Das, Swarga Jyoti; (2002) The role of keratinocyte growth factor and receptor in gingival hyperplasia. Doctoral thesis (Ph.D), UCL (University College London).

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Abstract

Gingival hyperplasia (GH) occurs almost exclusively as an adverse side-effect of the administration of three different types of drug with anti-epileptic, immunosuppressive and calcium channel-blocking activity. The most commonly used drugs under these categories are phenytoin, cyclosporin A and nifedipine, respectively. In order to prevent the occurrence and to improve the efficacy of clinical treatment of GH, it is essential to understand the molecular basis of GH; however, the precise mechanism(s) by which these drugs cause GH is not yet known. GH is characterised by a markedly increased thickness of the epithelium with elongated finger-like projections extending deep into the underlying connective tissue, suggesting the involvement of mitogenic factors for epithelial cells. Keratinocyte growth factor (KGF) is a potent and specific growth factor, which is produced by mesenchymal cells and acts exclusively on epithelial cells via the KGF receptor (KGFR). KGF and KGFR both have been implicated in benign prostate, mammary and other hyperplasias, and it is possible that this growth factor and its receptor could also be involved in the pathogenesis of GH. The present study was therefore undertaken to compare the expression of KGF and KGFR in GH tissues with that in normal gingiva (NG) at both the protein and RNA levels, using immunohistochemistry and the reverse transcriptase-polymerase chain reaction (RT-PCR), respectively. Enzyme-linked immunosorbant assay (ELISA) and flow cytometry (FCM) were used to evaluate the effects of the different drugs on the production of KGF and KGFR by normal human gingival fibroblasts and epithelial cells, respectively, and effects of the drugs were also examined on the activities of KGF and KGFR genes in vitro. The results have shown that KGF and KGFR are up-regulated in GH compared with NG tissues and also in response to the drugs in vitro, and suggest that KGF and its receptor play a fundamental part in the molecular pathology of GH.

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