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INTRODUCTION: Nifedipine is a relatively new and increasingly used medication for treatment of all kinds of angina pectoris and arterial hypertension. The principal action of nifedipine is to inhibit the influx of extracellular calcium ions across the membranes of cardiac and vascular smooth muscle cells, without changing serum calcium concentration (1). One of the side effects of this drug is gingival hyperplasia which was first described in 1984 by Lederman (2). He noted that gingival hyperplasia is mostly marked on the labial gingiva of the upper and lower anterior teeth and appeared 1 to 2 months after nifedipine therapy began at a dose of 90 mg per day, and never occurs in edentulous areas. This paper reports gingival hyperplasia in a patient treated with nifedipine. CASE REPORT: A 73-year-old man referred to the dental clinic for evaluation of gingival enlargement in the maxillar left quadrant which he had noticed about 3 months after starting the nifedipine therapy. Clinical examination showed gingival enlargement around the teeth 22, 23, 24 and 27, but with normal edentulous area (Fig. 1). The enlarged gingiva was red, smooth and shiny, with no pain on touch, and bled easily on probing. There were metal crowns with overhanging margins and pseudopockets--6 mm with dental plaque and calculus. Radiographs showed moderate alveolar bone resorption of horizontal type. The patient's maxillar left first premolar exhibited severe bone loss, resulting in a hopeless prognosis. This tooth was extracted under local anesthesia. The dental treatment included replacement of the ill-fitting metal crowns, scaling and root planning, and instructions on appropriate method for brushing teeth. 6 weeks later, the hyperplastic tissues were removed surgically. In a 1-year follow-up period, the patient was recalled at regular intervals for control, and no signs of recurrence of gingival hyperplasia have been observed in spite of continued nifedipine treatment. Biopsies taken from the gingivectomy specimens were handled with standard histological method. Histological examination showed a thick epithelium with parakeratosis and acanthosis, and irregular elongation of the rete peg. The underlying connective tissues contained dense fibers with inflammatory cell infiltrate mainly composed of plasma cells. DISCUSSION: The exact mechanism of action of nifedipine in causing gingival enlargement is unknown at present. There is also no answer to the question why gingival enlargement appears in some patients treated with nifedipine, but in others not. The clinical findings (3, 4, 5, 6, 7) and results of in vitro study (8) and this case report showed that hyperplastic change of gingiva started only in areas displaying signs of inflammation, but not in healthy and edentulous areas. These observations suggest that local factors and associated inflammation is essential for onset of the nifedipine-induced gingival hyperplasa. Moreover, it was suggested that duration of nifedipine therapy (more than 2 months) and drug dosage (90 mg per day) could be important (1,2,3). This case report also demonstrates that no signs of recurrence of hyperplasia were observed after elimination of the local inflammatory factors: extensive dental pluque control and surgical removal of the hyperplastic gingival tissue even though administration of nifedipine was continued. CONCLUSION: It was concluded that gingival enlargement occurs in patients with nifedipine therapy only in the areas where local inflammatory factors are present.