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Nifedipine and Cyclosporin Affect Fibroblast Calcium and Gingiva

¹ Department of Periodontology, Facultad de Odontologia, University of Sevilla, c/Avicena s/n, 41009 Sevilla, Spain;
² Institute of Anatomy and Pathologic Histology, Università Politecnica delle Marche, Ancona, Italy;
³ Institute of Biochemistry, Università Politecnica delle Marche, Ancona, Italy;
⁴ Department of Medical Physiology and Biophysics, University of Sevilla, Spain; and
⁵ Emeritus Professor of Periodontology and Preventive Dentistry, University of London, UK

^* corresponding author, pbullon{at}us.es

It has been stated that cyclosporin and nifedipine produce gingival overgrowth. However, the specific pathogenic mechanism remains uncertain. We used an experimental rat model to test the hypothesis that changes in collagen metabolism and numbers of gingival blood vessels are not mediated by intracellular calcium concentration (ratiometric Fura-2 AM measurement) in gingival fibroblasts. In the cyclosporin group, both width (364.2 ± 67.5 µm) and microvessel density (number of vessels/mm², stained with anti-CD34 antibody) (41.6 ± 5.1) of gingiva were statistically different when compared with those in the control group (width = 184.3 ± 35.2 µm, microvessel density = 19.6 ± 2.4). The nifedipine group showed the highest content of collagen (proportion of total stroma occupied by collagen, stained with Picro-Mallory) (nifedipine group = 66.3 ± 9.4, cyclosporin group = 55.2 ± 7.9, control group = 30.1 ± 10.2). Freshly cultured fibroblasts from the cyclosporin group exhibited higher ratiometric values of fluorescence than did both the control and nifedipine groups (p = 0.03). Our results support the hypothesis that changes in gingival collagen metabolism are not mediated by calcium intracellular oscillations.

KEY WORDS: nifedipine • cyclosporin A • gingival overgrowth • Fura • intracellular calcium