Background: Gingival enlargement is a known side effect of nifedipine use. This study was conducted to determine the prevalence and risk factors for gingival enlargement in nifedipinetreated patients.Methods: A cross-sectional study was conducted in a primary care center. Data from 65 patients taking nifedipine were compared with 147 controls who had never received the drug. All patients were examined for the presence of gingival enlargement using 2 different indices: vertical gingival overgrowth index (GO) in 6 points around each tooth, and horizontal MB index in the interdental area. Gingival index, plaque index, and probing depth were also evaluated.Results: The prevalence of gingival enlargement was significantly higher in nifedipine-treated cases than in controls (GO index, 33.8% versus 4.1%; MB index, 50.8% versus 7.5%, respectively). Higher gingival and plaque indices were observed in patients taking nifedipine. Among the possible risk factors, only the gingival index showed a significant association with gingival enlargement. The risk (odds ratio [OR]) of gingival enlargement associated with nifedipine therapy was 10.6 (3.8-29.1) for the GO index and 14.4 (6-34.6) for the MB index. Gingival index-adjusted ORs were 9.6 (3.3-28.1) and 9.7 (3.9-23.3), respectively. In the subset of high nifedipine exposure patients, the odds ratio for gingival enlargement increased to 17.4 (5.3-56.3) for the 3) for the MB index. The concordance between GO and MB indices showed a kappa value of 0.689 in controls and 0.642 in patients treated with nifedipine.Conclusions: Patients taking nifedipine are at high risk for gingival enlargement, and gingivitis acts as a predisposing factor. J Periodontol 2001;72:605-611.
Gingival enlargement, an abnormal growth of the periodontal tissue, is mainly associated with dental plaque-related inflammation and drug therapy. Its true incidence in the general population is unknown. Gingival enlargement produces aesthetic changes, pain, gingival bleeding and periodontal disorders. Although gingival overgrowth has been traditionally recognised as an adverse effect of phenytoin therapy, it has recently been reported in association with the use of cyclosporin and calcium antagonists. These 3 classes of drugs produce important changes in fibroblast function, which induce an increase in the extracellular matrix of the gingival connective tissue. In the majority of those patients for whom dosage reduction, or drug discontinuation or substitution is not possible, and for whom prophylactic measures have failed, surgical excision of gingival tissue remains the only treatment of choice.
This study reports significant differences in the prevalence and severity of gingival overgrowth in two groups of patients, one treated with phenytoin, and another treated with other anticonvulsants. Gingival inflammation is a significant risk factor for gingival enlargement in these patients.
Patients taking diltiazem are at high risk for gingival enlargement and gingivitis has a stronger effect than the drug treatment on gingival enlargement risk.
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