Evidence map›Paper›PMID 35403480›Full record

ArticleJournal of dental research2022

CGRP and Shh Mediate the Dental Pulp Cell Response to Neuron Stimulation.

E R Moore, B Michot, O Erdogan, A Ba, J L Gibbs, Y Yang

Open access · greenAbstract read
In one paragraph

Article in Journal of dental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 15% 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, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Expression of Calcitonin Gene-related Peptide and Its Application to Cochlear Implantation Under Local Anesthesia With Monitored Anesthesia Care in the Very Elderly: The University of California, Los Angeles, Experience.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Impaired Tertiary Dentin Secretion after Shallow Injury inInternational journal of molecular sciences · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. The anatomy, neurophysiology, and cellular mechanisms of intradental sensation.Frontiers in pain research (Lausanne, Switzerland) · 2024
    Review
  17. Review
  18. GαBiomolecules · 2022
    Article
  19. Review
  20. 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 1 institution in 1 country.

E R MooreHarvard School of Dental Medicine, Research and Education Building, Boston, MA, USA.
B MichotHarvard School of Dental Medicine, Research and Education Building, Boston, MA, USA.
O ErdoganHarvard School of Dental Medicine, Research and Education Building, Boston, MA, USA.
A BaHarvard School of Dental Medicine, Research and Education Building, Boston, MA, USA.
J L GibbsHarvard School of Dental Medicine, Research and Education Building, Boston, MA, USA.
Y YangHarvard School of Dental Medicine, Research and Education Building, Boston, MA, USA.
Harvard University · US

Funding

Gas-Hedgehog signaling in intramembranous bone formation and expansionR01DE025866 · NIDCR · HARVARD MEDICAL SCHOOL · PI Yingzi Yang · 2016 to 2026
$5.3M
Targeting the source: bacterial specific pain mechanisms in dental pulpR56DE027368 · NIDCR · HARVARD MEDICAL SCHOOL · PI GIBBS, JENNIFER LYNN · 2018 to 2018
$396k
NIDCR NIH HHS R01 DE025866NIDCR NIH HHS R56 DE027368
6 · The paper itself

Abstract

Dental pain is a persistent, detrimental public health issue that requires a better understanding of the mechanisms of tooth pain and inflammation in order to develop more effective treatments. Calcitonin gene-related peptide (CGRP) and dental pulp cells are promising candidates for mediating tooth pain and generating reparative dental tissues, respectively, but their behavior in the context of pulpitis remains elusive. The mouse incisor requires Sonic hedgehog (Shh) secreted from sensory nerves to continuously regenerate. However, it is unknown whether sensory nerves also regulate the comparatively nonregenerative mouse molar through CGRP and Shh. This is an important knowledge gap to fill since mouse incisors differ biologically from human teeth, while mouse and human molars are similar. In this work, we identified that molar pulp cells express CGRP receptor and Gli1, a Hedgehog (Hh) signaling protein found to label a dental stem cell population in the mouse incisor. We also observed in a mouse molar injury model that Hh signaling was activated and Shh expression was upregulated in vivo. We then determined in vitro that Shh and CGRP regulate differentiation of primary mouse molar and incisor pulp cells and a human dental pulp stem cell line. Furthermore, conditioned media from stimulated sensory neurons induced Hh signaling activation and inflammatory gene expression in primary molar pulp cells, which was abolished by inhibition of either Shh or CGRP. Our results suggest that CGRP and Shh signaling may promote an inflammatory response after injury in the molar and that activated sensory nerves secrete CGRP and Shh to regulate molar pulp cell expansion and differentiation into odontoblast-like cells for dentin repair. Thus, CGRP/Shh signaling should be considered for new strategies that seek to manage pain or dentin regeneration in the molar.

Indexed as

Calcitonin Gene-Related PeptideDental PulpAnimalsHedgehog ProteinsHumansIncisorMiceNeurons, AfferentPainCalcitonin Gene-Related PeptideHedgehog ProteinsSHH protein, humanShh protein, mousedentininflammationmolarodontogenesisregenerationtransgenic mouse

Identifiers

PMID35403480
PMCPMC9305843
OpenAlexW4223482723

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.