International Poster Journal of Dentistry and Oral Medicine



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Int Poster J Dent Oral Med 8 (2006), No. 4     15. Dec. 2006
Int Poster J Dent Oral Med 8 (2006), No. 4  (15.12.2006)

Poster 339, Language: English

Is the genetic background of the proinflammatory cytokine TNF-α a predictor for the development of aggressive and/or chronic periodontitis?
Schulz, Susanne/Machulla, Helmut/Klapproth, Jana/Zimmermann, Uta/Schaller, Hans-Günter/Altermann, Wolfgang/Reichert, Stefan
Periodontitis is a chronic inflammatory disorder of the periodontal supporting tissue of teeth. That's why several factors of the immune response and their genetic background have been proposed as potential markers for the development of this disease. However, existing data are very inconsistent. Therefore, the aim of the present study was to evaluate the importance of genomic variants of the potent proinflammatory cytokine TNF-a for the incidence of chronic and aggressive periodontitis. Methods: In the present study 66 periodontitis patients (chronic: n=34, mean age: 47+10.1y, 38.2% males; aggressive: n=32, mean age: 36.6+7.3y, 40.6% males) and 32 control probands without periodontitis (mean age: 41.6+10.3y, 40.6% males) were included. We investigated genotype, allele and haplotype frequencies of the TNFα-SNP -308G>A and -238G>A by use of PCR-SSP (CTS). Results: Hardy-Weinberg criteria were fulfilled for both SNPs in the patient groups. Investigating genotype and allele frequencies of both SNPs no significant disease specific differences could be detected in comparison with healthy controls. However, in the control group a distinct increase in the prevalence of the mutant genotypes (-308G>A: AG+AA; -238G>A: AG) and alleles (-308G>A: A, -238G>A: A), respectively could be described comparing with patients with chronic (-308G>A: 84.8%, -238G>A: 24.4%) and aggressive periodontitis (-308G>A: 39%, -238G>A: 133%). Compared with chronic (p=0.047), aggressive (p=0.024) and total patient group (p=0.015) in the control group a significant increase in carriers of the mutant haplotypes (haplotypes containing mutant A-allele vs. wildtype GG-GG) could be observed. Conclusions: The significant higher prevalence of carriers of the mutant haplotypes in the control group could be an indication for an altered, possibly more effective immune response to periodontal pathogens since these SNPs were considered to trigger the TNF-a production.

Keywords: TNF-alpha, haplotype, aggressive periodontitis, chronic periodontitis

17. Tagung der Deutschen Gesellschaft für Humangenetik