Evidence map›Paper›PMID 30937213›Full record

ArticleBone research2019

Pathological mechanisms and therapeutic outlooks for arthrofibrosis.

Kayley M Usher, Sipin Zhu, Georgios Mavropalias, John A Carrino, Jinmin Zhao, Jiake Xu

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

Article in Bone research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
131citing papers in PubMed, 4 pooled it
19.4field-weighted citation impact, top 1% 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

131 citing papers in PubMed, 4 syntheses or guidelines pooled it, 256 citations in OpenAlex.

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  11. A practical toolbox for modelling fibrosis in vitro.Nature biomedical engineering · 2026
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71 more citing papers are in PubMed but not listed here.

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 5 institutions in 3 countries.

Kayley M Usher1School of Biomedical Sciences, University of Western Australia, Crawley, Western Australia Australia.
Sipin Zhu2Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang China.
Georgios Mavropalias3School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia Australia.
John A Carrino4Hospital for Special Surgery, New York, NY USA.
Jinmin Zhao5Guangxi Key Laboratory of Regenerative Medicine, Guangxi Medical University, Nanning, Guangxi China.
Jiake Xu1School of Biomedical Sciences, University of Western Australia, Crawley, Western Australia Australia.
Guangxi Medical University · CNEdith Cowan University · AUHospital for Special Surgery · USUniversity of Western Australia · AUWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arthrofibrosis is a fibrotic joint disorder that begins with an inflammatory reaction to insults such as injury, surgery and infection. Excessive extracellular matrix and adhesions contract pouches, bursae and tendons, cause pain and prevent a normal range of joint motion, with devastating consequences for patient quality of life. Arthrofibrosis affects people of all ages, with published rates varying. The risk factors and best management strategies are largely unknown due to a poor understanding of the pathology and lack of diagnostic biomarkers. However, current research into the pathogenesis of fibrosis in organs now informs the understanding of arthrofibrosis. The process begins when stress signals stimulate immune cells. The resulting cascade of cytokines and mediators drives fibroblasts to differentiate into myofibroblasts, which secrete fibrillar collagens and transforming growth factor-β (TGF-β). Positive feedback networks then dysregulate processes that normally terminate healing processes. We propose two subtypes of arthrofibrosis occur: active arthrofibrosis and residual arthrofibrosis. In the latter the fibrogenic processes have resolved but the joint remains stiff. The best therapeutic approach for each subtype may differ significantly. Treatment typically involves surgery, however, a pharmacological approach to correct dysregulated cell signalling could be more effective. Recent research shows that myofibroblasts are capable of reversing differentiation, and understanding the mechanisms of pathogenesis and resolution will be essential for the development of cell-based treatments. Therapies with significant promise are currently available, with more in development, including those that inhibit TGF-β signalling and epigenetic modifications. This review focuses on pathogenesis of sterile arthrofibrosis and therapeutic treatments.

Identifiers

PMID30937213
PMCPMC6433953
OpenAlexW2923746368

What OpenQuestion holds

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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.