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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2013
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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. |
format | Online Article Text |
id | pubmed-3652200 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
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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