Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations

G.M. Richter; C. Graetz; P. Pohler; M. Nothnagel; H. Dommisch; M.L. Laine; M. Folwaczny; B. Noack; P. Eickholz; B. Groessner-Schreiber; S. Jepsen; B.G. Loos; S. Schreiber; A.S. Schaefer

doi:10.1111/j.1600-051X.2011.01846.x

Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations

G.M. Richter, C. Graetz, P. Pohler, M. Nothnagel, H. Dommisch, M.L. Laine, M. Folwaczny, B. Noack, P. Eickholz, B. Groessner-Schreiber, S. Jepsen, B.G. Loos, S. Schreiber, A.S. Schaefer

Research output: Contribution to Journal › Article › Academic › peer-review

Abstract

Aim
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.

Materials and 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.

Conclusion
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.

Original language	English
Pages (from-to)	315-322
Journal	Journal of Clinical Periodontology
Volume	39
Issue number	4
DOIs	https://doi.org/10.1111/j.1600-051X.2011.01846.x
Publication status	Published - 2012

Bibliographical note

With supporting information

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10.1111/j.1600-051X.2011.01846.x

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Richter, G. M., Graetz, C., Pohler, P., Nothnagel, M., Dommisch, H., Laine, M. L., Folwaczny, M., Noack, B., Eickholz, P., Groessner-Schreiber, B., Jepsen, S., Loos, B. G., Schreiber, S., & Schaefer, A. S. (2012). Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations. Journal of Clinical Periodontology, 39(4), 315-322. https://doi.org/10.1111/j.1600-051X.2011.01846.x

@article{c9dfdab9ee5b41d3b200bd6c29931bfc,

title = "Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations",

abstract = "AimInvolvement 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.Materials and methodsThe 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.ResultsUpon 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.ConclusionCommon 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.",

author = "G.M. Richter and C. Graetz and P. Pohler and M. Nothnagel and H. Dommisch and M.L. Laine and M. Folwaczny and B. Noack and P. Eickholz and B. Groessner-Schreiber and S. Jepsen and B.G. Loos and S. Schreiber and A.S. Schaefer",

note = "With supporting information",

year = "2012",

doi = "10.1111/j.1600-051X.2011.01846.x",

language = "English",

volume = "39",

pages = "315--322",

journal = "Journal of Clinical Periodontology",

issn = "0303-6979",

publisher = "Blackwell Munksgaard",

number = "4",

}

Richter, GM, Graetz, C, Pohler, P, Nothnagel, M, Dommisch, H, Laine, ML, Folwaczny, M, Noack, B, Eickholz, P, Groessner-Schreiber, B, Jepsen, S, Loos, BG, Schreiber, S & Schaefer, AS 2012, 'Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations', Journal of Clinical Periodontology, vol. 39, no. 4, pp. 315-322. https://doi.org/10.1111/j.1600-051X.2011.01846.x

TY - JOUR

T1 - Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations

AU - Richter, G.M.

AU - Graetz, C.

AU - Pohler, P.

AU - Nothnagel, M.

AU - Dommisch, H.

AU - Laine, M.L.

AU - Folwaczny, M.

AU - Noack, B.

AU - Eickholz, P.

AU - Groessner-Schreiber, B.

AU - Jepsen, S.

AU - Loos, B.G.

AU - Schreiber, S.

AU - Schaefer, A.S.

N1 - With supporting information

PY - 2012

Y1 - 2012

N2 - AimInvolvement 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.Materials and methodsThe 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.ResultsUpon 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.ConclusionCommon 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.

AB - AimInvolvement 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.Materials and methodsThe 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.ResultsUpon 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.ConclusionCommon 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.

U2 - 10.1111/j.1600-051X.2011.01846.x

DO - 10.1111/j.1600-051X.2011.01846.x

M3 - Article

SN - 0303-6979

VL - 39

SP - 315

EP - 322

JO - Journal of Clinical Periodontology

JF - Journal of Clinical Periodontology

IS - 4

ER -

Common genetic risk variants of TLR2 are not associated with periodontitis in large European case-control populations

Abstract

Bibliographical note

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