Evidence map›Paper›PMID 23852764›Full record

ArticleAnnals of the rheumatic diseases2014

Augmented pain behavioural responses to intra-articular injection of nerve growth factor in two animal models of osteoarthritis.

Sadaf Ashraf, Paul Ian Mapp, James Burston, Andrew John Bennett, Victoria Chapman, David Andrew Walsh

Open access · hybridAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
4.4field-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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.

  1. Pooled it
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  10. Assessment of osteoarthritis functional outcomes and intra-articular injection volume in the rat anterior cruciate ligament transection model.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022
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  16. Monoclonal Antibodies for Chronic Pain Treatment: Present and Future.International journal of molecular sciences · 2021
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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

6 authors at 3 institutions in 1 country.

Sadaf AshrafArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK Department of Academic Rheumatology, University of Nottingham, Nottingham, UK Centre for Vision and Vascular Sciences, Institute of Clinical Science, Royal Victoria Hospital, Belfast, UK.
Paul Ian MappArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK Department of Academic Rheumatology, University of Nottingham, Nottingham, UK.
James BurstonArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK School of Biomedical Sciences, University of Nottingham, Nottingham, UK.
Andrew John BennettSchool of Biomedical Sciences, University of Nottingham, Nottingham, UK.
Victoria ChapmanArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK School of Biomedical Sciences, University of Nottingham, Nottingham, UK.
David Andrew WalshArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK Department of Academic Rheumatology, University of Nottingham, Nottingham, UK.
University of Nottingham · GBVersus Arthritis · GBRoyal Victoria Hospital · GB

Funding

Medical Research Council MR/K00414X/1
6 · The paper itself

Abstract

objectivesNerve growth factor (NGF) is a promising analgesic target, particularly in osteoarthritis (OA) where existing therapies are inadequate. We hypothesised that pain responses to NGF are increased in OA joints. Here, NGF-evoked pain behaviour was compared in two rodent models of OA, and possible mechanisms underlying altered pain responses were examined.

methodsOA was induced in rat knees by meniscal transection (MNX) or intra-articular monosodium iodoacetate injection (MIA). Once OA pathology was fully established (day 20), we assessed pain behaviour (hindlimb weight-bearing asymmetry and hindpaw mechanical withdrawal thresholds) evoked by intra-articular injection of NGF (10 µg). Possible mechanisms underlying alterations in NGF-induced pain behaviour were explored using indomethacin pretreatment, histopathological evaluation of synovitis, and rtPCR for NGF receptor (tropomyosin receptor kinase (Trk)-A) expression in dorsal root ganglia (DRG).

resultsBoth the MIA and MNX models of OA displayed reduced ipsilateral weight bearing and hindpaw mechanical withdrawal thresholds, mild synovitis and increased TrkA expression in DRG. NGF injection into OA knees produced a prolonged augmentation of weight-bearing asymmetry, compared to NGF injection in non-osteoarthritic knees. However, hindpaw mechanical withdrawal thresholds were not further decreased by NGF. Pretreatment with indomethacin attenuated NGF-facilitated weight-bearing asymmetry and reversed OA-induced ipsilateral TrkA mRNA up-regulation.

conclusionsOA knees were more sensitive to NGF-induced pain behaviour compared to non-osteoarthritic knees. Cyclo-oxygenase products may contribute to increased TrkA expression during OA development, and the subsequent increased NGF sensitivity. Treatments that reduce sensitivity to NGF have potential to improve OA pain.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalArthritis, ExperimentalBehavior, AnimalDose-Response Relationship, DrugGanglia, SpinalIndomethacinInjections, Intra-ArticularMaleNerve Growth FactorOsteoarthritisPainPain MeasurementPain ThresholdRatsRats, Sprague-DawleyAnti-Inflammatory Agents, Non-SteroidalIndomethacinNerve Growth FactorReceptor, trkARNA, MessengerCorticosteroidsKnee OsteoarthritisSynovitis

Identifiers

PMID23852764
PMCPMC4145450
OpenAlexW2167774723

What OpenQuestion holds

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Registered trials

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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.