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The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth

Gingival overgrowth is a side effect of certain medications. The most fibrotic drug-induced lesions develop in response to therapy with phenytoin, the least fibrotic lesions are caused by cyclosporin A, and the intermediate fibrosis occurs in nifedipine-induced gingival overgrowth. Fibrosis is one o...

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Autores principales: Subramani, Tamilselvan, Rathnavelu, Vidhya, Alitheen, Noorjahan Banu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652200/
https://www.ncbi.nlm.nih.gov/pubmed/23690667
http://dx.doi.org/10.1155/2013/639468
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author Subramani, Tamilselvan
Rathnavelu, Vidhya
Alitheen, Noorjahan Banu
author_facet Subramani, Tamilselvan
Rathnavelu, Vidhya
Alitheen, Noorjahan Banu
author_sort Subramani, Tamilselvan
collection PubMed
description Gingival overgrowth is a side effect of certain medications. The most fibrotic drug-induced lesions develop in response to therapy with phenytoin, the least fibrotic lesions are caused by cyclosporin A, and the intermediate fibrosis occurs in nifedipine-induced gingival overgrowth. Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During connective tissue repair, activated gingival fibroblasts synthesize and remodel newly created extracellular matrix. Proteins such as transforming growth factor (TGF), endothelin-1 (ET-1), angiotensin II (Ang II), connective tissue growth factor (CCN2/CTGF), insulin-like growth factor (IGF), and platelet-derived growth factor (PDGF) appear to act in a network that contributes to the development of gingival fibrosis. Since inflammation is the prerequisite for gingival overgrowth, mast cells and its protease enzymes also play a vital role in the pathogenesis of gingival fibrosis. Drugs targeting these proteins are currently under consideration as antifibrotic treatments. This review summarizes recent observations concerning the contribution of TGF-β, CTGF, IGF, PDGF, ET-1, Ang II, and mast cell chymase and tryptase enzymes to fibroblast activation in gingival fibrosis and the potential utility of agents blocking these proteins in affecting the outcome of drug-induced gingival overgrowth.
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spelling pubmed-36522002013-05-20 The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth Subramani, Tamilselvan Rathnavelu, Vidhya Alitheen, Noorjahan Banu Mediators Inflamm Review Article Gingival overgrowth is a side effect of certain medications. The most fibrotic drug-induced lesions develop in response to therapy with phenytoin, the least fibrotic lesions are caused by cyclosporin A, and the intermediate fibrosis occurs in nifedipine-induced gingival overgrowth. Fibrosis is one of the largest groups of diseases for which there is no therapy but is believed to occur because of a persistent tissue repair program. During connective tissue repair, activated gingival fibroblasts synthesize and remodel newly created extracellular matrix. Proteins such as transforming growth factor (TGF), endothelin-1 (ET-1), angiotensin II (Ang II), connective tissue growth factor (CCN2/CTGF), insulin-like growth factor (IGF), and platelet-derived growth factor (PDGF) appear to act in a network that contributes to the development of gingival fibrosis. Since inflammation is the prerequisite for gingival overgrowth, mast cells and its protease enzymes also play a vital role in the pathogenesis of gingival fibrosis. Drugs targeting these proteins are currently under consideration as antifibrotic treatments. This review summarizes recent observations concerning the contribution of TGF-β, CTGF, IGF, PDGF, ET-1, Ang II, and mast cell chymase and tryptase enzymes to fibroblast activation in gingival fibrosis and the potential utility of agents blocking these proteins in affecting the outcome of drug-induced gingival overgrowth. Hindawi Publishing Corporation 2013 2013-04-16 /pmc/articles/PMC3652200/ /pubmed/23690667 http://dx.doi.org/10.1155/2013/639468 Text en Copyright © 2013 Tamilselvan Subramani et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Subramani, Tamilselvan
Rathnavelu, Vidhya
Alitheen, Noorjahan Banu
The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth
title The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth
title_full The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth
title_fullStr The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth
title_full_unstemmed The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth
title_short The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth
title_sort possible potential therapeutic targets for drug induced gingival overgrowth
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3652200/
https://www.ncbi.nlm.nih.gov/pubmed/23690667
http://dx.doi.org/10.1155/2013/639468
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