Polymorphisms in the IL-6 and FcγRIIIa genes in aggressive periodontitis

*0478 Polymorphisms in the IL-6 and FcγRIIIa genes in aggressive periodontitis*
B. GROESSNER-SCHREIBER¹, S. JEPSEN², C. SCHOLZ¹, C. SCHAEFER², K. SCHENCK³, U. VAN DER VELDEN⁴, J. HAMPE¹, B.G. LOOS⁴, and S. SCHREIBER¹, ¹ University of Kiel, Germany, ² University of Bonn, Germany, ³ University of Oslo, Norway, ⁴ ACTA, Amsterdam, Netherlands Objectives: Several lines of research have suggested that susceptibility to periodontitis has a genetic basis. Recent association studies on small patient cohorts report positive correlations, in some population groups, with polymorphisms of genes, which modulate inflammation. These include several interleukin and FcgR genes. The purpose of this study was to examine two important genes in inflammation pathophysiology. SNP's in the IL-6 and FcgRIIIa genes have also been implied in the genetic etiology of other inflammatory diseases. A large patient cohort with a pronounced disease phenotype for early-onset, aggressive periodontitis was studied. Methods: 270 unrelated European Caucasian patients with aggressive periodontitis were recruited through the European Periodontal Genetics (EPG) consortium. Patients needed to be £35 years of age at the time of diagnosis and must have ³2 teeth with ³50% bone loss on dental radiographs. A reference control group was recruited through anonymous blood donors also from European Caucasian descent with unknown periodontal status (n=360-720). Two SNP's in the promoter of IL-6 (-174 and -572), and one SNP in FcgRIIIa (rs396991) were genotyped using Taqman technology. Results: The results of this case-control study showed a weakly significant association between aggressive periodontitis and the IL-6 promoter polymorphism at position –174. Allele 1 prevalence for the SNP at position –174 was 62% for the patients and 55% for the controls (P=0.06. Allele 1 frequency for the SNP at position -572 was 5% for both patients and controls. Genotyping of the FcgRIIIa polymorphism revealed no significant differences between patients and controls. Conclusions: A trend for increased prevalence of allele 1 at -174 in the IL-6 promoter warrants further investigation, as IL-6 is an important mediator in inflammation pathophysiology.
Seq #46 - Periodontal Research 11:30 AM-1:30 PM, Saturday, 28 August 2004 Crowne Plaza Hotel SEDEF I
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