Evidence map›Paper›PMID 26879798›Full record

ArticleOsteoarthritis and cartilage2016

Loss of spatial organization and destruction of the pericellular matrix in early osteoarthritis in vivo and in a novel in vitro methodology.

T Felka, M Rothdiener, S Bast, T Uynuk-Ool, S Zouhair, B G Ochs, P De Zwart, U Stoeckle, W K Aicher, M L Hart and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Osteoarthritis and cartilage, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
–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

25 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

18 authors.

T FelkaSiegfried Weller Institute for Trauma Research, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: tino579@yahoo.de.
M RothdienerSiegfried Weller Institute for Trauma Research, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: miriam.rothdiener@uni-tuebingen.de.
S BastSiegfried Weller Institute for Trauma Research, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: sina.bast@gmx.net.
T Uynuk-OolSiegfried Weller Institute for Trauma Research, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: tanya_u@web.de.
S ZouhairDepartment of Cardiac, Thoracic and Vascular Sciences, University of Padua, Padua, Italy. Electronic address: sabra.zouhair@gmail.com.
B G OchsClinic for Trauma and Restorative Surgery, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: gochs@bgu-tuebingen.de.
P De ZwartClinic for Trauma and Restorative Surgery, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: PdeZwart@bgu-tuebingen.de.
U StoeckleClinic for Trauma and Restorative Surgery, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany. Electronic address: ustoeckle@bgu-tuebingen.de.
W K AicherDepartment of Urology, University of Tuebingen, Tuebingen, Germany. Electronic address: aicher@uni-tuebingen.de.
M L HartDepartment of Urology, University of Tuebingen, Tuebingen, Germany. Electronic address: melaniehar@gmail.com.
T ShiozawaInstitute of Clinical Anatomy and Cell Analysis, University of Tuebingen, Tuebingen, Germany. Electronic address: thomas.shiozawa@uni-tuebingen.de.
A J GrodzinskyCenter for Biomedical Engineering, Massachusetts Institute of Technology, Cambridge, USA. Electronic address: alg@mit.edu.
K Schenke-LaylandDepartment of Women's Health, Research Institute for Women's Health, University of Tuebingen, Tuebingen, Germany; Department of Cell and Tissue Engineering, Fraunhofer Institute for Interfacial Engineering and Biotechnology (IGB), Stuttgart, Germany. Electronic address: katja.schenke-layland@igb.fraunhofer.de.
J K VenkatesanCenter of Experimental Orthopaedics, Saarland University Medical Center, Homburg, Germany. Electronic address: jegadish.venki@gmail.com.
M CucchiariniCenter of Experimental Orthopaedics, Saarland University Medical Center, Homburg, Germany. Electronic address: mmcucchiarini@hotmail.com.
H MadryCenter of Experimental Orthopaedics, Saarland University Medical Center, Homburg, Germany. Electronic address: Henning.Madry@uniklinikum-saarland.de.
B KurzAnatomical Institute, Christian-Albrecht-University Kiel, Kiel, Germany. Electronic address: bkurz@anat.uni-kiel.de.
B RolauffsSiegfried Weller Institute for Trauma Research, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany; Clinic for Trauma and Restorative Surgery, BG Trauma Clinic Tuebingen, University of Tuebingen, Tuebingen, Germany; Center for Biomedical Engineering, Massachusetts Institute of Technology, Cambridge, USA. Electronic address: berndrolauffs@googlemail.com.

Funding

Cartilage Repair Using Self Assembling Peptide ScaffoldsR01AR060331 · NIAMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI GRODZINSKY, ALAN J. · 2012 to 2016
$1.7M
NIAMS NIH HHS R01 AR060331
6 · The paper itself

Abstract

objectivesCurrent repair procedures for articular cartilage (AC) cannot restore the tissue's original form and function because neither changes in its architectural blueprint throughout life nor the respective biological understanding is fully available. We asked whether two unique elements of human cartilage architecture, the chondrocyte-surrounding pericellular matrix (PCM) and the superficial chondrocyte spatial organization (SCSO) beneath the articular surface (AS) are congenital, stable or dynamic throughout life. We hypothesized that inducing chondrocyte proliferation in vitro impairs organization and PCM and induces an advanced osteoarthritis (OA)-like structural phenotype of human cartilage.

methodsWe recorded propidium-iodine-stained fetal and adult cartilage explants, arranged stages of organization into a sequence, and created a lifetime-summarizing SCSO model. To replicate the OA-associated dynamics revealed by our model, and to test our hypothesis, we transduced specifically early OA-explants with hFGF-2 for inducing proliferation. The PCM was examined using immuno- and auto-fluorescence, multiphoton second-harmonic-generation (SHG), and scanning electron microscopy (SEM).

resultsSpatial organization evolved from fetal homogeneity, peaked with adult string-like arrangements, but was completely lost in OA. Loss of organization included PCM perforation (local micro-fibrillar collagen intensity decrease) and destruction [regional collagen type VI (CollVI) signal weakness or absence]. Importantly, both loss of organization and PCM destruction were successfully recapitulated in FGF-2-transduced explants.

conclusionInduced proliferation of spatially characterized early OA-chondrocytes within standardized explants recapitulated the full range of loss of SCSO and PCM destruction, introducing a novel in vitro methodology. This methodology induces a structural phenotype of human cartilage that is similar to advanced OA and potentially of significance and utility.

Indexed as

OsteoarthritisCartilage, ArticularChondrocytesExtracellular MatrixFibroblast Growth Factor 2HumansFibroblast Growth Factor 2Articular cartilageCellular distributionChondrocyteEarly osteoarthritisPericellular matrixSuperficial zone

Identifiers

PMID26879798
PMCPMC4907798

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.