Evidence map›Paper›PMID 27730452›Full record

ReviewCurrent osteoporosis reports2016

Emerging Targets for the Management of Osteoarthritis Pain.

Anne-Marie Malfait, Richard J Miller

Abstract readReview
In one paragraph

Review in Current osteoporosis reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
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  5. Review
  6. NaNature · 2024
    Article
  7. Review
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  15. Review
  16. Article
  17. Review
  18. Review
  19. What is new in pain modification in osteoarthritis?Rheumatology (Oxford, England) · 2018
    Review
  20. Osteoarthritis pain: What are we learning from animal models?Best practice & research. Clinical rheumatology · 2017
    Review
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

2 authors at 2 institutions in 1 country.

Anne-Marie MalfaitDepartment of Internal Medicine, Division of Rheumatology, Rush University Medical Center, 1611 W Harrison Street, Suite 510, Chicago, IL, 60612, USA. anne-marie_malfait@rush.edu.
Richard J MillerDepartment of Pharmacology, Northwestern University, Robert H. Lurie Medical Research Center, 303 E. Superior, Chicago, IL, 60613, USA.
Northwestern University · USRush 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
NIAMS NIH HHS R01 AR060364NIAMS NIH HHS R01 AR064251
6 · The paper itself

Abstract

Worldwide, osteoarthritis (OA) is one of the leading causes of chronic pain, for which adequate relief is not available. Ongoing peripheral input from the affected joint is a major factor in OA-associated pain. Therefore, this review focuses predominantly on peripheral targets emerging in the preclinical and clinical arena. Nerve growth factor is the most advanced of these targets, and its blockade has shown tremendous promise in clinical trials in knee OA. A number of different types of ion channels, including voltage-gated sodium channels and calcium channels, transient receptor potential channels, and acid-sensing ion channels, are important for neuronal excitability and play a role in pain genesis. Few channel blockers have been tested in preclinical models of OA, with varying results. Finally, we discuss some examples of G-protein coupled receptors, which may offer attractive therapeutic strategies for OA pain, including receptors for bradykinin, calcitonin gene-related peptide, and chemokines. Since many of the pathways described above can be selectively and potently targeted, they offer an exciting opportunity for pain management in OA, either systemically or locally.

Indexed as

Acid Sensing Ion Channel BlockersAcid Sensing Ion ChannelsArthralgiaBradykinin Receptor AntagonistsCalcitonin Gene-Related Peptide Receptor AntagonistsCalcium Channel BlockersCalcium ChannelsHumansMolecular Targeted TherapyNerve Growth FactorOsteoarthritisReceptors, BradykininReceptors, Calcitonin Gene-Related PeptideReceptors, ChemokineReceptors, G-Protein-CoupledTransient Receptor Potential ChannelsAcid Sensing Ion Channel BlockersAcid Sensing Ion ChannelsBradykinin Receptor AntagonistsCalcitonin Gene-Related Peptide Receptor AntagonistsCalcium Channel BlockersCalcium ChannelsNerve Growth FactorReceptors, BradykininReceptors, Calcitonin Gene-Related PeptideReceptors, ChemokineReceptors, G-Protein-CoupledTransient Receptor Potential ChannelsVoltage-Gated Sodium Channel BlockersVoltage-Gated Sodium ChannelsGPCRsIon channelsNerve growth factorOsteoarthritisPainTargets

Identifiers

PMID27730452
PMCPMC5335491
OpenAlexW2531574227

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.