REGRESSION OF NIFEDIPINE-INDUCED GINGIVAL HYPERPLASIA FOLLOWING SWITCH TO A SAME CLASS CALCIUM-CHANNEL BLOCKER, ISRADIPINE

Citation
P. Westbrook et al., REGRESSION OF NIFEDIPINE-INDUCED GINGIVAL HYPERPLASIA FOLLOWING SWITCH TO A SAME CLASS CALCIUM-CHANNEL BLOCKER, ISRADIPINE, Journal of periodontology, 68(7), 1997, pp. 645-650
Citations number
38
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
Journal title
ISSN journal
00223492
Volume
68
Issue
7
Year of publication
1997
Pages
645 - 650
Database
ISI
SICI code
0022-3492(1997)68:7<645:RONGHF>2.0.ZU;2-2
Abstract
PATIENTS WITH NIFEDIPINE-INDUCED gingival hyperplasia (GH) often requi re continued calcium channel blocker therapy. Switches to diltiazem an d verapamil have been described; however, these drugs are of a differe nt chemical class and present therapeutic limitations in some patients . The purpose of this study was to evaluate the effect on nifedipine-i nduced GH of a switch to a dihydropyridine derivative with a low incid ence of GH. Fourteen patients with nifedipine-induced GH were given a medical exam and a periodontal exam. The following parameters were ass essed: probing depth (PD), gingival margin (GM), gingival thickness (G T), plaque index (PI), and gingival index (GI). Intraoral photographs, study models, and a gingival biopsy for histological examination were taken. Following baseline measures, patients were randomized to conti nued treatment with nifedipine or an equivalent dose of isradipine in a single-blind fashion. Biweekly periodontal parameters were taken for 8 weeks. At the end of 8 weeks, some patients elected to receive 4 we eks of open label isradipine therapy, with biweekly examination contin uing through the open label phase. The isradipine treatment arm showed a mean decrease in PD of 0.59 mm at week 8 (P < 0.05). No other measu red parameter (GM, GT, PI, GI) was significantly changed, compared eit her to baseline or to the alternate treatment arm. Clinically, 60% of patients treated with isradipine exhibited a decrease in hyperplasia, while 66% of patients treated with nifedipine demonstrated an increase in hyperplasia, a significant difference (F < 0.05). When combined wi th open label data, patients switching therapy to isradipine exhibited an increase in GM (increase in recession) of 0.74 mm from baseline to week 12 (P < 0.05). No patients treated with isradipine exhibited an increase in gingival overgrowth. All patients exhibited adequate contr ol of hypertension. We conclude that in hypertensive patients with nif edipine-induced GH, switching hypertensive therapy to isradipine may r esult in a regression of GH. When coupled with aggressive oral hygiene treatment, this drug may provide a reasonable option for patients req uiring dihydropyridine treatment.