Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Seles, M.
Expression of the Vascular Endothelial Growth Factor (VEGF) in a Drill Hole Lesion of the Growth Plate
Humanmedizin; [ Diplomarbeit/Master Thesis ] Medical University of Graz; 2010. pp.104.
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- Autor*innen der Med Uni Graz:
- Seles Maximilian
- Betreuer*innen:
- Weinberg Annelie-Martina
- Altmetrics:
- Abstract:
- Introduction: Injuries to the growth plate may occur either as a result of trauma or as the consequence of the treatment of physeal fractures. These injuries can initiate the formation of bone bridges resulting in bone length discrepancy, axis deviation or joint deformity. In this context, Vascular Endothelial Growth Factor (VEGF) is one important factor as it is one of the key players in angiogenesis, facture healing and bone growth. Aim: The aim was to investigate if VEGF is involved in the formation of a bone bridge after a trauma to the growth plate. After this was proven, the focus was set on the localization and the expression of VEGF in the fracture gap, its content and the chondroblasts of the growth plate at different points of time. Materials and Methods: 35 male Sprague Dawley rats at an average age of 4 weeks and a weight of 100g (+/-5g) were anaesthetized and an axial hole was drilled through the proximal growth plate of the tibia. The animals were euthanized on days 1, 3, 7, 14, 28 and 82 and their left and right tibiae were extracted. Sections of the growth plate at the level of the lesion were stained with anti-VEGF antibodies using immunohistochemical methods. Sections of the growth plate of the other leg were used as controls and were stained and examined the same way. All sections were analysed under the microscope. Results: On days 1 and 3, VEGF was strongly expressed in the fracture haematoma. The displaced bone bruise showed VEGF expression from day 1 until their remodelling on day 14. Thereafter, the trabeculae crossing the growth plate as well as the following bone-bridge also expressed VEGF, although this was limited to the surface of the trabeculae of the bone-bridge. VEGF was not expressed in the first 2 to 4 columns of chondroblasts of the growth plate adjoining the lesion on day 1 and day 3. Discussion: This study clearly documents that VEGF is involved in post-traumatic bone bridge formation of the growth plate. Vascular Endothelial Growth Factor may be an important and even crucial factor for the healing of growth plate defects. Further investigation should be done on this topic, as it may be a target of therapy to prevent the formation of bone bridge bridges and its side effects in our already injured young patients.