Evidence map›Paper›PMID 33774802›Full record

ReviewMolecular biology reports2021

Osteoblast role in the pathogenesis of rheumatoid arthritis.

S Berardi, A Corrado, N Maruotti, D Cici, F P Cantatore

Open access · hybridAbstract readReview
In one paragraph

Review in Molecular biology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.8field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. Article
  3. A novel small molecule KMU-11361 attenuates rheumatoid arthritis by mechanistic inhibition of the TAK1-NF-κB-NLRP3 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Comparative analysis ofFrontiers in pharmacology · 2025
    Article
  15. Review
  16. Article
  17. Bone equilibria and disruptions.Journal of the Pediatric Orthopaedic Society of North America · 2024
    Article
  18. Review
  19. Review
  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

5 authors at 1 institution in 1 country.

S Berardi *Rheumatology Clinic - Department of Medical and Surgical Sciences, University of Foggia - Policlinico Riuniti Foggia, Viale Pinto 1, 71121, Foggia, Italy. scaraberard@gmail.com.
A Corrado *Rheumatology Clinic - Department of Medical and Surgical Sciences, University of Foggia - Policlinico Riuniti Foggia, Viale Pinto 1, 71121, Foggia, Italy.
N MaruottiRheumatology Clinic - Department of Medical and Surgical Sciences, University of Foggia - Policlinico Riuniti Foggia, Viale Pinto 1, 71121, Foggia, Italy.
D CiciRheumatology Clinic - Department of Medical and Surgical Sciences, University of Foggia - Policlinico Riuniti Foggia, Viale Pinto 1, 71121, Foggia, Italy.
F P CantatoreRheumatology Clinic - Department of Medical and Surgical Sciences, University of Foggia - Policlinico Riuniti Foggia, Viale Pinto 1, 71121, Foggia, Italy.
University of Foggia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the pathogenesis of several rheumatic diseases, such as rheumatoid arthritis, spondyloarthritis, osteoarthritis, osteoporosis, alterations in osteoblast growth, differentiation and activity play a role. In particular, in rheumatoid arthritis bone homeostasis is perturbed: in addition to stimulating the pathologic bone resorption process performed by osteoclasts in course of rheumatoid arthritis, proinflammatory cytokines (such as Tumor Necrosis factor-α, Interleukin-1) can also inhibit osteoblast differentiation and function, resulting in net bone loss. Mouse models of rheumatoid arthritis showed that complete resolution of inflammation (with maximal reduction in the expression of pro-inflammatory factors) is crucial for bone healing, performed by osteoblasts activity. In fact, abnormal activity of factors and systems involved in osteoblast function in these patients has been described. A better understanding of the pathogenic mechanisms involved in osteoblast dysregulation could contribute to explain the generalized and focal articular bone loss found in rheumatoid arthritis. Nevertheless, these aspects have not been frequently and directly evaluated in studies. This review article is focused on analysis of the current knowledge about the role of osteoblast dysregulation occurring in rheumatoid arthritis: a better knowledge of these mechanisms could contribute to the realization of new therapeutic strategies.

Indexed as

AnimalsArthritis, RheumatoidBone and BonesBone ResorptionHomeostasisHumansOsteoblastsSignal TransductionBone lossCytokinesOsteoblastsRANKL/RANKRheumatoid arthritis

Identifiers

PMID33774802
PMCPMC8060181
OpenAlexW3144523164

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.