Evidence map›Paper›PMID 29294296›Full record

ArticleJournal of dental research2018

Integration of Murine and Human Studies for Mapping Periodontitis Susceptibility.

A Nashef, R Qabaja, Y Salaymeh, M Botzman, M Munz, H Dommisch, B Krone, P Hoffmann, J Wellmann, M Laudes and 16 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of dental research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
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  11. Systems genetics analysis of oral squamous cell carcinoma susceptibility using the mouse model: current position and new perspective.Mammalian genome : official journal of the International Mammalian Genome Society · 2021
    Review
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  15. Review
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  18. Review
  19. Article
  20. The Collaborative Cross mouse model for dissecting genetic susceptibility to infectious diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2018
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

26 authors at 14 institutions in 5 countries.

A Nashef1 Department of Prosthodontics, Hadassah Faculty of Dental Medicine, Hebrew University, Jerusalem, Israel.
R Qabaja1 Department of Prosthodontics, Hadassah Faculty of Dental Medicine, Hebrew University, Jerusalem, Israel.
Y Salaymeh2 Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
M Botzman3 Department of Cell Research and Immunology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
M Munz4 Department of Periodontology and Synoptic Medicine, Institute for Dental and Craniofacial Sciences, Charité-University Medicine Berlin, Berlin, Germany.
H Dommisch4 Department of Periodontology and Synoptic Medicine, Institute for Dental and Craniofacial Sciences, Charité-University Medicine Berlin, Berlin, Germany.
B Krone6 Institute of Medical Informatics, Biometry and Epidemiology, University Clinic Essen, Essen, Germany.
P Hoffmann7 Institute of Human Genetics, University of Bonn, Bonn, Germany.
J Wellmann9 Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany.
M Laudes10 Clinic of Internal Medicine, University Clinic Schleswig-Holstein, Kiel, Germany.
K Berger9 Institute of Epidemiology and Social Medicine, University of Münster, Münster, Germany.
T Kocher11 Unit of Periodontology, Department of Restorative Dentistry, Periodontology, Endodontology, Preventive Dentistry and Pedodontics, Dental School, University Medicine Greifswald, Greifswald, Germany.
B Loos12 Department of Periodontology and Oral Biochemistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and VU University Amsterdam, Amsterdam, the Netherlands.
N van der Velde13 Department of Internal Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
A G Uitterlinden13 Department of Internal Medicine, Erasmus Medical Center, Rotterdam, the Netherlands.
L C P G M de Groot15 Department of Epidemiology and the EMGO Institute of Health and Care Research, VU University Medical Center, Amsterdam, the Netherlands.
A Franke16 Institute of Clinical Molecular Biology, Christian-Albrechts-University, Kiel, Germany.
S Offenbacher17 School of Dentistry, Department of Periodontology, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.
W Lieb18 Institute of Epidemiology, Biobank popgen, Christian-Albrechts-University, Kiel, Germany.
K Divaris19 Gillings School of Global Public Health, Department of Epidemiology, University of North Carolina-Chapel Hill, Chapel Hill, NC, USA.ORCID 0000-0003-1290-7251
R Mott21 Genetics Institute, University Collage of London, London, UK.
I Gat-Viks3 Department of Cell Research and Immunology, George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel Aviv, Israel.
E Wiess22 Maurice and Gabriella Goldschleger School of Dental Medicine, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
A Schaefer4 Department of Periodontology and Synoptic Medicine, Institute for Dental and Craniofacial Sciences, Charité-University Medicine Berlin, Berlin, Germany.
F A Iraqi2 Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
Y H Haddad1 Department of Prosthodontics, Hadassah Faculty of Dental Medicine, Hebrew University, Jerusalem, Israel.
Tel Aviv University · ILHebrew University of Jerusalem · ILCharité - Universitätsmedizin Berlin · DEErasmus MC · NLUniversity of Münster · DEUniversity of North Carolina at Chapel Hill · USAcademic Center for Dentistry Amsterdam · NLAmsterdam Public Health · NLChristian-Albrechts-Universität zu Kiel · DEInstitute for Integrative and Experimental Genomics · DEInstitut für Medizinische Informatik, Biometrie und Epidemiologie · DEUniversitätsmedizin Greifswald · DEUniversity Hospital Schleswig-Holstein · DEUniversity of Bonn · DE

Funding

North Carolina Translational & Clinical Sciences Institute (NC TraCS)UL1TR001111 · NCATS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BUSE, JOHN BERNARD, CAREY, TIMOTHY S · 2013 to 2017
$43.9M
Training Program for the Next Generation of Oral Health Researches (NextGen)R90DE022527 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI EVERETT, ERIC T. · 2011 to 2016
$672k
GENOME-WIDE ASSOCIATION STUDY OF PERIODONTAL DISEASER01DE021418 · NIDCR · UNIV OF NORTH CAROLINA CHAPEL HILL · PI OFFENBACHER, STEVEN · 2011 to 2012
$658k
NCATS NIH HHS UL1 TR001111NIDCR NIH HHS R01 DE021418NIDCR NIH HHS R90 DE022527
6 · The paper itself

Abstract

Periodontitis is one of the most common inflammatory human diseases with a strong genetic component. Due to the limited sample size of available periodontitis cohorts and the underlying trait heterogeneity, genome-wide association studies (GWASs) of chronic periodontitis (CP) have largely been unsuccessful in identifying common susceptibility factors. A combination of quantitative trait loci (QTL) mapping in mice with association studies in humans has the potential to discover novel risk loci. To this end, we assessed alveolar bone loss in response to experimental periodontal infection in 25 lines (286 mice) from the Collaborative Cross (CC) mouse population using micro-computed tomography (µCT) analysis. The orthologous human chromosomal regions of the significant QTL were analyzed for association using imputed genotype data (OmniExpress BeadChip arrays) derived from case-control samples of aggressive periodontitis (AgP; 896 cases, 7,104 controls) and chronic periodontitis (CP; 2,746 cases, 1,864 controls) of northwest European and European American descent, respectively. In the mouse genome, QTL mapping revealed 2 significant loci (-log P = 5.3; false discovery rate = 0.06) on chromosomes 1 ( Perio3) and 14 ( Perio4). The mapping resolution ranged from ~1.5 to 3 Mb. Perio3 overlaps with a previously reported QTL associated with residual bone volume in F2 cross and includes the murine gene Ccdc121. Its human orthologue showed previously a nominal significant association with CP in humans. Use of variation data from the genomes of the CC founder strains further refined the QTL and suggested 7 candidate genes ( CAPN8, DUSP23, PCDH17, SNORA17, PCDH9, LECT1, and LECT2). We found no evidence of association of these candidates with the human orthologues. In conclusion, the CC populations enabled mapping of confined QTL that confer susceptibility to alveolar bone loss in mice and larger human phenotype-genotype samples and additional expression data from gingival tissues are likely required to identify true positive signals.

Indexed as

Alveolar Bone LossAnimalsChromosome MappingDisease Models, AnimalFemaleGenetic Association StudiesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMaleMiceMiddle AgedPeriodontitisQuantitative Trait LociX-Ray Microtomographyalveolar bone lossanimal modelCollaborative CrossgeneticGWASQTL mapping

Identifiers

PMID29294296
PMCPMC6728575
OpenAlexW2782388955

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.