Evidence map›Paper›PMID 23588785›Full record

ArticleEuropean cells & materials2013

Cartilage constructs engineered from chondrocytes overexpressing IGF-I improve the repair of osteochondral defects in a rabbit model.

H Madry, G Kaul, D Zurakowski, G Vunjak-Novakovic, M Cucchiarini

Open access · goldAbstract read
In one paragraph

Article in European cells & materials, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 65 citations in OpenAlex.

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  16. New trends in articular cartilage repair.Journal of experimental orthopaedics · 2015
    Article
  17. Bioactive IGF-1 release from collagen-GAG scaffold to enhance cartilage repair in vitro.Journal of materials science. Materials in medicine · 2015
    Article
  18. 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

5 authors at 3 institutions in 2 countries.

H MadryCentre of Experimental Orthopaedics, Medical Faculty, Building 37, Saarland University, D-66421 Homburg, Germany. henning.madry@uks.eu
G Kaul
D Zurakowski
G Vunjak-Novakovic
M Cucchiarini
Saarland University · DEBoston Children's Hospital · USColumbia University · US

Funding

Translational Bioreactors - Engineering Complex TissuesP41EB002520 · NIBIB · TUFTS UNIVERSITY MEDFORD · PI KAPLAN, DAVID L. · 2004 to 2018
$16.7M
Craniofacial Tissue EngineeringR01DE016525 · NIDCR · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI VUNJAK-NOVAKOVIC, GORDANA · 2005 to 2017
$5.5M
NIBIB NIH HHS P41 EB002520NIDCR NIH HHS R01 DE016525
6 · The paper itself

Abstract

Tissue engineering combined with gene therapy is a promising approach for promoting articular cartilage repair. Here, we tested the hypothesis that engineered cartilage with chondrocytes overexpressing a human insulin-like growth factor I (IGF-I) gene can enhance the repair of osteochondral defects, in a manner dependent on the duration of cultivation. Genetically modified chondrocytes were cultured on biodegradable polyglycolic acid scaffolds in dynamic flow rotating bioreactors for either 10 or 28 d. The resulting cartilaginous constructs were implanted into osteochondral defects in rabbit knee joints. After 28 weeks of in vivo implantation, immunoreactivity to ß-gal was detectable in the repair tissue of defects that received lacZ constructs. Engineered cartilaginous constructs based on IGF-I-overexpressing chondrocytes markedly improved osteochondral repair compared with control (lacZ) constructs. Moreover, IGF-I constructs cultivated for 28 d in vitro significantly promoted osteochondral repair vis-à-vis similar constructs cultivated for 10 d, leading to significantly decreased osteoarthritic changes in the cartilage adjacent to the defects. Hence, the combination of spatially defined overexpression of human IGF-I within a tissue-engineered construct and prolonged bioreactor cultivation resulted in most enhanced articular cartilage repair and reduction of osteoarthritic changes in the cartilage adjacent to the defect. Such genetically enhanced tissue engineering provides a versatile tool to evaluate potential therapeutic genes in vivo and to improve our comprehension of the development of the repair tissue within articular cartilage defects. Insights gained with additional exploration using this model may lead to more effective treatment options for acute cartilage defects.

Indexed as

Tissue EngineeringWound HealingAnimalsbeta-GalactosidaseBioreactorsCartilage, ArticularCell CountChondrocytesChondrogenesisCollagen Type IIDisease Models, AnimalHumansImmunohistochemistryInsulin-Like Growth Factor IMaleProsthesis Implantationbeta-GalactosidaseCollagen Type IIInsulin-Like Growth Factor I

Identifiers

PMID23588785
PMCPMC4476264
OpenAlexW105600474

What OpenQuestion holds

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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.