Int Poster J Dent Oral Med 9 (2007), No. 4 15. Dec. 2007
Int Poster J Dent Oral Med 9 (2007), No. 4 (15.12.2007)
Poster 384, Language: English
No association of genetic variants of interleukin 6 and the susceptibility
Schulz, Susanne/Zimmermann, Uta/Schaller, Hans-Günter/Machulla, Helmut/Altermann, Wolfgang/Gläser, Christiane/Reichert, Stefan
No association of genetic variants of interleukin 6 and the susceptibility to periodontitisS Schulz1, J Klapproth1, U Zimmermann1, HG Schaller1, HKG Machulla2, W Altermann2, C Gläser3, S Reichert11 University School of Dental Medicine, Department of Operative Dentistry and Periodonto-logy, 2 Interbranch HLA Laboratory - Department GHATT, and3 Institute of Human Genetics and Medical Biology, Medical School, Martin-Luther-University, Halle, GermanyPeriodontitis as a chronic inflammatory disorder is influenced by environmental and genetic factors. Several factors of the immune response and their genetic background have been proposed as potential markers for the susceptibility to this disease.The aim of the present study was to evaluate the importance of genomic variants of the potent proinflammatory cytokine interleukin 6 (IL6) for the incidence of chronic and aggressive periodontitis. Patients and Methods: In the present study 107 periodontitis patients (chronic: n=48, mean age: 48.1+10.1y, 33.3% males; aggressive: n=59, mean age: 41.6+9.8y, 35.6% males) and 40 control probands without periodontitis (mean age: 43.9+11.1y, 40 % males) were included. Clinical parameter including smoking status, plaque and bleeding indexes, pocket depth and attachment loss were assessed. Subgingival bacterial colonization was analyzed molecular biologically using the micro-Ident® test (Hain-Diagnostik, Nehren). We investigated genotype, allele and haplotype frequencies of the IL6-promotor SNP-174G>C and -597G>A by use of PCR-SSP (CTS-Kit, Heidelberg). Results: Hardy-Weinberg criteria were fulfilled for both SNPs. Investigating genotype, haplotype and allele frequencies no significant disease specific differences could be detected in comparison with healthy controls. Furthermore, the genetic background of IL6 was not associated with clinical and microbiological parameters investigated except attachment loss. In the group of patients suffering from aggressive periodontitis heterozygous genotypes were significantly associated with increased attachment loss (-174G>C: p=0.035; -597G>A: p=0.04) Conclusions: Although, the genetic background of IL6 was associated with attachment loss representing a clinical parameter of periodontitis the genetic variants -174G>C and -597G>A could not be described as independent risk factors for chronic or aggressive periodontitis.
Keywords: interleukin 6, genetic, aggressive periodontitis, chronic periodontitis
Jahrestagung der Deutschen Gesellschaft für Humangenetik