title: Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations.
abstract: OBJECTIVE
  Involvement of TLR2 in the pathophysiology of periodontitis has widely been discussed, but hitherto, no validated genetic associations were reported. Previous association studies lacked sufficient statistical power and adequate haplotype information to draw unambiguous conclusions. The aim of this study was to comprehensively investigate TLR2 linkage disequilibrium (LD) regions for their potential associations with periodontitis in two large analysis populations of aggressive (AgP) and chronic periodontitis (CP) of North West European descent.
  
  
  METHODS
  The study population comprised 598 AgP patients, 914 CP patients and 1804 healthy controls. Analysis of TLR2 LD regions was performed with haplotype tagging SNPs (tagSNPs) using SNPlex and TaqMan genotyping assays. Genotypic, dominant, multiplicative, and recessive genetic models were tested. The genotypes were adjusted for the covariates smoking, diabetes, and gender. Resequencing was performed by Sanger technology.
  
  
  RESULTS
  Upon covariate adjustment and correction for multiple testing, no tagSNPs showed significant associations with AgP or CP. Targeted resequencing of exon 3 in 47 AgP cases identified carriership of two common and three rare variants.
  
  
  CONCLUSIONS
  Common LD regions of TLR2 do not show genetic associations with periodontitis in the North West European population. Resequencing of exon 3 could not identify disease-associated rare variants in TLR2.
authors.affiliation: Christian-Albrechts-University, Institute for Clinical Molecular Biology, Kiel, Germany.
authors.forename: Gesa M
authors.initials: GM
authors.lastname: Richter
authors.forename: Christian
authors.initials: C
authors.lastname: Graetz
authors.forename: Pia
authors.initials: P
authors.lastname: Pohler
authors.forename: Michael
authors.initials: M
authors.lastname: Nothnagel
authors.forename: Henrik
authors.initials: H
authors.lastname: Dommisch
authors.forename: Marja L
authors.initials: ML
authors.lastname: Laine
authors.forename: Mathias
authors.initials: M
authors.lastname: Folwaczny
authors.forename: Barbara
authors.initials: B
authors.lastname: Noack
authors.forename: Peter
authors.initials: P
authors.lastname: Eickholz
authors.forename: Birte
authors.initials: B
authors.lastname: Groessner-Schreiber
authors.forename: Søren
authors.initials: S
authors.lastname: Jepsen
authors.forename: Bruno G
authors.initials: BG
authors.lastname: Loos
authors.forename: Stefan
authors.initials: S
authors.lastname: Schreiber
authors.forename: Arne S
authors.initials: AS
authors.lastname: Schaefer
mesh_terms: D000328:Adult; D010520:Aggressive Periodontitis / Q000235:genetics*; D016022:Case-Control Studies; D055113:Chronic Periodontitis / Q000235:genetics*; D005091:Exons / Q000235:genetics; D005260:Female; D005787:Gene Frequency; D005858:Germany; D006801:Humans; D015810:Linkage Disequilibrium; D008297:Male; D008875:Middle Aged; D008957:Models, Genetic; D009426:Netherlands; D020641:Polymorphism, Single Nucleotide; D017422:Sequence Analysis, DNA; D051195:Toll-Like Receptor 2 / Q000235:genetics*; D044465:White People / Q000235:genetics
chemical_list: D051195:Toll-Like Receptor 2