Epithelial to mesenchymal transition in human gingival overgrowth
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Abstract
Drug induced gingival overgrowth is a side-effect and unwanted outcome of systemic medication. Among the hypotheses which explain pathogenesis of drug induced gingival overgrowth, the idea that "EMT may play a role in drug induced gingival hyperplasia" has recently drawn attention. In this study, we have investigated the EMT markers (SLUG, SNA IL, SMAD3, [gamma]-catenin) in patients whose gingival overgrowth was induced by systemic administration of phenytoin, nifedipine, or cyclosporin A. We have observed reduced expressions of SLUG in the oral epithelium of the phenytoin induced gingival overgrowth tissues compared with non-overgrowth groups and reduced SNAIL expression in the apical part of the oral epithelium of the phenytoin induced gingival overgrowth tissues compared with control groups. Higher expression m cyclosporin A induced gingival overgrowth and lower SMAD3 expression in phenytoin overgrowth tissues compared to control was also found. In [gamma]-catenin expression, phenytoin and nifedipine overgrowth tissues showed reduced [gamma]-catenin expression than non-overgrowth tissue and up-regulation in cyclosporin A samples. Current findings have led to the insight that drug induced gingival overgrowth is less likely to be explained by direct effects of the drugs but explained by various cytokine imbalances due to secondary effects of the drugs. In spite of the inconsistency between in vitro and in vivo studies that is mainly due to limitation of experimental design in the in-vivo study, it is a valuable finding that various cytokines and inflammatory mediators are involved in drug induced gingival overgrowth and interact together.
Description
Thesis (MSD) --Boston University, Henry M. Goldman School of Dental Medicine, 2011 (Department of Oral Biology and Periodontology).
Includes bibliographic references: leaves 66-78.
Includes bibliographic references: leaves 66-78.
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This work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author.