Evidence map›Paper›PMID 31621560›Full record

ReviewClinical and experimental rheumatology

Innate inflammation and synovial macrophages in osteoarthritis pathophysiology.

Timothy M Griffin, Carla R Scanzello

Open access · greenAbstract readReview
In one paragraph

Review in Clinical and experimental rheumatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 3 pooled it
16.6field-weighted citation impact, top 1% 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

140 citing papers in PubMed, 3 syntheses or guidelines pooled it, 178 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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  6. Review
  7. Article
  8. Article
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  11. Synovial fibroblasts modulate endothelial activation in an acute injury-on-a-chip model.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  12. Article
  13. Review
  14. Article
  15. Article
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  17. Pro-resolving Annexin A1-derived peptide Ac2-26 reduces nociception and mitigates joint damage in experimental osteoarthritis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  18. Article
  19. Review
  20. Review

80 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

2 authors at 2 institutions in 1 country.

Timothy M GriffinAging and Metabolism Research Program, Oklahoma Medical Research Foundation, and Reynolds Oklahoma Center on Aging, Department of Biochemistry and Molecular Biology, Dept.of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Tim-Griffin@omrf.org.
Carla R ScanzelloTranslational Musculoskeletal Research Center & Dept. of Medicine, Corporal Michael J. Crescenz Department of Veterans Affairs Medical Center, Philadelphia, and Div. of Rheumatology, Univ. of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA.
Oklahoma Medical Research Foundation · USPhiladelphia VA Medical Center · US

Funding

Chondrocyte Metabolic Stress in the Development of OsteoarthritisR01AG049058 · NIA · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GRIFFIN, TIMOTHY M · 2015 to 2019
$1.9M
Biomechanical Regulation of Intra-Articular Adipose Tissue InflammationR03AR066828 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GRIFFIN, TIMOTHY M · 2014 to 2016
$257k
The Impact of C-C Chemokine Receptor 7 (CCR7) on Synovitis and Osteoarthritis (OA)I21RX001757 · VA · PHILADELPHIA VA MEDICAL CENTER · PI SCANZELLO, CARLA ROSE · 2015 to 2018
–
NIAMS NIH HHS R03 AR066828NIA NIH HHS R01 AG049058RRD VA I21 RX001757
6 · The paper itself

Abstract

Although osteoarthritis (OA) was historically referred to as the non-inflammatory arthritis, it is now considered a condition involving persistent low-grade inflammation and activation of innate inflammatory pathways. Synovitis increases the risk of OA onset and progression and involves the recruitment of monocytes, lymphocytes, and other leukocytes. In particular, macrophages are important mediators of synovial inflammatory activity and pathologic cartilage and bone responses that are characteristic of OA. Advances in understanding how damage-associated molecular patterns (DAMPs) trigger monocyte/macrophage recruitment and activation in joints provide opportunities for disease-modifying therapies. However, the complexity and plasticity of macrophage phenotypes that exist in vivo have thus far prevented the successful development of macrophage-targeted treatments. Current studies show that synovial macrophages are derived from distinct cellular lineages, which correspond to unique functional roles for maintaining joint homeostasis. An improved understanding of the aetiology of synovial inflammation in specific OA-subtypes, such as with obesity or genetic risk, is a potential strategy for developing patient selection criteria for future precision therapies.

Indexed as

OsteoarthritisSynovitisHumansInflammationMacrophagesMonocytes

Identifiers

PMID31621560
PMCPMC6842324
OpenAlexW2986302359

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.