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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| Format: | Article |
| Language: | English |
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Hindawi Publishing Corporation
2013
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| Online Access: | http://psasir.upm.edu.my/id/eprint/28096/ http://psasir.upm.edu.my/id/eprint/28096/1/28096.pdf |
| _version_ | 1848846021682003968 |
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| author | Subramani, Tamilselvan Rathnavelu, Vidhya Mohammed Alitheen, Noorjahan Banu |
| author_facet | Subramani, Tamilselvan Rathnavelu, Vidhya Mohammed Alitheen, Noorjahan Banu |
| author_sort | Subramani, Tamilselvan |
| building | UPM Institutional Repository |
| collection | Online Access |
| 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. |
| first_indexed | 2025-11-15T08:56:05Z |
| format | Article |
| id | upm-28096 |
| institution | Universiti Putra Malaysia |
| institution_category | Local University |
| language | English |
| last_indexed | 2025-11-15T08:56:05Z |
| publishDate | 2013 |
| publisher | Hindawi Publishing Corporation |
| recordtype | eprints |
| repository_type | Digital Repository |
| spelling | upm-280962016-06-20T06:12:58Z http://psasir.upm.edu.my/id/eprint/28096/ The possible potential therapeutic targets for drug induced gingival overgrowth Subramani, Tamilselvan Rathnavelu, Vidhya Mohammed Alitheen, Noorjahan Banu 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 Article PeerReviewed application/pdf en http://psasir.upm.edu.my/id/eprint/28096/1/28096.pdf Subramani, Tamilselvan and Rathnavelu, Vidhya and Mohammed Alitheen, Noorjahan Banu (2013) The possible potential therapeutic targets for drug induced gingival overgrowth. Mediators of Inflammation, 2013. art. no. 639468. pp. 1-9. ISSN 0962-9351; ESSN: 1466-1861 http://www.hindawi.com/journals/mi/2013/639468/abs/ 10.1155/2013/639468 |
| spellingShingle | Subramani, Tamilselvan Rathnavelu, Vidhya Mohammed 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 |
| url | http://psasir.upm.edu.my/id/eprint/28096/ http://psasir.upm.edu.my/id/eprint/28096/ http://psasir.upm.edu.my/id/eprint/28096/ http://psasir.upm.edu.my/id/eprint/28096/1/28096.pdf |