TLR4 and IL-18 gene variants in aggressive periodontitis

• Published in: Journal of clinical periodontology Vol. 35; no. 12; pp. 1020 - 1026
• Main Authors: Noack, Barbara, Görgens, Heike, Lorenz, Katrin, Ziegler, Andreas, Hoffmann, Thomas, Schackert, Hans Konrad
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.12.2008; Blackwell
• Subjects: Adult; aggressive periodontitis; Aggressive Periodontitis - genetics; Aggressive Periodontitis - immunology; Biological and medical sciences; Case-Control Studies; Dentistry; European Continental Ancestry Group; Facial bones, jaws, teeth, parodontium: diseases, semeiology; Female; Gene Frequency; Genetic Predisposition to Disease; genetic risk; Genotype; Humans; IL-18 gene; innate immune response; Interleukin-18 - genetics; Logistic Models; Male; Medical sciences; Middle Aged; Mutation, Missense; Non tumoral diseases; Otorhinolaryngology. Stomatology; Polymorphism, Single Nucleotide; Promoter Regions, Genetic; TLR4 gene; Toll-Like Receptor 4 - genetics; Immune response; Stomatology; TLR4 gene; Dentistry; IL-18 gene; Periodontal disease; Gene; Periodontitis; innate immune response; Risk factor; genetic risk; Genetics; aggressive periodontitis
• ISSN: 0303-6979; 1600-051X
• DOI: 10.1111/j.1600-051X.2008.01334.x

Aim: We aimed to assess the association of different genotypes with increased aggressive periodontitis susceptibility by studying functional relevant variants in the pathogen‐recognition receptor Toll‐like receptor 4 (TLR4) and variants in the promoter region of the pro‐inflammatory cytokine interleukin‐18 (IL‐18). Material and Methods: One hundred and eleven patients with aggressive periodontitis and 80 periodontally healthy controls were genotyped for four functional variants in the TLR4 gene (c.896A>G and c.1196C>T) and in the IL‐18 promoter (c.−368G>C and c.−838C>A). The genotype and allele frequencies, as well as the frequency of combined genotypes were compared between study groups. Results: There were no statistical differences in genotype and allele frequencies within the four variants between the groups. All study subjects were further classified into carriers and non‐carriers of at least one variant of both genes. The logistic regression analysis adjusted for gender and smoking showed no association between carrier status of at least one variant of both genes and periodontal status (OR=1.41, 95% CI: 0.43–4.70). Conclusions: Our results reject the hypothesis that functionally relevant IL‐18 and TLR4 gene mutations have a major effect on aggressive periodontitis susceptibility alone or in combination.