The role of SNPs in TGF-ß1 at codon 10 and 25 and the occurrence of severe periodontitis

TGF-ß1 is a pleiotropic cytokine that exerts its effects on bone and connective tissue metabolism which are of great importance in periodontal diseases. The expression of TGF-ß1 has been shown to be under genetic control. Two SNPs at codon 10 (L10P) and codon 25 (R25P) represent functionally important genetic variants. Therefore, the aim of this study was to evaluate links between genetic variants of TGF-ß1 and chronic/aggressive periodontitis and its clinical features. Patients and methods: One hundred and forty nine periodontitis patients (chronic: n=68, mean age=48.9+9.6y, 64.2% females; aggressive: n=81, mean age=40+9.5y, 63% females) and 82 healthy controls (mean age=46.6+10.7y, 53.7% females) without periodontitis were included in the study. TGF-ß1 polymorphisms and haplotypes were determined using PCR-SSP (CTS-Kit, Heidelberg, Germany). The clinical investigation included smoking status, plaque (API) and bleeding indexes (BOP), pocket depth (PD) and clinical attachment loss (CAL). Subgingival bacterial colonization was evaluated molecularbiologically using the micro-Ident®test (HAIN-Diagnostik, Nehren, Germany). Results: Hardy-Weinberg criteria were fulfilled for both SNPs. Comparing TGF-ß1 genotype and haplotype distribution no significant association with the occurrence of aggressive and chronic periodontitis could be proven in our study. However, there was a trend for a higher occurrence of the CC-genotype L10P among periodontitis-free controls compared to patients suffering from aggressive periodontitis (18.3% vs. 11.1%, n.s.). Furthermore, the genetic background of TGF-ß1 was not significantly associated with the subgingival colonization of periodontopathogens. However, among patients with chronic periodontitis bacteria of the red complex (P. gingivalis+T. forsythia. denticola) occurred less frequently in carriers of the TG haplotype (TG: 77.5% vs. CG+CC: 91.5%, p=0.042, pkorr.=0.073). Conclusions: Although, associations of the genetic background of TGF-ß1 and periodontitis and periodontopathogens could be shown in bivariate analyses in binary logistic regression analyses the SNPs L10P and R25P and corresponding haplotypes could not be proved as independent risk factors for chronic or aggressive periodontitis. Schlagwörter: periodontitis, SNP, TGF-ß1