Der -94 ins/delATTG Promotor-polymorphismus im Transkriptionsfaktor NF-kB bei Patienten mit aggressiver oder chronischer Parodontitis

The transcription factor NF-kB is involved in the regulation of the expression of inflammatory genes. Its expression is influenced, among others, by a -94 ins/delATTG polymorphism in the promoter region of the gene. Therefore, the aim of the present study was to evaluate the importance of this genomic variant for the incidence of chronic and aggressive periodontitis and its clinical markers. Patients and Methods: In the present study 73 patients with aggressive periodontitis (mean age: 41+9.8y, 37.4% males), 59 patients with chronic periodontitis (mean age: 48.8+9.8y, 33.9% males) and 75 control probands without periodontitis (mean age: 46.3+10.6y, 46.7 % 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 and allele frequencies of the polymorphism by analysis of the fragment length in polyacrylamide gel electrophoresis. Results: Bivariate statistical analyses showed no association of this polymorphism with the incidence of chronic or aggressive periodontitis. Investigating a del-dominant genetic model (ins/ins vs. ins/del + del/del), it could be shown, that carrier of del-genotypes and del-allele had an increased risk for subgingival colonization with A.a. (genotype: p=0.04, allele: p=0.03) und P.i. (genotype: p=0.037, allel: p=0.042). In multivariate analyses considering confounding factors (age, gender, smoking status and pocket depth), del-genotypes and del-allele could be proven as independent risk factors for subgingival colonization with A.a. and P.i. Conclusions: The results suggest, that carriers of del-genotypes and del-allele, respectively, show an increased bacterial colonization with A.a. and P.i. This finding could be possibly caused by an alteration in immune response due to a del-associated decrease in promoter activity. Parole chiave: Parodontitis, NF-kB, Polymorphismus