Evidence map›Paper›PMID 29319609›Full record

ArticlePain2018

Joint nociceptor nerve activity and pain in an animal model of acute gout and its modulation by intra-articular hyaluronan.

Aida Marcotti, Ana Miralles, Eduardo Dominguez, Eliseo Pascual, Ana Gomis, Carlos Belmonte, Elvira de la Peña

Open access · hybridAbstract read
In one paragraph

Article in Pain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. 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

7 authors at 2 institutions in 1 country.

Aida MarcottiInstituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain.
Ana MirallesInstituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain.
Eduardo DominguezInstituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain.
Eliseo PascualSección de Reumatología, Hospital General Universitario de Alicante, Alicante, Spain.
Ana GomisInstituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain.
Carlos BelmonteInstituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain.
Elvira de la PeñaInstituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain.
Universitat de Miguel Hernández d'Elx · ESHospital General Universitario de Alicante Doctor Balmis · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms whereby deposition of monosodium urate (MSU) crystals in gout activates nociceptors to induce joint pain are incompletely understood. We tried to reproduce the signs of painful gouty arthritis, injecting into the knee joint of rats suspensions containing amorphous or triclinic, needle MSU crystals. The magnitude of MSU-induced inflammation and pain behavior signs were correlated with the changes in firing frequency of spontaneous and movement-evoked nerve impulse activity recorded in single knee joint nociceptor saphenous nerve fibers. Joint swelling, mechanical and cold allodynia, and hyperalgesia appeared 3 hours after joint injection of MSU crystals. In parallel, spontaneous and movement-evoked joint nociceptor impulse activity raised significantly. Solutions containing amorphous or needle-shaped MSU crystals had similar inflammatory and electrophysiological effects. Intra-articular injection of hyaluronan (HA, Synvisc), a high-MW glycosaminoglycan present in the synovial fluid with analgesic effects in osteoarthritis, significantly reduced MSU-induced behavioral signs of pain and decreased the enhanced joint nociceptor activity. Our results support the interpretation that pain and nociceptor activation are not triggered by direct mechanical stimulation of nociceptors by MSU crystals, but are primarily caused by the release of excitatory mediators by inflammatory cells activated by MSU crystals. Intra-articular HA decreased behavioral and electrophysiological signs of pain, possibly through its viscoelastic filtering effect on the mechanical forces acting over sensitized joint sensory endings and probably also by a direct interaction of HA molecules with the transducing channels expressed in joint nociceptor terminals.

Indexed as

Acute PainAdjuvants, ImmunologicAnimalsAntioxidantsDisease Models, AnimalFlow CytometryGoutHyaluronic AcidInflammationInjections, Intra-ArticularKnee JointMaleNerve FibersPain ThresholdPhysical StimulationRatsAdjuvants, ImmunologicAntioxidantsHyaluronic AcidUric Acid

Identifiers

PMID29319609
PMCPMC5895116
OpenAlexW2784215662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.