AIMS: The relationship between gingival overgrowth (GO) induced by cyclosporine A (CsA) and transforming growth factor-beta1 (TGF-beta1) remains unclear. The aims of the present study were to evaluate TGF-beta1 gene expression under different immunosuppressive treatments and its association with TGF-beta1 gene functional polymorphism and GO in renal transplant recipients. MATERIAL AND METHODS: The study included 98 CsA-treated renal transplant recipients (with and without GO) and 44 tacrolimus-treated transplant patients (without GO). TGF-beta1 mRNA expression was measured using a real-time quantitative polymerase chain reaction assay. The levels were correlated with TGF-beta1 gene polymorphisms at codons 10 and 25, with different immunosuppressive treatment and GO. RESULTS: The level of TGF-beta1 gene expression was insignificantly lower in the CsA-treated group compared with the tacrolimus group, and significantly lower in the group with GO compared with patients without GO. In tacrolimus- and CsA-treated patients, but not in patients with GO, the level of TGF-beta1 gene expression was associated with functional phenotypes of TGF-beta1. The incidence, degree and extent of GO were higher in recipients with lower TGF-beta1 gene expression. CONCLUSIONS: Lower level TGF-beta1 gene expression, not functional polymorphism, in patients treated with CsA may be considered to be a risk factor for GO.
AIMS: The relationship between gingival overgrowth (GO) induced by cyclosporine A (CsA) and transforming growth factor-beta1 (TGF-beta1) remains unclear. The aims of the present study were to evaluate TGF-beta1 gene expression under different immunosuppressive treatments and its association with TGF-beta1 gene functional polymorphism and GO in renal transplant recipients. MATERIAL AND METHODS: The study included 98 CsA-treated renal transplant recipients (with and without GO) and 44 tacrolimus-treated transplant patients (without GO). TGF-beta1 mRNA expression was measured using a real-time quantitative polymerase chain reaction assay. The levels were correlated with TGF-beta1 gene polymorphisms at codons 10 and 25, with different immunosuppressive treatment and GO. RESULTS: The level of TGF-beta1 gene expression was insignificantly lower in the CsA-treated group compared with the tacrolimus group, and significantly lower in the group with GO compared with patients without GO. In tacrolimus- and CsA-treated patients, but not in patients with GO, the level of TGF-beta1 gene expression was associated with functional phenotypes of TGF-beta1. The incidence, degree and extent of GO were higher in recipients with lower TGF-beta1 gene expression. CONCLUSIONS: Lower level TGF-beta1 gene expression, not functional polymorphism, in patients treated with CsA may be considered to be a risk factor for GO.