Tm. Quinn et al., EFFECTS OF INJURIOUS COMPRESSION ON MATRIX TURNOVER AROUND INDIVIDUALCELLS IN CALF ARTICULAR-CARTILAGE EXPLANTS, Journal of orthopaedic research, 16(4), 1998, pp. 490-499
The effects of mechanical injury on the metabolism of cartilage matrix
are of interest for understanding the pathogenesis of osteoarthrosis
and the development of strategies for cartilage repair. The purpose of
the present study was to examine the effects of injury on matrix turn
over in a calf articular cartilage explant system for which the effect
s of mechanical loading on cell activity and the cell-mediated pathway
s of matrix metabolism are already well characterized. New methods of
quantitative autoradiography were used in combination with established
biochemical and biomechanical techniques for the analysis of cell and
matrix responses to acute mechanical injury,with particular attention
to the processes of localized matrix turnover in the cell-associated
matrices of individual chondrocytes. Matrix deposition and turnover ar
ound cells in control explants was spatially dependent, with the highe
st rates of proteoglycan deposition and turnover and the lowest rates
of collagen deposition (as indicated by [H-3]proline autoradiography)
occurring in the pericellular matrix. Injurious compression was associ
ated with (a) an abrupt decrease in the tensile load-carrying capacity
of the collagen matrix, apparently associated with mechanical failure
of the tissue, (b) a considerable but subtotal decrease in cell viabi
lity, marked by the emergence of an apparently inactive cell populatio
n interspersed within catabolically active but abnormally large cells,
and (c) sustained, elevated rates of proteoglycan turnover, particula
rly in the cell-associated matrices of apparently viable cells, which
involved the increased release of aggregating species in addition to a
spectrum of degradation fragments that were also in controls. These r
esults may represent an in vitro model for the responses of chondrocyt
es and the cartilage extracellular matrix to mechanical injury.