Evidence map›Paper›PMID 31862470›Full record

ReviewOsteoarthritis and cartilage2020

The innate immune response as a mediator of osteoarthritis pain.

R J Miller, A-M Malfait, R E Miller

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Osteoarthritis and cartilage, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

58 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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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

3 authors.

R J MillerNorthwestern University, Chicago, IL, USA.
A-M MalfaitRush University Medical Center, Chicago, IL, USA. Electronic address: Anne-marie_malfait@rush.edu.
R E MillerRush University Medical Center, Chicago, IL, USA. Electronic address: Rachel_Miller@rush.edu.

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
The nervous joint: New concepts in the development of osteoarthritisR61AR073576 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MALFAIT, ANNE-MARIE, MILLER, RICHARD J · 2018 to 2019
$798k
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 AR064251NIAMS NIH HHS R61 AR073576
6 · The paper itself

Abstract

In this narrative review, we discuss the emerging role of innate immunity in osteoarthritis (OA) joint pain. First, we give a brief description of the pain pathway in the context of OA. Then we consider how neuro-immune signaling pathways may promote OA pain. First, activation of neuronal Pattern Recognition Receptors by mediators released in a damaged joint can result in direct excitation of nociceptors, as well as in production of chemokines and cytokines. Secondly, indirect neuro-immune signaling may occur when innate immune cells produce algogenic factors, including chemokines and cytokines, that act on the pain pathway. Neuro-immune crosstalk occurs at different levels of the pathway, starting in the joint but also in the innervating dorsal root ganglia and in the dorsal horn. Synovitis is characterized by recruitment of immune cells, including macrophages, mast cells, and CD4+ lymphocytes, which may contribute to nociceptor sensitization and OA pain through production of algogenic factors that amplify the activation of sensory neurons. We discuss examples where this scenario has been suggested by findings in human OA and in animal models. Overall, increasing evidence suggests that innate immune pathways play an initiating as well as facilitating role in pain, but information on how these pathways operate in OA remains limited. Since these innate pathways are eminently targetable, future studies in this area may provide fruitful leads towards a better management of symptomatic OA.

Indexed as

AnimalsArthralgiaCytokinesGanglia, SpinalHumansImmunity, InnateNeuroimmunomodulationNociceptorsOsteoarthritisReceptors, Pattern RecognitionSpinal Cord Dorsal HornSynovitisCytokinesReceptors, Pattern RecognitionInnate immunityNeuroinflammationOsteoarthritisPainSensitizationToll-like receptors

Identifiers

PMID31862470
PMCPMC6951330

What OpenQuestion holds

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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.