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CDKN2BAS is associated with periodontitis in different European populations and is activated by bacterial infection
  1. Arne S Schaefer1,
  2. Gesa M Richter1,
  3. Henrik Dommisch2,
  4. Markus Reinartz2,
  5. Michael Nothnagel3,
  6. Barbara Noack4,
  7. Marja L Laine5,
  8. Mathias Folwaczny6,
  9. Birte Groessner-Schreiber7,
  10. Bruno G Loos5,
  11. Søren Jepsen2,
  12. Stefan Schreiber1
  1. 1Christian-Albrechts-University Kiel, Institute for Clinical Molecular Biology, Kiel, Germany
  2. 2Department of Periodontology, Operative and Preventive Dentistry, University of Bonn, Bonn, Germany
  3. 3University Medical Center Schleswig-Holstein, Campus Kiel, Institute of Medical Informatics and Statistics, Kiel, Germany
  4. 4University Medical Center Carl Gustav Carus der Technischen Universität Dresden, Zentrum für Zahn-, Mund- und Kieferheilkunde, Poliklinik für Zahnerhaltung, Dresden, Germany
  5. 5Department of Periodontology, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University, Amsterdam, the Netherlands
  6. 6Department of Preventive Dentistry and Periodontology, University of Munich, Munich, Germany
  7. 7University Medical Center Schleswig-Holstein, Campus Kiel, Department of Operative Dentistry and Periodontology, Kiel, Germany
  1. Correspondence to Dr Arne S Schaefer, Christian-Albrechts-University Kiel, Institute for Clinical Molecular Biology, Arnold-Heller-Str. 3, 24105 Kiel, Germany; a.schaefer{at}ikmb.uni-kiel.de

Footnotes

  • Funding This study was supported by a research grant from the “Research Center for Inflammation Medicine” of the Medical Faculty, Christian-Albrechts-University, University Medical Center Schleswig-Holstein, Campus Kiel, (Arne S Schaefer, Gesa M Richter), by the German Ministry of Education and Research (BMBF) through a National Genome Research Network (NGFN) grant (Michael Nothnagel, 01GS0809), by grants of the German Research Foundation (DFG) (KFO208) (TP3: Arne S Schaefer, Gesa M Richter, Søren Jepsen) (TP2: Henrik Dommisch, Markus Reinartz, Søren Jepsen), by the BMBF through the POPGEN biobank project (01GR0468), by a grant from BONFOR of the Medical Faculty, University of Bonn (Søren Jepsen), and a grant from the ARPA Research Foundation (Birte Grössner-Schreiber, Søren Jepsen), Regensburg, Germany.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the Medical Ethical Committee, Universities of Bonn, Dresden, Kiel and Munich, Germany, and Medical Ethical Committee, Academic Medical Center, University of Amsterdam, the Netherlands.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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Footnotes

  • Funding This study was supported by a research grant from the “Research Center for Inflammation Medicine” of the Medical Faculty, Christian-Albrechts-University, University Medical Center Schleswig-Holstein, Campus Kiel, (Arne S Schaefer, Gesa M Richter), by the German Ministry of Education and Research (BMBF) through a National Genome Research Network (NGFN) grant (Michael Nothnagel, 01GS0809), by grants of the German Research Foundation (DFG) (KFO208) (TP3: Arne S Schaefer, Gesa M Richter, Søren Jepsen) (TP2: Henrik Dommisch, Markus Reinartz, Søren Jepsen), by the BMBF through the POPGEN biobank project (01GR0468), by a grant from BONFOR of the Medical Faculty, University of Bonn (Søren Jepsen), and a grant from the ARPA Research Foundation (Birte Grössner-Schreiber, Søren Jepsen), Regensburg, Germany.

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the Medical Ethical Committee, Universities of Bonn, Dresden, Kiel and Munich, Germany, and Medical Ethical Committee, Academic Medical Center, University of Amsterdam, the Netherlands.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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