TGF‐β1 gene polymorphism in renal transplant patients with and without gingival overgrowth

Abstract

Oral Diseases (2011) 17, 414–419 Background: The incidence of gingival overgrowth among renal transplant patients treated with cyclosporine A ranges from 13% to 84.6%, and the overgrowth is not only esthetic but also a medical problem. We studied the determination of association between TGF‐β1 (TGFB1) gene polymorphism and gingival overgrowth in kidney transplant patients medicated with cyclosporin A. Methods: Eighty‐four kidney transplant patients with gingival overgrowth and 140 control transplant patients without overgrowth were enrolled into the case control study. TGFB1 polymorphism was determined using the PCR‐RFLP assay for +869T>C in codon 10 and +915G>C in codon 25 as well as TaqMan real‐time PCR assays for promoter −800G>A and −509C>T SNPs. Results: In kidney transplant patients suffering from gingival overgrowth, mean score of gingival overgrowth was 1.38 ± 0.60, whereas in control subjects it was 0.0. The patients with gingival overgrowth were characterized by similar distribution of TGFB1 genotypes and allele in comparison to subjects without gingival overgrowth. Among 16 potentially possible haplotypes of TGFB1 gene, only four were observed in the studied sample of kidney transplant patients: G_C_T_G, G_T_C_G, G_C_C_C, and A_C_T_G, with similar frequency in patients with and without gingival overgrowth. Conclusion: No association between the TGFB1 gene polymorphism and gingival overgrowth was revealed in kidney transplant patients administered cyclosporine A.

Cyclosporine A‐induced gingival overgrowth in renal transplant patients accompanied by epithelial‐to‐mesenchymal transition

“…In addition to influential clinical factors, such as age, sex, the blood CsA concentration, the degree of renal injury, any drug combinations, and plaque-induced inflammation, studies have mainly focused on tissue fibrosis, oxidative stress, and the epithelial-tomesenchymal transition (EMT). 2,5,[10][11][12][13] The histopathological manifestations of drug-induced GO indicate that treatment with CsA thickens the gingival epithelium and increases the gingival fibroblasts in the lamina propria and collagen deposition. 14 It has been reported that CsA upregulates the expression of the fibrosis marker glutaminase 2 in gingival fibroblasts.…”