Background: Periodontitis is initiated by the subgingival occurrence of periodontopathogens. It is triggered by specific host dependent immune response which is influenced by the genetic predisposition. Polymorphisms in the interleukin 1 (IL-1) gene cluster have been suggested to influence the pathogenesis of periodontitis. Patients and methods: A total of 159 periodontitis patients (chronic: n=73, aggressive: n=86) and 89 periodontitisfree controls were included in the study. Polymorphisms IL-1a (rs1800587), IL-1b (rs16944, rs1143634), IL-1 receptor (rs2234650), and IL-1 receptor antagonist (rs315952) were determined by polymerase chain reaction with sequence-specific primers (PCR-SSP). Subgingival bacterial colonization was assessed using a polymerase chain reaction (PCR)/DNA probe test (micro-Ident®). Haplotype block structure was determined using Haploview 4.2. Statistical analyses were performed applying SPSS 17.0 considering dominant, recessive and codominant genetic models. Results: In this case-control-study no association between genomic variants of the IL-1 gene cluster and the incidence of severe periodontitis could be shown. Carriers of the rare genotypes of rs1800587 (pcorr.=0.009), rs1143634 (pcorr.=0.009) and composite genotype (rs1800587+rs1143634) (pcorr.=0.031) had a 2-fold higher risk for subgingival occurrence of A. actinomycetemcomitans. In forward stepwise binary logistic regression analyses considering age, gender, smoking, approximal plaque index as potential confounders these significant associations were proven. Conclusions: Despite the genetic background of IL-1 gene cluster could be shown to be associated with subgingival colonization of A. actinomycetemcomitans there is no evidence that it is an independent risk indicator for periodontitis. Keywords: interleukin-1, genetic, A. actinomycetemcomitans