title: Immunolocalizaiton of c-Myc and bcl-2 proto-oncogene products in gingival hyperplasia induced by nifedipine and phenytoin.
abstract: BACKGROUND
  Hyperplastic gingival tissues show the histopathological characteristics of thick parakeratinized squamous epithelia with acanthosis and rete pegs elongated into the lamina propria. However, the pathogenic factors that contribute to the epithelial morphogenesis of this disease are obscure and remain to be studied.
  
  
  METHODS
  We immunohistochemically examined the expression of both c-Myc and bcl-2 oncoprotein, which can exert influence on the epithelial morphogenesis and homeostasis, in 12 hyperplastic gingival tissues induced by nifedipine and phenytoin as well as 5 control tissues using avidin-biotin-peroxidase complex methods.
  
  
  RESULTS
  Four specimens out of 5 nifedipine-induced and 5 out of 7 phenytoin-induced hyperplastic gingival tissues revealed the expression of c-Myc oncoprotein, whereas no significant immunostaining of c-Myc oncoprotein was found in 5 control tissues. The c-Myc oncoprotein-positive cells were observed to be localized in the basal and suprabasal cell layers of the hyperplastic gingival epithelia. Although all of the 12 hyperplastic gingival epithelia showed the distribution of bcl-2 oncoprotein in the basal and suprabasal layer cells, in 5 control epithelia the bcl-2 oncoprotein expression was slight and confined to the basal layer cells.
  
  
  CONCLUSIONS
  The results of our present study indicate that the synergistic overexpression of c-Myc and bcl-2 oncoprotein may be related to the pathogenesis of gingival hyperplasia induced by nifedipine and phenytoin, especially to the morphogenesis of hyperplastic epithelia.
authors.affiliation: Department of Preventive Dentistry, School of Dentistry, Tohoku University, Sendai, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Saito
authors.forename: S
authors.initials: S
authors.lastname: Mori
authors.forename: N
authors.initials: N
authors.lastname: Tanda
authors.forename: S
authors.initials: S
authors.lastname: Sakamoto
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000927:Anticonvulsants / Q000009:adverse effects*; D002121:Calcium Channel Blockers / Q000009:adverse effects*; D004847:Epithelial Cells / Q000378:metabolism / Q000473:pathology; D004848:Epithelium / Q000378:metabolism / Q000473:pathology; D005260:Female; D005786:Gene Expression Regulation; D005881:Gingiva / Q000378:metabolism / Q000473:pathology; D005885:Gingival Hyperplasia / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology*; D006706:Homeostasis; D006801:Humans; D007124:Immunoenzyme Techniques; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009024:Morphogenesis; D009543:Nifedipine / Q000009:adverse effects*; D010672:Phenytoin / Q000009:adverse effects*; D000090063:Proto-Oncogene Mas; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis* / Q000235:genetics; D016271:Proto-Oncogene Proteins c-myc / Q000032:analysis* / Q000235:genetics
chemical_list: D000927:Anticonvulsants; D002121:Calcium Channel Blockers; C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D019253:Proto-Oncogene Proteins c-bcl-2; D016271:Proto-Oncogene Proteins c-myc; D010672:Phenytoin; D009543:Nifedipine