Evidence map›Paper›PMID 25384124›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2015

Development of non-traumatic osteonecrosis of the femoral head requires toll-like receptor 7 and 9 stimulations and is boosted by repression on nuclear factor kappa B in rats.

Shunichiro Okazaki, Satoshi Nagoya, Hiroshi Matsumoto, Keisuke Mizuo, Mikito Sasaki, Satoshi Watanabe, Toshihiko Yamashita, Hiromasa Inoue

Open access · hybridAbstract read
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  16. A Human Chondrocyte-Derived In Vitro Model of Alcohol-Induced and Steroid-Induced Femoral Head Necrosis.Medical science monitor : international medical journal of experimental and clinical research · 2018
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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

8 authors at 1 institution in 1 country.

Shunichiro Okazaki1] Department of Musculoskeletal Biomechanics and Surgical Development, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Department of Legal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Satoshi NagoyaDepartment of Musculoskeletal Biomechanics and Surgical Development, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiroshi MatsumotoDepartment of Legal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Keisuke MizuoDepartment of Legal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Mikito Sasaki1] Department of Musculoskeletal Biomechanics and Surgical Development, Sapporo Medical University School of Medicine, Sapporo, Japan [2] Department of Orthopedic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Satoshi WatanabeDepartment of Legal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Toshihiko YamashitaDepartment of Orthopedic Surgery, Sapporo Medical University School of Medicine, Sapporo, Japan.
Hiromasa InoueDepartment of Legal Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-traumatic osteonecrosis of the femoral head (ONFH) often occurs after corticosteroid therapy in patients with inflammatory diseases. Recent studies suggest that toll-like receptor (TLR) signaling may contribute to the pathogenesis of inflammatory diseases, and that the reason for corticosteroid therapy for inflammatory diseases is related to the anti-inflammatory activities of corticosteroids through the reduction of NF-κB. We hypothesized that the administration of TLR ligands in combination with corticosteroid causes ONFH and that transcription factors may contribute to the pathogenesis of ONFH. The aim of the study was to evaluate (1) the incidence of ONFH in rats after the administration of TLR7 or TLR9 ligands together with methylprednisolone (MPSL) and (2) whether transcription factors contribute to the development of ONFH. Male Wistar rats (n=148) were divided into five groups as follows: Group 1: Saline+MPSL, Group 2: Imiquimod+Saline, Group 3: Imiquimod+MPSL, Group 4: CpG-C+MPSL, Group 5: Imiquimod+BAY11-7082+MPSL. As a result, ONFH was observed in 0 of 12 rats in Group 1, in 1 of 10 in Group 2, in 6 of 12 in Group 3, in 4 of 12 in Group 4, in 0 of 9 in Group 5. MPSL treatment did not significantly affect IRF7 activity, whereas NF-κB activity was significantly repressed in Group 2 and Group 3. Furthermore, the repression in interferon regulatory factor 7 (IRF7) activity by BAY11-7082 interfered with the development of ONFH simultaneously with the MPSL treatment-induced repression in NF-κB activity. In conclusion, in the present study, corticosteroid treatment after the administration of TLR7 or TLR9 ligands caused ONFH. Repression in NF-κB activity by corticosteroid treatment boosted the development of ONFH.

Indexed as

AnimalsBase SequenceDNA ProbesElectrophoretic Mobility Shift AssayFemur HeadMaleNF-kappa BOsteonecrosisRatsRats, WistarToll-Like Receptor 7Toll-Like Receptor 9DNA ProbesNF-kappa BTLR7 protein, ratTlr9 protein, ratToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID25384124
PMCPMC7100527
OpenAlexW2023688854

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.