Mechanism of drug-induced gingival overgrowth revisited: a unifying hypothesis

被引:52
|
作者
Brown, R. S. [1 ,2 ,3 ]
Arany, P. R. [4 ]
机构
[1] Howard Univ, Coll Dent, Dept Comprehens Dent, Div Oral Diag, Washington, DC 20059 USA
[2] Georgetown Univ, Med Ctr, Dept Otolaryngol, Washington, DC 20007 USA
[3] NHLBI, Hematol Branch, NIH, Bethesda, MD 20892 USA
[4] NIDCR, NIH, Bethesda, MD USA
关键词
drug-induced gingival overgrowth; folic acid; matrix metalloproteins; calcineurin inhibitors; calcium channel blocking agents; phenytoin; FOLIC-ACID SUPPLEMENTATION; NONINSTITUTIONALIZED EPILEPTIC CHILDREN; CONNECTIVE-TISSUE METABOLISM; GENE-EXPRESSION; EXTRACELLULAR-MATRIX; PLAQUE CONTROL; CALCIUM-ANTAGONISTS; ACTIVATOR PROTEIN-1; CYCLOSPORINE; PHENYTOIN;
D O I
10.1111/odi.12264
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Drug-induced gingival overgrowth (DIGO) is a disfiguring side effect of anti-convulsants, calcineurin inhibitors, and calcium channel blocking agents. A unifying hypothesis has been constructed which begins with cation flux inhibition induced by all three of these drug categories. Decreased cation influx of folic acid active transport within gingival fibroblasts leads to decreased cellular folate uptake, which in turn leads to changes in matrix metalloproteinases metabolism and the failure to activate collagenase. Decreased availability of activated collagenase results in decreased degradation of accumulated connective tissue which presents as DIGO. Studies supporting this hypothesis are discussed.
引用
收藏
页码:E51 / E61
页数:11
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