Expression of matrix metalloproteinases in human growth plate chondrocytes is enhanced at high levels of mechanical loading

A possible explanation for overuse injuries in children

K. Pichler, V. Herbert, B. Schmidt, E. E. Fischerauer, A. Leithner, A-M. Weinberg


Matrix metalloproteinases (MMPs), responsible for extracellular matrix remodelling and angiogenesis, might play a major role in the response of the growth plate to detrimental loads that lead to overuse injuries in young athletes. In order to test this hypothesis, human growth plate chondrocytes were subjected to mechanical forces equal to either physiological loads, near detrimental or detrimental loads for two hours. In addition, these cells were exposed to physiological loads for up to 24 hours. Changes in the expression of MMPs -2, -3 and -13 were investigated.

We found that expression of MMPs in cultured human growth plate chondrocytes increases in a linear manner with increased duration and intensity of loading. We also showed for the first time that physiological loads have the same effect on growth plate chondrocytes over a long period of time as detrimental loads applied for a short period.

These findings confirm the involvement of MMPs in overuse injuries in children. We suggest that training programmes for immature athletes should be reconsidered in order to avoid detrimental stresses and over-expression of MMPs in the growth plate, and especially to avoid physiological loads becoming detrimental.

Cite this article: Bone Joint J 2013;95-B:568–73.


  • The authors would like to thank Mr D. Kummer for his valuable technical assistance in artwork preparation. Furthermore the authors acknowledge support from the Land Steiermark, research grant number GZ: 16.Z-19/2012-3.

    No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article.

    This article was primary edited by J. Scott and first-proof edited by G. Scott.

  • Received August 14, 2012.
  • Accepted December 11, 2012.
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