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Updated: Dec 7, 2025

Real-time Visualization and Analysis of Chondrocyte Injury Due to Mechanical Loading in Fully Intact Murine Cartilage Explants
Published on: January 7, 2019
Layer dependence in strain distribution and chondrocyte damage in porcine articular cartilage exposed to excessive
Wenjing Huang1, Mia Warner2, Hikaru Sasaki3
1Department of Bioengineering, School of Engineering, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-8656, Japan.
Abstract:
Exposure to excessive stress is associated with the pathogenesis of osteoarthritis, a joint disease involved in the degeneration of articular cartilage. Mechanical properties of mature articular cartilage are known to be depth zone-dependent. Although chondrocyte death was observed in articular cartilage after excessive stress loading in vitro, few studies have investigated the correlation between chondrocyte death and local mechanical strains in a depth dependent manner. Here, we developed a real-time observation system of cut cartilage samples under an excessive stress loading (18 MPa) at low (3.5%/s) and high (35%/s) strain rates on the microscope stage, which is regarded as injurious compression in vivo. Using this system, real-time monitoring of local deformations was conducted during compression, and local chondrocyte death was investigated after short-term culture. The results showed that the dead cells were mainly observed in the surface layer at a high strain rate. In contrast, the dead cells were relatively concentrated not in the surface layer but in the middle layer at a low strain rate. The local strain measurements showed that the dead cell distributions were correlated with depth-dependent local strain rates at both low and high strain rates. Moreover, when the surface layer was removed, both depth-dependence in dead cell distributions and in local strain rates disappeared at low and high strain rates. Although the mechanisms underlying mechanically induced osteoarthritis are still elusive, those results suggest a correlation between local chondrocyte death and transient strain rates in a depth dependent manner, and the surface layer played a crucial role in regulating chondrocyte damages and local strains in middle and deep layers. Our study, therefore, could contribute to an analytical understanding of cartilage degeneration under excessive stress loadings.
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