During the last decades numerous studies have reported the critical impact of physical activity on bone repair. While most studies have evaluated the tissue response to the local mechanical environment within the fracture gap, there is a lack of information on the systemic role of physical activity during fracture healing. Therefore, the aim of this study was to standardize the mechanical environment in the fracture gap by developing a rotationally and axially stable murine fracture model, and thereby to analyze the systemic influence of physical activity on early bone repair. After stable fixation of a closed femoral fracture, mice (n=18) were housed in cages supplied with running wheels (running distance >
500m/d). At 2 weeks animals were sacrificed and bones were prepared for histomorphometric (n=7), biomechanical (n=7), and protein biochemical analyses (n=4). Additional mice (n=22), which were housed in standard cages, served as controls. Histomorphometric evaluation showed no influence of increased physical activity on bone repair in terms of callus size and tissue composition. Accordingly, also biomechanical testing of the callus revealed no differences between both groups in rotational stiffness, peak rotation angle, and load at failure. Western blot analyses demonstrated no alterations in callus expression of proliferating cell nuclear antigen (PCNA) and vascular endothelial growth factor (VEGF) after daily running when compared to controls. We conclude that increased physical activity under standardized mechanical conditions in the fracture gap does not affect early bone repair in mice.
The aspirates were examined with a commercially available assay using a Multiplex Reader. The interleukins Il-1 beta, -2, -5, -6, -10, -12, -13, -15,-17 and IL-1 receptor antagonist (Il-1ra) were measured. Further G-CSF, GM-CSF, IFN gamma, MIP 1 beta, MIP alpha, MCP 1, and TNF alpha were assayed.
