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Updated: Jun 5, 2026
A Rat Tibial Growth Plate Injury Model to Characterize Repair Mechanisms and Evaluate Growth Plate Regeneration Strategies
Published on: July 4, 2017
Growth factor release in extra- and intramedullary osteosynthesis following tibial fracture
K Sarahrudi1, A Thomas, T Heinz
1Department of Traumatology, Medical University of Vienna, Waehringer Guertel 18-20, Vienna, Austria. kambiz.sarahrudi@meduniwien.ac.at
Introduction:
Recent studies indicate alterations of local and systemic growth factor level during fracture healing. As a result, osteogenic and angiogenic growth factors allow us to monitor fracture healing on a molecular level. We hypothesised that closed intramedullary (IM) reaming and nail fixation, in contrast to open reduction and internal plate fixation (ORIF), could exert an effect on the cellular elements present in the intramedullary canal, leading to increased release of mediators. The purpose of the study was to investigate whether different osteosynthesis techniques influence the released quantity of cytokines.
Patients And Methods:
A total of 34 patients with tibia fractures treated with IM fixation and 19 patients treated with ORIF were included in the study. In addition to clinical and radiological examination, serum concentrations of transforming growth factor beta 1(TGF-β1), macrophage-colony stimulating factor (M-CSF) and vascular endothelial growth factor (VEGF), were analysed at 1, 2, 4, 6, 8, 12, and 24 weeks after surgery.
Results:
Expression of TGF-β1 and M-CSF was increased during the first 2 weeks of fracture healing in patients treated with the IM fixation technique compared with those treated by ORIF. After 24 weeks, M-CSF levels in patients with IM fixation were clearly higher. Conversely, VEGF levels were higher during the first 2 weeks of fracture healing in patients treated by ORIF compared with IM fixation. However, these results were not significant.
Conclusion:
Our results show that 1 week after surgery neither reamed IM fixation nor ORIF of the tibia could increase the expression of VEGF, M-CSF and TGF-β1 in its favour.
