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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Wiley
2013-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2013/639468 |
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| author | Tamilselvan Subramani Vidhya Rathnavelu Noorjahan Banu Alitheen |
| author_facet | Tamilselvan Subramani Vidhya Rathnavelu Noorjahan Banu Alitheen |
| author_sort | Tamilselvan Subramani |
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| 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 | Article |
| id | doaj-art-cfafaddd9d554e798265ceb093c56a8b |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
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| series | Mediators of Inflammation |
| spelling | doaj-art-cfafaddd9d554e798265ceb093c56a8b2025-02-03T05:46:19ZengWileyMediators of Inflammation0962-93511466-18612013-01-01201310.1155/2013/639468639468The Possible Potential Therapeutic Targets for Drug Induced Gingival OvergrowthTamilselvan Subramani0Vidhya Rathnavelu1Noorjahan Banu Alitheen2Department of Cell and Molecular Biology, Faculty of Biotechnology and Biomolecular Sciences, University Putra Malaysia, 43400 Serdang, Selangor, MalaysiaDepartment of Oral and Maxillofacial Pathology, Faculty of Dental Science, Sri Ramachandra University, Porur, Chennai 600116, IndiaDepartment of Cell and Molecular Biology, Faculty of Biotechnology and Biomolecular Sciences, University Putra Malaysia, 43400 Serdang, Selangor, MalaysiaGingival 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.http://dx.doi.org/10.1155/2013/639468 |
| spellingShingle | Tamilselvan Subramani Vidhya Rathnavelu Noorjahan Banu Alitheen The Possible Potential Therapeutic Targets for Drug Induced Gingival Overgrowth Mediators of Inflammation |
| 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 |
| url | http://dx.doi.org/10.1155/2013/639468 |
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