetes mellitus (GDM). Although periodontitis and GDM share the common feature of systemic inflammation, the molecular mechanistic link of this association has not been completely clarified. This review aims to examine the potential biological mechanisms involved in the association between periodontitis and GDM, highlighting the contribution of both diseases to systemic inflammation and the role of new molecular participants, such as extracellular vesicles and non-coding RNAs, which could act as novel molecular intercellular linkers between periodontal and placental tissues. MDPI 2021-10-31 /pmc/articles/PMC8584134/ /pubmed/34769262 http://dx.doi.org/10.3390/ijms222111831 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Bendek, María José
Canedo-Marroquín, Gisela
Realini, Ornella
Retamal, Ignacio N.
Hernández, Marcela
Hoare, Anilei
Busso, Dolores
Monteiro, Lara J.
Illanes, Sebastián E.
Chaparro, Alejandra
Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle
title Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle
title_full Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle
title_fullStr Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle
title_full_unstemmed Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle
title_short Periodontitis and Gestational Diabetes Mellitus: A Potential Inflammatory Vicious Cycle
title_sort periodontitis and gestational diabetes mellitus: a potential inflammatory vicious cycle
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8584134/
https://www.ncbi.nlm.nih.gov/pubmed/34769262
http://dx.doi.org/10.3390/ijms222111831
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