Evidence map›Paper›PMID 26481971›Full record

ReviewSeminars in cell & developmental biology2016

Mediators of inflammation and bone remodeling in rheumatic disease.

Anita T Shaw, Ellen M Gravallese

Abstract readReview
In one paragraph

Review in Seminars in cell & developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
7.5field-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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Investigating the Osteoregenerative Properties ofJournal of functional biomaterials · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. STING-dependent interferon signatures restrict osteoclast differentiation and bone loss in mice.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. Article
  20. Article
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 1 institution in 1 country.

Anita T ShawDepartment of Medicine, Division of Rheumatology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: anita.shaw1@umassmed.edu.
Ellen M GravalleseDepartment of Medicine, Division of Rheumatology, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: ellen.gravallese@umassmed.edu.
University of Massachusetts Chan Medical School · US

Funding

Inhibition of osteoblast function in bone erosion in rheumatoid arthritisR01AR055952 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI GRAVALLESE, ELLEN M · 2009 to 2013
$1.7M
NIAMS NIH HHS NIHR01-AR055952NIAMS NIH HHS R01 AR055952
6 · The paper itself

Abstract

Remodeling of bone is a continuous process that occurs throughout life. Under normal physiologic conditions, bone-resorbing osteoclasts and bone-forming osteoblasts are tightly coupled and regulated to ensure proper balance, such that there is no net change in bone mass. However, inflammation perturbs normal bone homeostasis. The impact of inflammation on bone is dependent upon the anatomic site affected, cell types, factors and cytokines present in the local microenvironment, and local mechanical forces. Cytokines are central to the pathogenesis of inflammation-induced bone loss and contribute to the uncoupling of osteoclast-mediated bone resorption and osteoblast-mediated bone formation, thereby disrupting normal remodeling. In this review, we will discuss the effects of cytokines on bone in two settings, rheumatoid arthritis and spondyloarthritis, a disease category that includes ankylosing spondylitis, psoriatic arthritis, reactive arthritis, inflammatory bowel disease, and juvenile onset spondyloarthropathy. The outcome for bone in these disease settings is quite different, and an understanding of the pathogenic mechanisms leading to the net impact on bone has been essential in developing new therapeutic approaches to bone health in these diseases.

Indexed as

AnimalsArthritis, RheumatoidBone ResorptionCytokinesHumansInflammation MediatorsOsteoblastsOsteoclastsSignal TransductionCytokinesInflammation MediatorsCytokinesInflammationOsteoblastsOsteoclastsRheumatoid arthritisSpondyloarthritis

Identifiers

PMID26481971
PMCPMC4761455
OpenAlexW1802864915

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.