Abstract
Abstract 
 
 Introduction: Gingival overgrowth is one of several oral side effects of phenytoin, a potent antiepileptic drug. Several mechanisms have been elucidated to understand the pathogenesis of drug induced gingival overgrowth. The frequency of gingival overgrowth associated with chronic phenytoin therapy remains controversial. and the possible subclinical effects of this drug on the gingival epithelium should be investigated histopathologically and immunohistochemically.
 Purpose of the study: To investigate the Bcl-2 for apoptosis rate and Ki-67 for the epithelial proliferative activity in epileptic patients.
 Materials and methods: Twenty four samples of gingival tissue from epileptic patients treated with phenytoin and in eight samples of gingival tissue from healthy patients who didn’t use phenytoin (control) were evaluated for Bcl-2 and Ki-67 immunohistochemically.
 Results: The results revealed moreproliferative activity of the overlying epithelium and an increased pattern of Bcl-2 and Ki-67 in phenytoin users compared to controls.
 Conclusion: These results concluded that the increased epithelial thickness observed in phenytoin induced gingival overgrowth is associated with increased apoptotic rate and mitotic activity , especially in the oral epithelium.
 
 Keywords: Gingival overgrowth, Bcl-2, Ki-67, Phenytoin.
Highlights
Gingival overgrowth is one of several oral side effects of phenytoin, a potent antiepileptic drug
Other series realized that the pathogenesis of Drug-induced gingival overgrowth (DIGO) has been related to the presence of a genetically determined subpopulation of drugsensitive fibroblasts, which may respond by increasing cell proliferation/survival or by altering the synthesis and remodeling of extracellular matrix.[27,28,29,30,31,32]
In an attempt to better understand the pathogenesis of phenytoin as a DIGO, the present study evaluates the immunohistochemical expression of antiapoptotic protein Bcl-2 and the cell proliferation rates (Ki-67) in gingival overgrowth of epileptic patients using phenytoin and compared the findings with those observed for clinically healthy gingiva
Summary
Gingival overgrowth is one of several oral side effects of phenytoin, a potent antiepileptic drug. Some studies proposed that DIGO could be induced by rupture of homeostasis between synthesis and degradation of collagen and other extracellular matrix components, as well as between cell proliferation and apoptosis involving the gingival epithelium and connective tissue.[21,22,23,24,25,26] Other series realized that the pathogenesis of DIGO has been related to the presence of a genetically determined subpopulation of drugsensitive fibroblasts, which may respond by increasing cell proliferation/survival or by altering the synthesis and remodeling of extracellular matrix.[27,28,29,30,31,32] In an attempt to better understand the pathogenesis of phenytoin as a DIGO, the present study evaluates the immunohistochemical expression of antiapoptotic protein Bcl-2 and the cell proliferation rates (Ki-67) in gingival overgrowth of epileptic patients using phenytoin and compared the findings with those observed for clinically healthy gingiva.
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