The gingival crevicular fluid levels of growth factors in patients with amlodipine-induced gingival overgrowth: A pilot study.

BACKGROUND: Amlodipine, calcium channel blocker (CCB), is used in the management of cardiovascular diseases which causes gingival overgrowth (GO). The growth factors may have a role in the pathogenesis of amlodipine-induced GO. OBJECTIVES: This pilot study aimed to investigate the growth factors including transforming growth factor-b1 (TGF-b1), platelet-derived growth factor-BB (PDGF-BB), and basic fibroblast growth factor (bFGF) in gingival crevicular fluid (GCF) of patients with amlodipine-induced GO and compare with of healthy subjects. METHODS: GCF samples were collected from 56 sites presenting GO (GO + group) and from 38 sites not presenting GO (GO- group) of 5 patients using amlodipine for more than one year, and from 45 sites (control group) of 5 healthy subjects. The levels of TGF-b1, PDGF-BB, and bFGF were determined by using ELISA kits. RESULTS: The mean concentration of TGF-b1 in GCF samples of GO + group (9.50 ± 7.30 ng/ml) was higher than both GO- group (2.07 ± 0.50 ng/ml) and control group (2.74 ± 1.01 ng/ml) (P = 0.014). No significant difference was found among the groups in the GCF levels of PDGF-BB (P = 0.767). bFGF was detected in only 33% of the sites from patients. CONCLUSION: These preliminary results suggest that TGF-b1 may play a crucial role in the pathogenesis of amlodipine-induced GO.

Expression of growth factors in the gingival crevice fluid of patients with phenytoin-induced gingival enlargement.

The mechanism underlying phenytoin (PHT)-induced gingival enlargement (GE) is not yet known. The aim of the present study was to investigate transforming growth factor-beta1 (TGF-beta1), platelet-derived growth factor-BB (PDGF-BB) and basic fibroblast growth factor (bFGF) profiles in the gingival crevice fluid (GCF) of patients with PHT-induced GE and to compare the results with healthy controls. Five PHT-treated patients and five healthy subjects with normal periodontal tissue were included in this study. GCF samples were collected from (i) enlarged gingival sites in patients receiving PHT (GE+); (ii) non-enlarged gingival sites in the same patients (GE-); (iii) normal gingival sites of healthy subjects (control). The levels of TGF-beta1, PDGF-BB and bFGF in the GCF samples were analysed by ELISA. The results showed that the total amounts of TGF-beta1 and PDGF-BB in the GE+ group were higher than in the GE- group and significantly higher than in the control group (P < 0.05). However, no significant differences were found between the groups when the concentrations of these growth factors were compared. bFGF levels were not compared as this growth factor could be detected in only 33, 41 and 44% of the GE+, GE- and control GCF samples, respectively. These results show that TGF-beta1 and PDGF-BB are readily detectable in GCF obtained from enlarged and non-enlarged sites of PHT recipients and suggest that since the amounts were markedly higher at the GE+ than the GE- sites, the systemic administration of PHT has a pronounced localised effect on the levels of these growth factors. Moreover, our findings provide evidence that both TGF-beta1 and PDGF-BB are closely associated with the clinical manifestation of PHT-induced GE.