The extent and distribution of cell death and matrix damage in impacted chondral explants varies with the presence of underlying bone

J. A. Krueger, P. Thisse, B. J. Ewers, D. Dvoracek-Driksna, M. W. Orth, Roger C. Haut

Research output: Contribution to journalArticlepeer-review

34 Scopus citations

Abstract

Excessive mechanical loading can lead to matrix damage and chondrocyte death in articular cartilage. Previous studies on chondral and osteochondral explants have not clearly distinguished to what extent the degree and the distribution of cell death are dependent on the presence of an underlying layer of bone. The current study hypothesized that the presence of underlying bone would decrease the amount of matrix damage and cell death. Chondral and osteochondral explants were loaded to 30 MPa at a high rate of loading (∼600 MPa/s) or at a low rate of loading (30 MPa/s). After 24 hours in culture, matrix damage was assessed by the total length and average depth of surface fissures. The explants were also sectioned and stained for cell viability in the various layers of the cartilage. More matrix damage was documented in chondral than osteochondral explants for each rate of loading experiment. The total amount of cell death was also less in osteochondral explants than chondral explants. The presence of underlying bone significantly reduced the extent of cell death in all zones in low rate of loading tests. The percentage of cell death was also reduced in the intermediate zone and deep zones of the explant by the presence of the underlying bone for a high rate of loading. This study indicated that the presence of underlying bone significantly limited the degree of matrix damage and cell death, and also affected the distribution of dead cells through the explant thickness. These data may have relevance to the applicability of experimental data from chondral explants to the in situ condition.

Original languageEnglish
Pages (from-to)114-119
Number of pages6
JournalJournal of Biomechanical Engineering
Volume125
Issue number1
DOIs
StatePublished - Feb 2003

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