• E Breburda, T Wirth, R Leiser, and P Griss.
• Department of Experimental Trauma Surgery, Justus Liebig University, Giessen, Germany. EdithBreburda@chiru.med.uni-giessen.de
• Arch Orthop Trauma Surg. 2001 Sep 1; 121 (8): 443-9.

AbstractIn vitro studies about the regenerative capacity of chondrocytes located in the growth plate of long bones revealed a potential for reparation. A measurable advance in the understanding of the physiologic processes in the bone growth plate and their modifications after defined lesions is based on the recognition of the role of the vascular architecture. Newly formed bridging arteries crossing from the metaphysis to the epiphysis through the growth plate are thought to be responsible for the cell proliferation observed after Salter-Harris I and II lesions. We aimed to examine the influence of mechanical microstimulations on the growth or inhibition of the proliferation of the chondrocytes in the tibial growth plate. We studied 22 tibial bone fractures, which were stabilized with a dynamic or a stable external fixateur. Proliferative changes in the bone tissue were examined by immunohistochemical classification using bromodeoxyuridine (BUdR), a thymidine analogue. Radiologic studies, computer tomography, and magnetic resonance imaging documented the results in comparison with histological examination. Cell proliferation in the growth plate was not stimulated in the 1st week after distraction. The histological studies revealed an initial increase in proliferation of chondrocytes, especially between the 2nd and the 4th week. This was more clearly seen with the use of the dynamic fixator. We conclude that a temporary ischemia with a reactive hyperemia takes place, which we could document by histological analysis and MRI. These results could modify the current clinical therapy of growth plate fractures.

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