Background: Currently, the etiology of drug-induced gingival overgrowth is not entirely understood but is clearly multifactorial. Phenytoin, one of the common drugs implicated in gingival enlargement, is metabolized mainly by cytochrome P450 (CYP)2C9 and partly by CYP2C19. The CYP2C9 and CYP2C19 genes are polymorphically expressed and most of the variants result in decreased metabolism of the respective substrates.
View Article and Find Full Text PDFBackground: Gingival recession is significantly more common among smokers, while cigarette smoking has been shown to negatively influence healing following periodontal therapeutic procedures as compared to non-smokers. The objective of this study was to evaluate the influence of cigarette smoking on the outcome of coronally positioned flap (CPF) in the treatment of Miller Class I gingival recession defects.
Materials And Methods: Ten current smokers (≥10 cigarettes daily for at least 5 years) and 10 non-smokers (never smokers), each with one 3 to 4-mm Miller Class I recession defect in an upper canine or bicuspid, were treated with CPF.