ArticleJB & JS open access
Fetal Cartilage Progenitor Cells in the Repair of Osteochondral Defects.
Article in JB & JS open access. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Chondrocyte metabolic transition from proliferation to quiescence revealed by FLIM in postnatal mouse knee joints.Journal of tissue engineeringArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Therapies for cartilage restoration are of great interest, but current options provide limited results. In salamanders, interzone (IZN) tissue can regenerate large joint lesions. The mammalian homolog to this tissue exists during fetal development and exhibits remarkable chondrogenesis in vitro. This study analyzed the potential of equine IZN and adjacent anlagen (ANL) cells to regenerate osteochondral defects. Methods: Osteochondral defects were created in the knee of immunosuppressed rats and were grafted with cell pellets from either equine fetal IZN, equine fetal ANL, adult fibroblasts, or adult chondrocytes, or they were left untreated. Osteochondral repair was assessed after 2, 6, and 16 weeks. Results: Untreated lesions unexpectedly failed to represent critical-sized defects and at 2 weeks exhibited new subchondral bone covered by a fibrocartilage layer that thinned over time. Fibroblast-treated defects filled with soft fibrous tissue. Chondrocyte-treated repair tissue exhibited strong proteoglycan and COL2 staining but poor integration to the adjacent bone. Defects treated with IZN, ANL, or chondrocyte pellets developed hyaline cartilage with increasing safranin-O and collagen II staining over time. IZN and ANL repair tissues exhibited some evidence of zonal architecture such as native cartilage and the best bone integration; nonetheless, they developed exuberant growth, often causing patellar instability and osteoarthritis. Conclusions: IZN or ANL cells exhibited some potential to recapitulate developmental features during cartilage repair. However, identifying regulatory determinants of IZN and ANL-derived overgrowths is necessary. Clinical Relevance: Studies grafting IZN or ANL tissues in larger animal models with regular immune functions may provide additional insights into improving osteochondral regeneration.
Identifiers
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Registered trials
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.