Evidence map›Paper›PMID 29480410›Full record

ReviewCurrent rheumatology reports2018

Peripheral Mechanisms Contributing to Osteoarthritis Pain.

Delfien Syx, Phuong B Tran, Rachel E Miller, Anne-Marie Malfait

Open access · bronzeAbstract readReview
In one paragraph

Review in Current rheumatology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Observational
  4. Review
  5. Review
  6. Osteoclast-Derived SLIT3 Mediates Osteoarthritis Pain and Degenerative Changes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  11. Article
  12. Review
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  16. Review
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6 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 2 countries.

Delfien SyxCenter for Medical Genetics, Ghent University, De Pintelaan 185, Ghent, Belgium.
Phuong B TranDepartment of Internal Medicine, Division of Rheumatology, Rush University Medical Center, 1611 W. Harrison St, Suite 510, Chicago, IL, 60612, USA.
Rachel E MillerDepartment of Internal Medicine, Division of Rheumatology, Rush University Medical Center, 1611 W. Harrison St, Suite 510, Chicago, IL, 60612, USA.
Anne-Marie MalfaitDepartment of Internal Medicine, Division of Rheumatology, Rush University Medical Center, 1611 W. Harrison St, Suite 510, Chicago, IL, 60612, USA. anne-marie_malfait@rush.edu.
Rush University Medical Center · US

Funding

Osteoarthritis Progression And Sensory Pathway AlterationsR01AR064251 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE, MILLER, RICHARD J · 2013 to 2025
$7.6M
Molecular Pathways of Pain Generation in OsteoarthritisR01AR060364 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE · 2011 to 2025
$6.0M
Biomechanical Pathways Associated with Osteoarthritis PainK01AR070328 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MILLER, RACHEL ELIZABETH · 2016 to 2020
$547k
NIAMS NIH HHS K01 AR070328NIAMS NIH HHS R01 AR060364NIAMS NIH HHS R01 AR064251
6 · The paper itself

Abstract

purpose of reviewOsteoarthritis (OA) is the most common form of arthritis and a major source of pain and disability worldwide. OA-associated pain is usually refractory to classically used analgesics, and disease-modifying therapies are still lacking. Therefore, a better understanding of mechanisms and mediators contributing to the generation and maintenance of OA pain is critical for the development of efficient and safe pain-relieving therapies. RECENT

findingsBoth peripheral and central mechanisms contribute to OA pain. Clinical evidence suggests that a strong peripheral nociceptive drive from the affected joint maintains pain and central sensitization associated with OA. Mediators present in the OA joint, including nerve growth factor, chemokines, cytokines, and inflammatory cells can contribute to sensitization. Furthermore, structural alterations in joint innervation and nerve damage occur in the course of OA. Several interrelated pathological processes, including joint damage, structural reorganization of joint afferents, low-grade inflammation, neuroplasticity, and nerve damage all contribute to the pain observed in OA. It can be anticipated that elucidating exactly how these mechanisms are operational in the course of progressive OA may lead to the identification of novel targets for intervention.

Indexed as

AnalgesicsAnimalsArthritis, ExperimentalChronic PainCytokinesHumansImmunity, InnateNeurons, AfferentNociceptionOsteoarthritisAnalgesicsCytokinesInflammationInnervationOsteoarthritisPainPeripheralSensitization

Identifiers

PMID29480410
PMCPMC6599517
OpenAlexW2789345994

What OpenQuestion holds

Textmetadata
LicenceTDM
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.