Evidence map›Paper›PMID 22145886›Full record

ArticleMolecular pain2011

Calcitonin gene-related peptide promotes cellular changes in trigeminal neurons and glia implicated in peripheral and central sensitization.

Ryan J Cady, Joseph R Glenn, Kael M Smith, Paul L Durham

2 registry-linked trialsOpen access · goldAbstract read
In one paragraph

Article in Molecular pain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
3.0field-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.

NCT05142228 phase2terminatednot on this mapstarted 2022, after this paper: background citation

Erenumab as a Therapeutic Approach for the Management of Trigeminal Neuropathic Pain (TNP)

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2022 to 2022Enrolled5ConditionsTrigeminal NeuropathyArmsErenumab-Aooe, Placebo
NCT05162027 phase2terminatednot on this mapstarted 2022, after this paper: background citation

Erenumab as a Therapeutic Approach for the Management of Painful Chronic Temporomandibular Disorders (TMD)

TypeinterventionalSponsorUniversity of Maryland, BaltimoreRan2022 to 2023Enrolled5ConditionsTemporomandibular DisordersArmsErenumab-Aooe 70 MG in 1 mL Prefilled Syringe, Placebo
3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 133 citations in OpenAlex.

  1. Mutual effect between neuropeptides and inflammatory cytokines in neurogenic SMSCs of human temporomandibular joint.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2014
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  5. Non-neuronal targets for migraine therapy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Review
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  8. Gut neuropeptide involvement in Parkinson's disease.American journal of physiology. Gastrointestinal and liver physiology · 2025
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  16. An Update on Temporomandibular Disorders (TMDs) and Headache.Current neurology and neuroscience reports · 2023
    Review
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22 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Ryan J CadyCenter for Biomedical & Life Sciences, Missouri State University, Boonville, Springfield, MO, USA. pauldurham@missouristate.edu
Joseph R Glenn
Kael M Smith
Paul L Durham
Missouri State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCalcitonin gene-related peptide (CGRP), a neuropeptide released from trigeminal nerves, is implicated in the underlying pathology of temporomandibular joint disorder (TMD). Elevated levels of CGRP in the joint capsule correlate with inflammation and pain. CGRP mediates neurogenic inflammation in peripheral tissues by increasing blood flow, recruiting immune cells, and activating sensory neurons. The goal of this study was to investigate the capability of CGRP to promote peripheral and central sensitization in a model of TMD.

resultsTemporal changes in protein expression in trigeminal ganglia and spinal trigeminal nucleus were determined by immunohistochemistry following injection of CGRP in the temporomandibular joint (TMJ) capsule of male Sprague-Dawley rats. CGRP stimulated expression of the active forms of the MAP kinases p38 and ERK, and PKA in trigeminal ganglia at 2 and 24 hours. CGRP also caused a sustained increase in the expression of c-Fos neurons in the spinal trigeminal nucleus. In contrast, levels of P2X3 in spinal neurons were only significantly elevated at 2 hours in response to CGRP. In addition, CGRP stimulated expression of GFAP in astrocytes and OX-42 in microglia at 2 and 24 hours post injection.

conclusionsOur results demonstrate that an elevated level of CGRP in the joint, which is associated with TMD, stimulate neuronal and glial expression of proteins implicated in the development of peripheral and central sensitization. Based on our findings, we propose that inhibition of CGRP-mediated activation of trigeminal neurons and glial cells with selective non-peptide CGRP receptor antagonists would be beneficial in the treatment of TMD.

Indexed as

AnimalsCalcitonin Gene-Related PeptideCentral Nervous System SensitizationImmunohistochemistryMaleRatsRats, Sprague-DawleyReceptors, Calcitonin Gene-Related PeptideSensory Receptor CellsTemporomandibular Joint DisordersTrigeminal GanglionCalcitonin Gene-Related PeptideReceptors, Calcitonin Gene-Related Peptide

Identifiers

PMID22145886
PMCPMC3267674
OpenAlexW2143790394

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.