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Age-Related Differences in Articular Cartilage Wound Healing: A Potential Role for Transforming Growth Factor β1 in Adult Cartilage Repair

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Tissue Engineering

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 585))

20.1. Abstract

Objective of this study was to investigate the early wound healing reactions of immature and mature articular cartilage on experimental wound healing in the New Zealand White rabbit. The proliferation potential and glycosaminoglycan production of isolated chondrocytes of these animals was studied in an alginate culture system. A band of tissue with death chondrocytes was observed at wound edges of immature articular cartilage, whereas mature cartilage showed a significant smaller amount of dead chondrocytes. A general increase in TGFβ1, FGF2 and IGF1 was observed throughout cartilage tissue with the exception of lesion edges. The observed immunonegative area appeared to correlate with the observed cell death in lesion edges. Repair in immature cartilage was indicated by chondrocyte proliferation in clusters and a decrease in defect size. No repair response was observed in mature articular cartilage defects. The alginate culture experiment demonstrated a higher proliferation rate of immature chondrocytes. Addition of recombinant TGFβ1 increased proliferation rate and GAG production of mature chondrocytes. We were not able to further stimulate immature chondrocytes. These results indicate that TGF 1 addition may contribute to induce cartilage repair responses in mature cartilage as observed in immature, developing cartilage.

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Bos, P.K., Verhaar, J.A.N., van Osch, G.J.V.M. (2006). Age-Related Differences in Articular Cartilage Wound Healing: A Potential Role for Transforming Growth Factor β1 in Adult Cartilage Repair. In: Fisher, J.P. (eds) Tissue Engineering. Advances in Experimental Medicine and Biology, vol 585. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-34133-0_20

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  • DOI: https://doi.org/10.1007/978-0-387-34133-0_20

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-0-387-32664-1

  • Online ISBN: 978-0-387-34133-0

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