Evidence map›Paper›PMID 27208420›Full record

ArticleOsteoarthritis and cartilage2016

The anti-NGF antibody muMab 911 both prevents and reverses pain behaviour and subchondral osteoclast numbers in a rat model of osteoarthritis pain.

L Xu, L N Nwosu, J J Burston, P J Millns, D R Sagar, P I Mapp, P Meesawatsom, L Li, A J Bennett, D A Walsh and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 63 citations in OpenAlex.

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  15. Monoclonal Antibodies for Chronic Pain Treatment: Present and Future.International journal of molecular sciences · 2021
    Review
  16. Review
  17. Crosstalk between Bone and Nerves within Bone.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

11 authors at 3 institutions in 1 country.

L XuArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
L N NwosuArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Medicine, University of Nottingham, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK.
J J BurstonArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
P J MillnsArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
D R SagarArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
P I MappArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Medicine, University of Nottingham, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK.
P MeesawatsomArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
L LiArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
A J BennettArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK.
D A WalshArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Medicine, University of Nottingham, Clinical Sciences Building, City Hospital, Hucknall Road, Nottingham, NG5 1PB, UK.
V ChapmanArthritis Research UK Pain Centre, University of Nottingham, Nottingham, UK; School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham, NG7 2UH, UK. Electronic address: victoria.chapman@nottingham.ac.uk.
Versus Arthritis · GBQueen's Medical Centre · GBUniversity of Nottingham · GB

Funding

Arthritis Research UK 18769
6 · The paper itself

Abstract

objectiveNerve growth factor (NGF) has a pivotal role in peripheral hyperalgesia and inflammation; anti-NGF antibodies attenuate pain responses in inflammatory pain models, and in people with osteoarthritis (OA) or low back pain. The aim of this study was to characterise the peripheral mechanisms contributing to the analgesic effects of anti-NGF antibody treatment in an established model of joint pain, which mimics key clinical features of OA.

designEffects of preventative vs therapeutic treatment with an anti-NGF antibody (monoclonal antibody 911: muMab 911 (10 mg/kg, s.c.)) on pain behaviour (weight bearing asymmetry and hindpaw withdrawal thresholds (PWT)), cartilage damage, synovitis and numbers of subchondral osteoclasts were investigated in the monosodium iodoacetate (MIA) model. Potential direct effects of NGF on receptor activator of nuclear factor kappa-B ligand (RANKL) mediated osteoclastogenesis were investigated in cultured human osteoclasts.

resultsIntra-articular MIA injection resulted in significant pain behaviour, cartilage damage, synovitis and increased numbers of subchondral osteoclasts. Both preventative and therapeutic treatment with muMab 911 significantly prevented, or reversed, MIA-induced pain behaviour, but did not alter cartilage or synovial pathology quantified at the end of the treatment period. NGF did not facilitate RANKL driven osteoclast differentiation in vitro, but preventative or therapeutic muMab 911 reduced numbers of TRAP positive osteoclasts in the subchondral bone.

conclusionsWe demonstrate that anti-NGF antibody treatment attenuates OA pain behaviour despite permitting cartilage damage and synovitis. Indirect effects on subchondral bone remodelling may contribute to the analgesic effects of NGF blockade.

Indexed as

PainAnimalsDisease Models, AnimalHumansNerve Growth FactorOsteoarthritisOsteoclastsRatsRats, Sprague-DawleyNerve Growth FactorBoneInflammationNerve growth factorOsteoarthritisPain

Identifiers

PMID27208420
PMCPMC5009895
OpenAlexW2401549699

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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.