Evidence map›Paper›PMID 19758243›Full record

ArticleEuropean journal of oral sciences2009

Consequences for enamel development and mineralization resulting from loss of function of ameloblastin or enamelin.

Charles E Smith, Rima Wazen, Yuanyuan Hu, Sylvia F Zalzal, Antonio Nanci, James P Simmer, Jan C-C Hu

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in European journal of oral sciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 63 citations in OpenAlex.

  1. Enam expression is regulated by Msx2.Developmental dynamics : an official publication of the American Association of Anatomists · 2023
    Article
  2. Article
  3. Article
  4. The phosphorylation of serineMatrix biology : journal of the International Society for Matrix Biology · 2022
    Article
  5. Article
  6. ENAM mutations and digenic inheritance.Molecular genetics & genomic medicine · 2019
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

7 authors at 2 institutions in 2 countries.

Charles E SmithLaboratory for the Study of Calcified Tissues and Biomaterials, Faculté de Médecine Dentaire, Université de Montréal, Montreal, QC, Canada. ce.smith@umontreal.ca
Rima Wazen
Yuanyuan Hu
Sylvia F Zalzal
Antonio Nanci
James P Simmer
Jan C-C Hu
Université de Montréal · CAUniversity of Michigan–Ann Arbor · US

Funding

Proteomics and Genetics of Enamel and DentinR01DE015846 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HU, JAN CHING CHUN · 2004 to 2019
$5.7M
ENAMEL WITHOUT ENAMELINR01DE011301 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HU, JAN C-C · 2003 to 2007
$1.5M
Enamel and EnamelinR56DE011301 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HU, JAN CHING CHUN · 2010 to 2010
$367k
PORCINE ENAMEL PROTEINSR29DE011301 · NIDCR · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI HU, JAN C-C · 1997 to 2001
$212k
CIHR 89811-1NIDCR NIH HHS DE11301NIDCR NIH HHS R01 DE011301NIDCR NIH HHS R01 DE015846NIDCR NIH HHS R29 DE011301NIDCR NIH HHS R56 DE011301
6 · The paper itself

Abstract

Although the nonamelogenin proteins, ameloblastin and enamelin, are both low-abundance and rapidly degrading components of forming enamel, they seem to serve essential developmental functions, as suggested by findings that an enamel layer fails to appear on teeth of mice genetically engineered to produce either a truncated form of ameloblastin (exons 5 and 6 deleted) or no enamelin at all (null). The purpose of this study was to characterize, by direct micro weighing, changes in enamel mineralization occurring on maxillary and mandibular incisors of mice bred for these alterations in nonamelogenin function (Ambn(+/+, +/-5,6, -5,6/-5,6), Enam(+/+, +/- ,-/-)). The results indicated similar changes to enamel-mineralization patterns within the altered genotypes, including significant decreases by as much as 50% in the mineral content of maturing enamel from heterozygous mice and the formation of a thin, crusty, and disorganized mineralized layer, rather than true enamel, on the labial (occlusal) surfaces of incisors and molars along with ectopic calcifications within enamel organ cells in Ambn(-5,6/-5,6) and Enam(-/-) homozygous mice. These findings confirm that both ameloblastin and enamelin are required by ameloblasts to create an enamel layer by appositional growth as well as to assist in achieving its unique high level of mineralization.

Indexed as

AmeloblastsAmelogenesisAnimalsDental EnamelDental Enamel ProteinsDentinEnamel OrganExonsFemaleGene DeletionGenotypeHeterozygoteHomozygoteIncisorMaleMandibleAmbn protein, mouseDental Enamel ProteinsMineralstuftelin

Identifiers

PMID19758243
PMCPMC2778578
OpenAlexW2109772938

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.