Evidence map›Paper›PMID 26521746›Full record

ArticleOsteoarthritis and cartilage2015

Intra-articular nerve growth factor regulates development, but not maintenance, of injury-induced facet joint pain & spinal neuronal hypersensitivity.

J V Kras, S Kartha, B A Winkelstein

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04542798 (Central Sensitization and Aberrant Nerve Sprouting Possible Explanations for RFA Failure of MBDR in CLBP of FJ Origin), which is not on this map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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.

NCT04542798 naunknown statusnot on this mapstarted 2020, after this paper: background citation

Central Sensitization and Aberrant Nerve Sprouting Possible Explanations for RFA Failure of MBDR in CLBP of FJ Origin: CRF Versus WCRF or PRF-DRG Randomized Clinical Trial

TypeinterventionalSponsorHospital General Universitario de ValenciaRan2020 to 2024Enrolled80ConditionsLow Back Pain, Recurrent, Neuropathic Pain, Facet Joint Pain, Central SensitisationArmsRadiofrequency COSMAN
3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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  16. Osteoarthritis pain: What are we learning from animal models?Best practice & research. Clinical rheumatology · 2017
    Review
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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

3 authors at 1 institution in 1 country.

J V KrasDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: jkras@seas.upenn.edu.
S KarthaDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: skartha@seas.upenn.edu.
B A WinkelsteinDepartment of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA; Department of Neurosurgery, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: winkelst@seas.upenn.edu.
University of Pennsylvania · US

Funding

Nociceptive Mechanisms In Whiplash InjuryR01AR056288 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI WINKELSTEIN, BETH A · 2009 to 2013
$1.6M
NIAMS NIH HHS AR056288NIAMS NIH HHS R01 AR056288
6 · The paper itself

Abstract

objectiveThe objective of the current study is to define whether intra-articular nerve growth factor (NGF), an inflammatory mediator that contributes to osteoarthritic pain, is necessary and sufficient for the development or maintenance of injury-induced facet joint pain and its concomitant spinal neuronal hyperexcitability.

methodMale Holtzman rats underwent painful cervical facet joint distraction (FJD) or sham procedures. Mechanical hyperalgesia was assessed in the forepaws, and NGF expression was quantified in the C6/C7 facet joint. An anti-NGF antibody was administered intra-articularly in additional rats immediately or 1 day following facet distraction or sham procedures to block intra-articular NGF and test its contribution to initiation and/or maintenance of facet joint pain and spinal neuronal hyperexcitability. NGF was injected into the bilateral C6/C7 facet joints in separate rats to determine if NGF alone is sufficient to induce these behavioral and neuronal responses.

resultsNGF expression increases in the cervical facet joint in association with behavioral sensitivity after that joint's mechanical injury. Intra-articular application of anti-NGF immediately after a joint distraction prevents the development of both injury-induced pain and hyperexcitability of spinal neurons. Yet, intra-articular anti-NGF applied after pain has developed does not attenuate either behavioral or neuronal hyperexcitability. Intra-articular NGF administered to the facet in naïve rats also induces behavioral hypersensitivity and spinal neuronal hyperexcitability.

conclusionFindings demonstrate that NGF in the facet joint contributes to the development of injury-induced joint pain. Localized blocking of NGF signaling in the joint may provide potential treatment for joint pain.

Indexed as

Gene Expression RegulationAnimalsArthralgiaBlotting, WesternDisease Models, AnimalDNAHyperalgesiaMaleNerve Growth FactorOsteoarthritisPain MeasurementRatsRats, Sprague-DawleyZygapophyseal JointDNANerve Growth FactorFacet jointNeuronal hyperexcitabilityNGFPainTrauma

Identifiers

PMID26521746
PMCPMC4630778
OpenAlexW2146667034

What OpenQuestion holds

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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.