Evidence map›Paper›PMID 25479552›Full record

ArticlePloS one2014

Inactivation of Fam20C in cells expressing type I collagen causes periodontal disease in mice.

Peihong Liu, Hua Zhang, Chao Liu, Xiaofang Wang, Li Chen, Chunlin Qin

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Ablation of FAM20C caused short root defects via suppressing the BMP signaling pathway in mice.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2023
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  5. Review
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  7. Article
  8. Article
  9. Article
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  11. Periodontal disease and FAM20A mutations.Journal of human genetics · 2017
    Article
  12. Article
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  14. Article
  15. Article
  16. Article
  17. 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

6 authors at 2 institutions in 2 countries.

Peihong LiuDepartment of Periodontics, Harbin Medical University School of Stomatology, Harbin, Heilongjiang, 150001, China; Department of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
Hua ZhangDepartment of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
Chao LiuDepartment of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
Xiaofang WangDepartment of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
Li ChenLongjiang Scholar Laboratory, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
Chunlin QinDepartment of Biomedical Sciences and Center for Craniofacial Research and Diagnosis, Texas A&M University Baylor College of Dentistry, Dallas, Texas, 75246, United States of America.
Texas A&M University · USFirst Affiliated Hospital of Harbin Medical University · CN

Funding

The Roles of FAM20C (DMP4) in Odontogenesis and OsteogenesisR01DE022549 · NIDCR · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI QIN, CHUNLIN · 2013 to 2017
$1.8M
NIDCR NIH HHS DE022549NIDCR NIH HHS R01 DE022549
6 · The paper itself

Abstract

backgroundFAM20C is a kinase that phosphorylates secretory proteins. Previous studies have shown that FAM20C plays an essential role in the formation and mineralization of bone, dentin and enamel. The present study analyzed the loss-of-function effects of FAM20C on the health of mouse periodontal tissues.

methodsBy crossbreeding 2.3 kb Col 1a1-Cre mice with Fam20Cfl/fl mice, we created 2.3 kb Col 1a1-Cre;Fam20Cfl/fl (cKO) mice, in which Fam20C was inactivated in the cells that express Type I collagen. We analyzed the periodontal tissues in the cKO mice using X-ray radiography, histology, scanning electron microscopy and immunohistochemistry approaches.

resultsThe cKO mice underwent a remarkable loss of alveolar bone and cementum, along with inflammation of the periodontal ligament and formation of periodontal pockets. The osteocytes and lacuno-canalicular networks in the alveolar bone of the cKO mice showed dramatic abnormalities. The levels of bone sialoprotein, osteopontin, dentin matrix protein 1 and dentin sialoprotein were reduced in the Fam20C-deficient alveolar bone and/or cementum, while periostin and fibrillin-1 were decreased in the periodontal ligament of the cKO mice.

conclusionLoss of Fam20C function leads to periodontal disease in mice. The reduced levels of bone sialoprotein, osteopontin, dentin matrix protein 1, dentin sialoprotein, periostin and fibrillin-1 may contribute to the periodontal defects in the Fam20C-deficient mice.

Indexed as

Alveolar Bone LossCalcium-Binding ProteinsExtracellular Matrix ProteinsAnimalsAntigens, DifferentiationCollagen Type ICollagen Type I, alpha 1 ChainMiceMice, KnockoutOsteocytesRadiographyAntigens, DifferentiationCalcium-Binding ProteinsCollagen Type ICollagen Type I, alpha 1 ChainExtracellular Matrix ProteinsFAM20C protein, mouse

Identifiers

PMID25479552
PMCPMC4257665
OpenAlexW2043051186

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Registered trials

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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.