Evidence map›Paper›PMID 12223101›Full record

ReviewArthritis research2002

The molecular mechanism of osteoclastogenesis in rheumatoid arthritis.

Nobuyuki Udagawa, Shigeru Kotake, Naoyuki Kamatani, Naoyuki Takahashi, Tatsuo Suda

Open access · diamondAbstract readReview
In one paragraph

Review in Arthritis research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

44 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
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  14. Novel Therapeutic Targets in Axial Spondyloarthritis.Current treatment options in rheumatology · 2018
    Review
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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

5 authors at 3 institutions in 1 country.

Nobuyuki UdagawaDepartment of Biochemistry, Matsumoto Dental University, Nagano, Japan. udagawa@po.mdu.ac.jp
Shigeru Kotake
Naoyuki Kamatani
Naoyuki Takahashi
Tatsuo Suda
Matsumoto Dental University · JPTokyo Women's Medical University · JPSaitama Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte-macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-kappaB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Recent studies have shown that T lymphocytes produce cytokines other than RANKL such as IL-17, granulocyte-macrophage colony-stimulating factor and IFN-gamma, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.

Indexed as

AnimalsArthritis, RheumatoidBone ResorptionCarrier ProteinsCell DifferentiationCells, CulturedCloning, MolecularCytokinesFibroblastsHumansLymphocyte ActivationMembrane GlycoproteinsMiceOsteoclastsRANK LigandReceptor Activator of Nuclear Factor-kappa BCarrier ProteinsCytokinesMembrane GlycoproteinsRANK LigandReceptor Activator of Nuclear Factor-kappa BTNFRSF11A protein, humanTnfrsf11a protein, mouseTNFSF11 protein, humanTnfsf11 protein, mouse

Identifiers

PMID12223101
PMCPMC128939
OpenAlexW1510491926

What OpenQuestion holds

Textmetadata
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.