Evidence map›Paper›PMID 24170372›Full record

ArticleJournal of dental research2014

Barrier formation: potential molecular mechanism of enamel fluorosis.

D M Lyaruu, J F Medina, S Sarvide, T J M Bervoets, V Everts, P Denbesten, C E Smith, A L J J Bronckers

Abstract read
In one paragraph

Article in Journal of dental research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. NaFrontiers in physiology · 2023
    Article
  8. Article
  9. Article
  10. Dental Fluorosis: the Risk of Misdiagnosis-a Review.Biological trace element research · 2021
    Review
  11. Review
  12. Fluoride exposure alters CaScience signaling · 2020
    Article
  13. Awareness of the Benefits and Risks Related to Using Fluoridated Toothpaste Among Doctors: A Population-Based Study.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  14. Article
  15. How pH is regulated during amelogenesis in dental fluorosis.Experimental and therapeutic medicine · 2018
    Review
  16. Review
  17. Review
  18. Review
  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

8 authors at 4 institutions in 4 countries.

D M LyaruuDepartment of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam, and MOVE Research Institute, VU University Amsterdam, Amsterdam, Netherlands.
J F Medina
S Sarvide
T J M Bervoets
V Everts
P Denbesten
C E Smith
A L J J Bronckers
Academic Center for Dentistry Amsterdam · NLUniversidad de Navarra · ESMcGill University · CAUniversity of California, San Francisco · US

Funding

ENAMEL FLUOROSIS;MECHANISMS OF ACTIONR01DE013508 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DEN BESTEN, PAMELA K · 2000 to 2013
$4.5M
Enamel Fluorosis: Mechanisms of ActionR56DE013508 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DEN BESTEN, PAMELA K · 2010 to 2010
$453k
NIDCR NIH HHS DE13508NIDCR NIH HHS R01 DE013508NIDCR NIH HHS R56 DE013508
6 · The paper itself

Abstract

Enamel fluorosis is an irreversible structural enamel defect following exposure to supraoptimal levels of fluoride during amelogenesis. We hypothesized that fluorosis is associated with excess release of protons during formation of hypermineralized lines in the mineralizing enamel matrix. We tested this concept by analyzing fluorotic enamel defects in wild-type mice and mice deficient in anion exchanger-2a,b (Ae2a,b), a transmembrane protein in maturation ameloblasts that exchanges extracellular Cl(-) for bicarbonate. Defects were more pronounced in fluorotic Ae2a,b (-/-) mice than in fluorotic heterozygous or wild-type mice. Phenotypes included a hypermineralized surface, extensive subsurface hypomineralization, and multiple hypermineralized lines in deeper enamel. Mineral content decreased in all fluoride-exposed and Ae2a,b(-/-) mice and was strongly correlated with Cl(-). Exposure of enamel surfaces underlying maturation-stage ameloblasts to pH indicator dyes suggested the presence of diffusion barriers in fluorotic enamel. These results support the concept that fluoride stimulates hypermineralization at the mineralization front. This causes increased release of protons, which ameloblasts respond to by secreting more bicarbonates at the expense of Cl(-) levels in enamel. The fluoride-induced hypermineralized lines may form barriers that impede diffusion of proteins and mineral ions into the subsurface layers, thereby delaying biomineralization and causing retention of enamel matrix proteins.

Indexed as

AmeloblastsAmelogenesisAnimalsBicarbonatesChloride-Bicarbonate AntiportersChloridesColoring AgentsDental EnamelDental Enamel ProteinsDiffusionFemaleFluoridesFluorosis, DentalHeterozygoteHomozygoteHydrogen-Ion ConcentrationBicarbonatesChloride-Bicarbonate AntiportersChloridesColoring AgentsDental Enamel Proteinsenamel matrix proteinsFluoridesIndicators and ReagentsMineralschloridehypermineralizationhypomineralizationpH regulationquantitative X-ray microanalysisSlc4a2

Identifiers

PMID24170372
PMCPMC3865793
OpenAlexW2146919007

What OpenQuestion holds

Textmetadata
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.