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Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?

There is documented evidence of significant associations between cancer of the lung, kidney, pancreas, hematological and oral cancers and periodontal diseases of the supporting structures of the teeth. Enhanced lipid peroxidation, raised levels of TBARS and the oxidative stress marker malondealdehyd...

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Autor principal: Soory, Mena
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835098/
https://www.ncbi.nlm.nih.gov/pubmed/24281088
http://dx.doi.org/10.3390/cancers2020670
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author Soory, Mena
author_facet Soory, Mena
author_sort Soory, Mena
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description There is documented evidence of significant associations between cancer of the lung, kidney, pancreas, hematological and oral cancers and periodontal diseases of the supporting structures of the teeth. Enhanced lipid peroxidation, raised levels of TBARS and the oxidative stress marker malondealdehyde have been detected in breast cancer with reduced antioxidant capacity, also characteristic of periodontal diseases. Antioxidants could overcome this deficit and attenuate disease progression by down regulating glutathione detoxification/redox buffering system and inhibiting key transcription factors. Periodontal disease may be a critical marker of a susceptible immune system, or initiate cancer risk with a pro-oxidant inflammatory profile.
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spelling pubmed-38350982013-11-21 Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis? Soory, Mena Cancers (Basel) Review There is documented evidence of significant associations between cancer of the lung, kidney, pancreas, hematological and oral cancers and periodontal diseases of the supporting structures of the teeth. Enhanced lipid peroxidation, raised levels of TBARS and the oxidative stress marker malondealdehyde have been detected in breast cancer with reduced antioxidant capacity, also characteristic of periodontal diseases. Antioxidants could overcome this deficit and attenuate disease progression by down regulating glutathione detoxification/redox buffering system and inhibiting key transcription factors. Periodontal disease may be a critical marker of a susceptible immune system, or initiate cancer risk with a pro-oxidant inflammatory profile. Molecular Diversity Preservation International 2010-04-26 /pmc/articles/PMC3835098/ /pubmed/24281088 http://dx.doi.org/10.3390/cancers2020670 Text en © 2010 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Soory, Mena
Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?
title Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?
title_full Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?
title_fullStr Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?
title_full_unstemmed Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?
title_short Oxidative Stress Induced Mechanisms in the Progression of Periodontal Diseases and Cancer: A Common Approach to Redox Homeostasis?
title_sort oxidative stress induced mechanisms in the progression of periodontal diseases and cancer: a common approach to redox homeostasis?
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835098/
https://www.ncbi.nlm.nih.gov/pubmed/24281088
http://dx.doi.org/10.3390/cancers2020670
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