Evidence map›Paper›PMID 42564269›Full record

ArticleFrontiers in immunology2026

TNF-α blockade with adalimumab restores bone metabolism in rheumatoid arthritis by regulating cytokines and inflammatory cell infiltration.

Akilan Krishnamurthy, Shankar Revu, Petra Neregård, Aase Hensvold, Erik Af Klint, Dimitrios Makrygiannakis, Anca I Catrina, Ioannis Parodis

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Akilan KrishnamurthyDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Shankar RevuDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Petra NeregårdDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Aase HensvoldDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Erik Af KlintDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Dimitrios MakrygiannakisDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Anca I Catrina *Division of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.
Ioannis ParodisDivision of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, and Center for Molecular Medicine (CMM), Stockholm, Sweden.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the mechanisms underlying the bone-sparing effects of the anti-TNF antibody adalimumab in rheumatoid arthritis (RA) by examining synovial tissue and its direct effect on osteoblasts and osteoclasts. Methods: Paired synovial biopsies from 12 patients with RA were obtained before and 8 weeks after initiation of adalimumab. Immune-cell infiltrates (CD163 Results: Adalimumab treatment led to a marked clinical improvement, with median DAS28 decreasing from 5.4 to 3.1. Semiquantitative analysis of synovial biopsies revealed a significant decrease in CD163 Conclusion: Adalimumab decreased synovial macrophage infiltration while it modulates pro-osteoclastogenic cytokines and inhibits osteoclastogenesis. These combined effects explain how TNF-α blockade ameliorates joint inflammation and prevents structural damage.

Indexed as

AdalimumabAntirheumatic AgentsArthritis, RheumatoidBone and BonesCytokinesTumor Necrosis Factor-alphaAdultAgedBone ResorptionFemaleHumansMacrophagesMaleMiddle AgedOsteoblastsOsteoclastsAdalimumabAntirheumatic AgentsCytokinesOsteoprotegerinRANK LigandTNFSF11 protein, humanTumor Necrosis Factor-alphaanti-TNF-αbiologicsbone erosionosteoblastsosteoclastsrheumatoid arthritissynovial inflammation

Identifiers

PMID42564269
PMCPMC13442820

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.