On the mechanism of drug-induced gingival hyperplasia.
Proposed mechanisms of the side effect of drug-induced gingival hyperplasia are reviewed. Hypotheses with regard to inflammation from bacterial plaque, increased sulfated glycosaminoglycans, immunoglobulins, gingival fibroblast phenotype population differences, epithelial growth factor, pharmacokinetics and tissuebinding, collagenase activation, disruption of fibroblast cellular sodium/calcium flux, folic acid and a combination hypothesis are evaluated.
Brown
R S
RS
Department of Oral Diagnostic Sciences, University of Texas, Houston.
Beaver
W T
WT
Bottomley
W K
WK
D003773:Dental Plaque / Q000382:microbiology; D004110:Diltiazem / Q000493:pharmacokinetics; D004815:Epidermal Growth Factor / Q000502:physiology; D005347:Fibroblasts / Q000737:chemistry / Q000473:pathology; D005492:Folic Acid / Q000502:physiology; D005885:Gingival Hyperplasia / Q000139:chemically induced* / Q000503:physiopathology*; D006025:Glycosaminoglycans / Q000502:physiology; D006801:Humans; D007132:Immunoglobulin Isotypes / Q000276:immunology; D003012:Microbial Collagenase / Q000378:metabolism; D009543:Nifedipine / Q000493:pharmacokinetics; D010672:Phenytoin / Q000493:pharmacokinetics
D006025:Glycosaminoglycans; D007132:Immunoglobulin Isotypes; D010672:Phenytoin; D004815:Epidermal Growth Factor; D005492:Folic Acid; D003012:Microbial Collagenase; D004110:Diltiazem; D009543:Nifedipine