Evidence map›Paper›PMID 28506841›Full record

ArticleOsteoarthritis and cartilage2017

Definition of a Critical Size Osteochondral Knee Defect and its Negative Effect on the Surrounding Articular Cartilage in the Rat.

H Katagiri, L F Mendes, F P Luyten

Open access · hybridAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

24 citing papers in PubMed, 66 citations in OpenAlex.

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  7. Effect of N-butyl cyanoacrylate on the regeneration of joint defects in mature male rats.Veterinary research forum : an international quarterly journal · 2025
    Article
  8. Review
  9. Article
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  11. Review
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  13. Article
  14. Hyperplastic Human Macromass Cartilage for Joint Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  15. Article
  16. Cell therapy for cartilage repair.Emerging topics in life sciences · 2021
    Review
  17. Article
  18. Article
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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

3 authors at 1 institution in 1 country.

H KatagiriTissue Engineering Laboratory, Skeletal Biology and Engineering Research Center, KU Leuven, Leuven, Belgium; Prometheus, Division of Skeletal Tissue Engineering, KU Leuven, Leuven, Belgium.
L F MendesTissue Engineering Laboratory, Skeletal Biology and Engineering Research Center, KU Leuven, Leuven, Belgium; Prometheus, Division of Skeletal Tissue Engineering, KU Leuven, Leuven, Belgium.
F P LuytenTissue Engineering Laboratory, Skeletal Biology and Engineering Research Center, KU Leuven, Leuven, Belgium; Prometheus, Division of Skeletal Tissue Engineering, KU Leuven, Leuven, Belgium. Electronic address: frank.luyten@uzleuven.be.
KU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundJoint trauma is predisposing to the incidence of osteoarthritis (OA) of the knee. There is a limited knowledge on the impact of posttraumatic osteochondral defects on the whole joint. This study was designed to define a critical size osteochondral defect in the knee of rats and to investigate a possible association between osteochondral defects and degeneration of the surrounding joint surface.

methodsCylindrical osteochondral defects of different sizes were created in the knee joint of rats. The natural course of these lesions was studied by macroscopic observation, histology, and immunohistochemistry. Gene expression of the articular cartilage surrounding the defects in vivo and of articular chondrocytes cultured in vitro in IL1β and fibroblast growth factor 2 (FGF2) supplemented media was evaluated by quantitative polymerase chain reaction (qPCR).

resultsIn defects of 0.9 mm diameter, spontaneous joint surface healing was observed but also upward advancing of the subchondral bone plate at 16 weeks. Larger 1.4 mm diameter defects were critical size, not resulting in successful healing at any time point. Importantly, the articular cartilage surrounding the defects expressed FGF2 and IL1β, but not ACAN and Col2. Chondrocytes cultured in IL1β and FGF2 supplemented media lost the natural fibroblast growth factor receptors - FGFr1/FGFr3 balance and showed decreased viability.

conclusionsA critical size osteochondral defect was defined as 1.4 mm in diameter in rat. Subchondral bone plate advancement occured rapidly. The articular cartilage surrounding osteochondral defects showed catabolic activity with expression of IL1β, FGF2 and a disturbed FGFr1/FGFr3 balance, potentially initiating a process of early osteoarthritic disease.

Indexed as

AnimalsArthritis, ExperimentalBone RegenerationCartilage, ArticularCells, CulturedChondrocytesCollagen Type IIFibroblast Growth Factor 2Interleukin-1betaKnee InjuriesMaleOsteoarthritisRats, Inbred LewWound HealingCollagen Type IIFibroblast Growth Factor 2Interleukin-1betaKneeOsteoarthritisOsteochondralTissue regeneration

Identifiers

PMID28506841
PMCPMC5754326
OpenAlexW2613784806

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.