Several factors of the immune response and their genetic background have been proposed as potential markers for the development of periodontitis. TGFb1 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 TGFb1 is influenced by SNPs located in codon 10 (L10P) and codon 25 (R25P) of this gene. The aim of this study was to evaluate links between genetic variants of TGFb1 and severe periodontitis and its clinical features. Patients/methods: Patients with severe periodontitis (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. TGFb1 polymorphisms and haplotypes were assessed using PCR-SSP (CTS-Kit, Heidelberg, Germany). Subgingival occurrence of periodontopathogens was evaluated molecularbiologically using the micro-Ident®test (HAIN-Diagnostik, Nehren, Germany). The clinical investigation included smoking status, plaque (API) and bleeding indexes (BOP), pocket depth (PD) and clinical attachment loss (CAL). Results: Associations between TGFb1 haplotype and the occurrence of periodontopathogens could be shown among patients with chronic periodontitis. Bacteria of the red complex (P.g.+T.f.+T.d.) occurred less frequently in carriers of the TG haplotype (TG: 77.5% vs. CG+CC: 91.5%, p=0.042). However, after Yates correction the association became not significant. (pkorr.=0.073). Comparing TGFb1 genotype and haplotype distribution no significant association with the occurrence of aggressive and chronic periodontitis could be proven. However, there was a trend for a higher occurrence of the CC-genotype L10P among controls compared to patients suffering from aggressive periodontitis (18.3% vs. 11.1%, n.s.). Conclusions: In binary logistic regression analyses the TGFb1 SNPs L10P and R25P and the corresponding haplotypes could not be proved as independent risk factors for bacterial colonization and chronic or aggressive periodontitis considering age, gender, smoking, and clinical attachment loss as cofactors. Keywords: periodontitis, genetic variants, TGFb1