Evidence map›Paper›PMID 28558827›Full record

ArticleBMC musculoskeletal disorders2017

Early anti-inflammatory intervention ameliorates axial disease in the proteoglycan-induced spondylitis mouse model of ankylosing spondylitis.

Hsu-Wen Tseng, Tibor T Glant, Matthew A Brown, Tony J Kenna, Gethin P Thomas, Allison R Pettit

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC musculoskeletal disorders, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. 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

6 authors at 2 institutions in 2 countries.

Hsu-Wen TsengThe University of Queensland Diamantina Institute, Translational Research Institute, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Tibor T GlantSection of Molecular Medicine, Department of Orthopedic Surgery, Rush University Medical Center, 1735 W. Harrison Str., Cohn Research Building, Chicago, IL, 60612, USA.
Matthew A BrownThe University of Queensland Diamantina Institute, Translational Research Institute, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Tony J KennaThe University of Queensland Diamantina Institute, Translational Research Institute, 37 Kent Street, Woolloongabba, QLD, 4102, Australia.
Gethin P ThomasThe University of Queensland Diamantina Institute, Translational Research Institute, 37 Kent Street, Woolloongabba, QLD, 4102, Australia. getthomas@csu.edu.au.
Allison R PettitMater Research Institute-The University of Queensland, Faculty of Medicine, Translational Research Institute, 37 Kent St, Woolloongabba, QLD, 4102, Australia. allison.pettit@mater.uq.edu.au.ORCID 0000-0003-4707-7892
Translational Research Institute · AURush University Medical Center · US

Funding

Identification of Genetic and Epigenetic Alterations in SpondyloarthritisR01AR062991 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI MIKECZ, KATALIN · 2013 to 2017
$1.6M
NIAMS NIH HHS R01 AR062991
6 · The paper itself

Abstract

backgroundAnkylosing spondylitis (AS) is characterised by immune-mediated arthritis and osteoproliferation, ultimately leading to joint ankylosis. Whether inflammation is necessary for osteoproliferation is controversial, fuelled by the unclear efficacy of anti-inflammatory treatments on radiographic progression. In proteoglycan-induced spondylitis (PGISp), a mouse model of AS, inflammation is the prerequisite for osteoproliferation as osteoproliferation was only observed following inflammation-driven intervertebral disc (IVD) destruction. We hypothesised that early intervention with a potent anti-inflammatory therapy would protect IVD integrity and consequently alter disease progression.

methodsPGISp mice received vehicle or a combination of etanercept (ETN) plus prednisolone (PRD) therapy for 2 or 6 weeks initiated at an early disease stage. Peripheral arthritis was scored longitudinally. Spinal disease was assessed using a semi-quantitative histological scoring regimen including inflammation, joint destruction and excessive tissue formation.

resultsETN + PRD therapy significantly delayed the onset of peripheral arthritis. IVD integrity was significantly protected when treatment was commenced in early disease. Six-weeks of treatment resulted in trends towards reductions in intervertebral joint damage and excessive tissue formation. IVD score distribution was dichotomized, likely reflecting the extent of axial disease at initiation of therapy. In the sub-group of mice with high IVD destruction scores, ETN + PRD treatment significantly reduced IVD destruction severity, inflammation and bone erosion and reduced cartilage damage and excessive tissue formation.

conclusionsEarly intervention with anti-inflammatory treatment not only improved inflammatory symptoms but also ameliorated structural damage of spine in PGISp mice. This preclinical observation suggests that early anti-inflammatory intervention may slow radiographic progression in AS patients.

Indexed as

Disease Models, AnimalAnimalsAnti-Inflammatory AgentsDrug Administration ScheduleDrug Therapy, CombinationEtanerceptFemaleHumansMiceMice, Inbred BALB CPrednisoloneProteoglycansSpondylitis, AnkylosingAnti-Inflammatory AgentsEtanerceptPrednisoloneProteoglycansAnkylosing spondylitisEarly interventionOsteoproliferationProteoglycan-induced spondylitis mouse modelSpondyloarthropathy

Identifiers

PMID28558827
PMCPMC5450150
OpenAlexW2619743864

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Registered trials

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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.