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Pro chondrogenic effect of mesenchymal stromal cell-based treatment of chondral defects under physioxia in a novel ex vivo organ model
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Pro chondrogenic effect of mesenchymal stromal cell-based treatment of chondral defects under physioxia in a novel ex vivo organ model
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Paper
Pro chondrogenic effect of mesenchymal stromal cell-based treatment of chondral defects under physioxia in a novel ex vivo organ model
2020
Overview
Abstract Objective High failure rates of (trauma induced) knee injuries highlight the need to improve current treatment strategies aiming to decrease the number of secondary osteoarthritis developed by patients in later stage [1-3]. In this controlled laboratory study the stimulative effect of mesenchymal stromal cells (MSC) on chondrocyte (CHON) extracellular matrix production was investigated in an ex vivo cartilage defect model (chondral vs. full thickness defects) cultured under normoxic (20 % O2) and physioxic (2 % O2) conditions. Design Porcine CHON or co-culture of 20 % CHON and 80 % MSC (MIX) were embedded in collagen type I hydrogel, implanted into 4 mm diameter cartilage defects of osteochondral explants and cultured with tissue specific media without addition of TGF-β under normoxia and physioxia. Chondral defects were induced automatically, while full thickness defects were created with biopsy punch. After 28 days of culture, samples were histologically processed, and treatments outcome was evaluated using international cartilage repair society (ICRS)-II scoring. Results Under physioxic conditions, cartilage repair scoring results of the MIX treatment (chondral 8.67 ± 2.42, full thickness 5.67 ± 1.21) were close to those of CHON treatment (chondral 8.17 ± 0.75, full thickness 7.33 ± 1.21). Overall, scoring results were higher in physioxia compared to normoxia conditions in chondral defects, but less or no prevalent for full thickness defects. Conclusion Co-culture of CHON with MSC represents a promising approach to stimulate chondrogenic repair and tissue formation in our ex vivo model and reduces total amount of CHON needed for cell-based treatment. Competing Interest Statement The authors have declared no competing interest. Footnotes * Andrea Schwab University Hospital Wuerzburg, Department Tissue Engineering and Regenerative Medicine, AO Research Institute Davos, Clavadelerstrasse 8, 7270 Davos, Switzerland E-Mail: andrea.schwabataofoundation.org * Alexa Buß University Hospital Wuerzburg, Department Tissue Engineering and Regenerative Medicine, Roentgenring 11, 97070 Wuerzburg, Germany, Klinikum Würzburg Mitte gGmbH, Juliusspital, Juliuspromenade 19, 97070 Wuerzburg, Germany, E-Mail: alexa.bussatkwm-klinikum.de * Oliver Pullig University Hospital Wuerzburg, Department Tissue Engineering and Regenerative Medicine, Roentgenring 11, 97070 Wuerzburg, Germany, Fraunhofer Institute for Silicate Research ISC, Translational Center Regenerative Therapies, Roentgenring 11, 97070 Wuerzburg, Germany, E-Mail: oliver.pulligatisc.fraunhofer.de
Publisher
Cold Spring Harbor Laboratory Press
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