| Research Abstract |
Biomechanical forces are thought to have significant effects on the growth of skeletal tissues. However, it is not known how biomechanical forces are translated in these tissues or what changes they cause in the cellular activities. Growth plate and articular cartilage are important as a growth center and a cushion, respectively. Therefore, we examined the effects of centrifugal force on the proliferation of growth-plate and articular chondrocytes and the syntheses of their extracellular matrix in pelleted cultures.
We have shown that pelleted growth-plate chondrocytes in centrifuge tubes can undergo terminal differentiation and then cause calcification of the extracellular matrix, but articular cbondrocytes show scarcely any terminal differentiation asd do not cause calcification. Centrifugation resulted in increased ^3H-thymidine incorporation into DNA in rabbit articular chondrocytes, but had little effect on DNA synthesis in growth-plate chondrocytes in pelleted cultures. Centrifuga
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tion of articular and growth-plate chondrocytes stimulated proteoglycan synthesis. The increase in proteoglycan synthesis by chondrocytes in response to mechanical forces may be necessary for an increase in the strength of cartilaginous tissue, because compressive stiffness of cartilages to mechanical forces has beerv shown to be associated with an increase in the concentration of glycosaminoglycans. The mechanism by which centrifugation stimulates proteoglycan synthesis by chondrocytes is not known. However, in pelleted rabbit chondrocyte cultures, indomethacin did not modulate the effect of centrifugation on ^<35>S-sulf'ate incorporation into proteoglycans. Therefore, it is not likely that prostaglandins are involved in these effect by centrifugal force. Because chondrocytes produce insulinlike growth factors (IGFs), transforming growth factor-beta, and chondromodulins, these factors may play a role in mediating the effect of mechanical forces. Our results provide evidence that mechanical forces act directly on chondrocytes to modulate their proliferation and extracellular matrix synthesis. Less
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