A genome-wide association study identifies nucleotide variants at SIGLEC5 and DEFA1A3 as risk loci for periodontitis
Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome....
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| Vydáno v: | Human molecular genetics Ročník 26; číslo 13; s. 2577 |
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| Médium: | Journal Article |
| Jazyk: | angličtina |
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England
01.07.2017
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| ISSN: | 1460-2083, 1460-2083 |
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| Abstract | Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome. Previous genome-wide association studies (GWAS) have reported several suggestive susceptibility loci. Here, we conducted a GWAS using a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare but highly severe and early-onset form of periodontitis, validated the associations in a German sample of severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls). Positive findings were replicated in a Turkish sample of AgP (223 cases, 564 controls). A locus at SIGLEC5 (sialic acid binding Ig-like lectin 5) and a chromosomal region downstream of the DEFA1A3 locus (defensin alpha 1-3) showed association with both disease phenotypes and were associated with periodontitis at a genome-wide significance level in the pooled samples, with P = 1.09E-08 (rs4284742,-G; OR = 1.34, 95% CI = 1.21-1.48) and P = 5.48E-10 (rs2738058,-T; OR = 1.28, 95% CI = 1.18-1.38), respectively. SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling. Alpha defensins are antimicrobial peptides with expression in neutrophils and mucosal surfaces and a role in phagocyte-mediated host defense. This study identifies the first shared genetic risk loci of AgP and CP with genome-wide significance and highlights the role of innate and adaptive immunity in the etiology of periodontitis. |
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| AbstractList | Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome. Previous genome-wide association studies (GWAS) have reported several suggestive susceptibility loci. Here, we conducted a GWAS using a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare but highly severe and early-onset form of periodontitis, validated the associations in a German sample of severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls). Positive findings were replicated in a Turkish sample of AgP (223 cases, 564 controls). A locus at SIGLEC5 (sialic acid binding Ig-like lectin 5) and a chromosomal region downstream of the DEFA1A3 locus (defensin alpha 1-3) showed association with both disease phenotypes and were associated with periodontitis at a genome-wide significance level in the pooled samples, with P = 1.09E-08 (rs4284742,-G; OR = 1.34, 95% CI = 1.21-1.48) and P = 5.48E-10 (rs2738058,-T; OR = 1.28, 95% CI = 1.18-1.38), respectively. SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling. Alpha defensins are antimicrobial peptides with expression in neutrophils and mucosal surfaces and a role in phagocyte-mediated host defense. This study identifies the first shared genetic risk loci of AgP and CP with genome-wide significance and highlights the role of innate and adaptive immunity in the etiology of periodontitis.Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome. Previous genome-wide association studies (GWAS) have reported several suggestive susceptibility loci. Here, we conducted a GWAS using a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare but highly severe and early-onset form of periodontitis, validated the associations in a German sample of severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls). Positive findings were replicated in a Turkish sample of AgP (223 cases, 564 controls). A locus at SIGLEC5 (sialic acid binding Ig-like lectin 5) and a chromosomal region downstream of the DEFA1A3 locus (defensin alpha 1-3) showed association with both disease phenotypes and were associated with periodontitis at a genome-wide significance level in the pooled samples, with P = 1.09E-08 (rs4284742,-G; OR = 1.34, 95% CI = 1.21-1.48) and P = 5.48E-10 (rs2738058,-T; OR = 1.28, 95% CI = 1.18-1.38), respectively. SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling. Alpha defensins are antimicrobial peptides with expression in neutrophils and mucosal surfaces and a role in phagocyte-mediated host defense. This study identifies the first shared genetic risk loci of AgP and CP with genome-wide significance and highlights the role of innate and adaptive immunity in the etiology of periodontitis. Periodontitis is one of the most common inflammatory diseases, with a prevalence of 11% worldwide for the severe forms and an estimated heritability of 50%. The disease is characterized by destruction of the alveolar bone due to an aberrant host inflammatory response to a dysbiotic oral microbiome. Previous genome-wide association studies (GWAS) have reported several suggestive susceptibility loci. Here, we conducted a GWAS using a German and Dutch case-control sample of aggressive periodontitis (AgP, 896 cases, 7,104 controls), a rare but highly severe and early-onset form of periodontitis, validated the associations in a German sample of severe forms of the more moderate phenotype chronic periodontitis (CP) (993 cases, 1,419 controls). Positive findings were replicated in a Turkish sample of AgP (223 cases, 564 controls). A locus at SIGLEC5 (sialic acid binding Ig-like lectin 5) and a chromosomal region downstream of the DEFA1A3 locus (defensin alpha 1-3) showed association with both disease phenotypes and were associated with periodontitis at a genome-wide significance level in the pooled samples, with P = 1.09E-08 (rs4284742,-G; OR = 1.34, 95% CI = 1.21-1.48) and P = 5.48E-10 (rs2738058,-T; OR = 1.28, 95% CI = 1.18-1.38), respectively. SIGLEC5 is expressed in various myeloid immune cells and classified as an inhibitory receptor with the potential to mediate tyrosine phosphatases SHP-1/-2 dependent signaling. Alpha defensins are antimicrobial peptides with expression in neutrophils and mucosal surfaces and a role in phagocyte-mediated host defense. This study identifies the first shared genetic risk loci of AgP and CP with genome-wide significance and highlights the role of innate and adaptive immunity in the etiology of periodontitis. |
| Author | Richter, Gesa M van der Velde, Nathalie Jepsen, Soeren Uitterlinden, André G Graetz, Christian Schaefer, Arne S Berger, Klaus Direskeneli, Haner Dommisch, Henrik Wellmann, Jürgen Laudes, Matthias Schreiber, Stefan Nohutcu, Rahime M Sawalha, Amr H Loos, Bruno G Bruckmann, Corinna Saruhan-Direskeneli, Güher Erdmann, Jeanette de Groot, Lisette C P G M Doerfer, Christof Holtfreter, Birte Meyle, Jörg Guzeldemir-Akcakanat, Esra Keceli, Huseyin Gencay Franke, Andre Lieb, Wolfgang Eickholz, Peter Krone, Bastian Jockel-Schneider, Yvonne Noack, Barbara Teumer, Alexander Staufenbiel, Ingmar Kocher, Thomas Hoffmann, Per Willenborg, Christina Munz, Matthias |
| Author_xml | – sequence: 1 givenname: Matthias surname: Munz fullname: Munz, Matthias organization: Institute for Integrative and Experimental Genomics, University Medical Center Schleswig-Holstein - Campus Lübeck, Germany – sequence: 2 givenname: Christina surname: Willenborg fullname: Willenborg, Christina organization: Institute for Integrative and Experimental Genomics, University Medical Center Schleswig-Holstein - Campus Lübeck, Germany – sequence: 3 givenname: Gesa M surname: Richter fullname: Richter, Gesa M organization: Department of Periodontology and Synoptic Dentistry, Institute of Dental, Oral and Maxillary Medicine, Charité - University Medicine Berlin, Germany – sequence: 4 givenname: Yvonne surname: Jockel-Schneider fullname: Jockel-Schneider, Yvonne organization: Department of Periodontology, Clinic of Preventive Dentistry and Periodontology, University Medical Center of the Julius-Maximilians-University, Würzburg, Germany – sequence: 5 givenname: Christian surname: Graetz fullname: Graetz, Christian organization: Department of Operative Dentistry and Periodontology, University Medical Center Schleswig-Holstein, Campus Kiel, Germany – sequence: 6 givenname: Ingmar surname: Staufenbiel fullname: Staufenbiel, Ingmar organization: Department of Conservative Dentistry, Periodontology and Preventive Dentistry, Hannover Medical School, Hannover, Germany – sequence: 7 givenname: Jürgen surname: Wellmann fullname: Wellmann, Jürgen organization: Institute of Epidemiology and Social Medicine, University Münster, Germany – sequence: 8 givenname: Klaus surname: Berger fullname: Berger, Klaus organization: Institute of Epidemiology and Social Medicine, University Münster, Germany – sequence: 9 givenname: Bastian surname: Krone fullname: Krone, Bastian organization: Institute of Medical Informatics, Biometry and Epidemiology, University Clinic Essen, Germany – sequence: 10 givenname: Per surname: Hoffmann fullname: Hoffmann, Per organization: Human Genomics Research Group, Department of Biomedicine, University Hospital of Basel, Switzerland – sequence: 11 givenname: Nathalie surname: van der Velde fullname: van der Velde, Nathalie organization: Department of Internal Medicine Section of Geriatrics, Amsterdam Medical Center, Amsterdam, The Netherlands – sequence: 12 givenname: André G surname: Uitterlinden fullname: Uitterlinden, André G organization: Department of Internal Medicine, Erasmus Medical Center, Rotterdam, The Netherlands – sequence: 13 givenname: Lisette C P G M surname: de Groot fullname: de Groot, Lisette C P G M organization: Department of Epidemiology and the EMGO Institute of Health and Care Research, VU University Medical Center, Amsterdam, The Netherlands – sequence: 14 givenname: Amr H surname: Sawalha fullname: Sawalha, Amr H organization: Center for Computational Medicine and Bioinformatics, University of Michigan Medical School, USA – sequence: 15 givenname: Haner surname: Direskeneli fullname: Direskeneli, Haner organization: Division of Rheumatology, Marmara University, School of Medicine, Istanbul, Turkey – sequence: 16 givenname: Güher surname: Saruhan-Direskeneli fullname: Saruhan-Direskeneli, Güher organization: Department of Physiology, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey – sequence: 17 givenname: Esra surname: Guzeldemir-Akcakanat fullname: Guzeldemir-Akcakanat, Esra organization: Department of Periodontology, Faculty of Dentistry, Kocaeli University, Turkey – sequence: 18 givenname: Huseyin Gencay surname: Keceli fullname: Keceli, Huseyin Gencay organization: Department of Periodontology, Faculty of Dentistry, Hacettepe University, Sihhiye, Ankara, Turkey – sequence: 19 givenname: Matthias surname: Laudes fullname: Laudes, Matthias organization: Clinic of Internal Medicine, University Clinic Schleswig-Holstein, Kiel, Germany – sequence: 20 givenname: Barbara surname: Noack fullname: Noack, Barbara organization: Clinic of Conservational Dentistry, Center of Dental, Oral and Maxillary Medicine, University Medical Center Carl-Gustav-Carus, Technical University Dresden, Germany – sequence: 21 givenname: Alexander surname: Teumer fullname: Teumer, Alexander organization: Institute for Community Medicine, University Medicine Greifswald, Germany – sequence: 22 givenname: Birte surname: Holtfreter fullname: Holtfreter, Birte organization: Unit of Periodontology, Department of Restorative Dentistry, Periodontology, Endodontology, Preventive Dentistry and Pedodontics, Dental School, University Medicine Greifswald, Germany – sequence: 23 givenname: Thomas surname: Kocher fullname: Kocher, Thomas organization: Unit of Periodontology, Department of Restorative Dentistry, Periodontology, Endodontology, Preventive Dentistry and Pedodontics, Dental School, University Medicine Greifswald, Germany – sequence: 24 givenname: Peter surname: Eickholz fullname: Eickholz, Peter organization: Department of Periodontology, Johann Wolfgang Goethe-University, Frankfurt am Main, Germany – sequence: 25 givenname: Jörg surname: Meyle fullname: Meyle, Jörg organization: Department of Periodontology, University Medical Center Giessen and Marburg, Germany – sequence: 26 givenname: Christof surname: Doerfer fullname: Doerfer, Christof organization: Department of Operative Dentistry and Periodontology, University Medical Center Schleswig-Holstein, Campus Kiel, Germany – sequence: 27 givenname: Corinna surname: Bruckmann fullname: Bruckmann, Corinna organization: Department of Conservative Dentistry and Periodontology, Medical University Vienna, School of Dentistry, Vienna, Austria – sequence: 28 givenname: Wolfgang surname: Lieb fullname: Lieb, Wolfgang organization: Institute of Epidemiology, Biobank PopGen, Christian-Albrechts-University, Kiel, Germany – sequence: 29 givenname: Andre surname: Franke fullname: Franke, Andre organization: Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany – sequence: 30 givenname: Stefan surname: Schreiber fullname: Schreiber, Stefan organization: Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany – sequence: 31 givenname: Rahime M surname: Nohutcu fullname: Nohutcu, Rahime M organization: Department of Periodontology, Faculty of Dentistry, Kocaeli University, Turkey – sequence: 32 givenname: Jeanette surname: Erdmann fullname: Erdmann, Jeanette organization: Institute for Integrative and Experimental Genomics, University Medical Center Schleswig-Holstein - Campus Lübeck, Germany – sequence: 33 givenname: Bruno G surname: Loos fullname: Loos, Bruno G organization: Department of Periodontology and Oral Biochemistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University Amsterdam, The Netherlands – sequence: 34 givenname: Soeren surname: Jepsen fullname: Jepsen, Soeren organization: Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany – sequence: 35 givenname: Henrik surname: Dommisch fullname: Dommisch, Henrik organization: Department of Periodontology and Synoptic Dentistry, Institute of Dental, Oral and Maxillary Medicine, Charité - University Medicine Berlin, Germany – sequence: 36 givenname: Arne S surname: Schaefer fullname: Schaefer, Arne S organization: Department of Periodontology and Synoptic Dentistry, Institute of Dental, Oral and Maxillary Medicine, Charité - University Medicine Berlin, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28449029$$D View this record in MEDLINE/PubMed |
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| Title | A genome-wide association study identifies nucleotide variants at SIGLEC5 and DEFA1A3 as risk loci for periodontitis |
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