title: Single nucleotide polymorphisms in interleukin-1gene cluster and subgingival colonization with Aggregatibacter actinomycetemcomitans in patients with aggressive periodontitis.
abstract: Periodontitis is initiated by the subgingival occurrence of periodontopathogens. It is triggered by a specific host-dependent immune response that is influenced by genetic predisposition. Polymorphisms in the interleukin-1 (IL-1) gene cluster have been suggested to influence the pathogenesis of periodontitis. A total of 159 periodontitis patients (chronic disease: n = 73, aggressive disease: n = 86) and 89 periodontitis-free controls were included in the study. Polymorphisms IL-1α (rs1800587), IL-1β (rs16944, rs1143634), IL-1 receptor (rs2234650), and IL-1 receptor antagonist (rs315952) were determined by polymerase chain reaction with sequence-specific primers (PCR-SSP). Subgingival bacterial colonization was assessed using a polymerase chain reaction/DNA probe test (micro-Ident). Haplotype block structure was determined using Haploview 4.2. Statistical analyses were performed applying SPSS 17.0 considering dominant, recessive, and codominant genetic models. In this case-control study, no association between genomic variants of the IL-1 gene cluster and the incidence of severe periodontitis could be shown. Carriers of the rare genotypes of rs1800587 (p(corr) = 0.009), rs1143634 (p(corr) = 0.009) and composite genotype (rs1800587+rs1143634) (p(corr) = 0.031) had a twofold higher risk for subgingival occurrence of Aggregatibacter actinomycetemcomitans. In forward stepwise binary logistic regression analyses considering age, gender, smoking, and approximal plaque index as potential confounders these significant associations were demonstrated. Despite the genetic background of IL-1 gene cluster could be shown to be associated with subgingival colonization of A actinomycetemcomitans, there is no evidence that it is an independent risk indicator for periodontitis.
authors.affiliation: Department of Operative Dentistry and Periodontology, University School of Dental Medicine, Martin-Luther University, Halle-Wittenberg, Halle, Germany. susanne.schulz@medizin.uni-halle.de
authors.forename: Susanne
authors.initials: S
authors.lastname: Schulz
authors.forename: Jamal M
authors.initials: JM
authors.lastname: Stein
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Altermann
authors.forename: Jana
authors.initials: J
authors.lastname: Klapproth
authors.forename: Uta
authors.initials: U
authors.lastname: Zimmermann
authors.forename: Yvonne
authors.initials: Y
authors.lastname: Reichert
authors.forename: Christiane
authors.initials: C
authors.lastname: Gläser
authors.forename: Hans-Günter
authors.initials: HG
authors.lastname: Schaller
authors.forename: Stefan
authors.initials: S
authors.lastname: Reichert
mesh_terms: D000189:Actinobacillus Infections / Q000150:complications / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D000328:Adult; D016976:Aggregatibacter actinomycetemcomitans / Q000502:physiology*; D010520:Aggressive Periodontitis / Q000453:epidemiology / Q000209:etiology / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D000483:Alleles; D016022:Case-Control Studies; D055113:Chronic Periodontitis / Q000453:epidemiology / Q000209:etiology / Q000235:genetics* / Q000276:immunology / Q000382:microbiology; D003774:Dental Plaque Index; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D005858:Germany; D006239:Haplotypes; D006801:Humans; D053582:Interleukin-1alpha / Q000235:genetics*; D053583:Interleukin-1beta / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D017472:Receptors, Interleukin-1 / Q000235:genetics*
chemical_list: D053582:Interleukin-1alpha; D053583:Interleukin-1beta; D017472:Receptors, Interleukin-1