Poster 489, Language: GermanSchulz, Susanne/Klapproth, Jana/Zimmermann, Uta/Reichert, Yvonne/Stein, Jamal M./Gläser, Christiane/Schaller, Hans-Günter/Reichert, StefanBackground: Periodontitis is characterized as a chronic inflammatory disease. Periodontopathogens induce innate responses amongst others via CD14 and 4 resulting in activation of NF-κB. Functional important SNPs are described for these genes. The aim of this study was to evaluate links between SNP and the subgingival occurrence of periodontopathogens.
Patients and Methods: 133 periodontitis patients (chronic periodontitis: n=60, mean age: 48.7+9.7y, aggressive periodontitis: n=73, mean age: 41+9.9y) and 80 healthy controls without periodontitis were included in the study. SNPs in CD14 (c.-159C>T), in TLR4 (Asp299Gly, Thr399Ile) were determined by RFLP. Subgingival bacterial colonization (A. actinomycetemcomitans, P. gingivalis, P. intermedia, T. forsythia, T. denticola) was analysed molecularbiologically using the micro-Ident®test.
Results: Associations between genotype and the occurrence of periodontopathogens could be shown: P. intermedia occurred less frequently in individuals positive for the TT genotype of CD14-SNP c.-159C>T (OR=0.36, 95%CI: 0.14-0.91, p=0.045). In binary logistic regression analyses, the associations for TT-genoytpe (OR=0.31, CI: 0.12-0.81, p=0.017) could be proven considering age, gender, smoking, and clinical attachment loss as confounding factors. No genotype dependent association with subgingival occurrence of periodontopathogens could be proven for SNPs in TLR4. However, no significant association with chronic and or aggressive periodontitis and polymorphisms in CD14 and TLR4 could be proven.
Conclusions: Although, the CD14 c.-159C>T polymorphism could be shown to be associated with subgingival colonization with P. intermedia there is no evidence that CD14 and TLR4 polymorphisms investigated are independent risk factors for chronic or aggressive periodontitis in German periodontitis patients.
Keywords: Parodontitis, SNP, CD14, TLR4, Pardontopathogene