4.5 Article

Evaluation of transforming growth factor-β1 level in crevicular fluid of cyclosporin A-treated patients

Journal

JOURNAL OF PERIODONTOLOGY
Volume 72, Issue 4, Pages 526-531

Publisher

AMER ACAD PERIODONTOLOGY
DOI: 10.1902/jop.2001.72.4.526

Keywords

cyclosporin A/adverse effects; gingival crevicular fluid/analysis; growth factors, transforming; gingival hyperplasia/etiology; kidney transplantation/complications

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Background: The aim of the present study was to investigate the level of transforming growth factor-beta1 (TGF-beta1) in gingival crevicular fluid (GCF) samples of cyclosporin A (CsA)-treated patients and to compare the results with control groups. Methods: Fourteen renal transplant patients exhibiting severe CsA-induced gingival overgrowth, 10 patients with chronic gingivitis, and 10 subjects with clinically healthy periodontium were included in the study. In CsA-treated patients, GCF samples were harvested from sites exhibiting gingival overgrowth (CsA GO+) and sites not exhibiting gingival overgrowth (CsA GO-). The TGF-beta1 levels in a total of 96 GCF samples from the 34 participants were analyzed by enzyme-linked immunosorbent assay. The results were expressed in terms of total amount (pg/2 sites) and concentration (ng/ml). Results: TGF-beta1 total amounts in CsA GO+ and CsA GO-sites were similar and significantly higher than that of healthy sites (P <0.02 and P <0.01, respectively). The total amount of TGF-beta1 was also higher in gingivitis sites compared to the healthy sites, but the difference was not statistically significant (P >0.05). CsA GO+ and CsA GO- sites exhibited higher total amount and concentration of TGF-beta1 than that of gingivitis sites, but the differences were insignificant (P >0.05). Conclusions: The results of the present study support the theory that CsA increases the synthesis of TGF-beta1 in GCF However, since the difference between CsA GO+ and CsA GO- sites was not statistically significant, it seems unlikely that GCF TGF-beta1 level is the sole factor responsible for the CsA-induced gingival overgrowth. Complex interactions between various mediators of inflammation and tissue modeling are possibly involved in the pathogenic mechanisms of this side effect.

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