Stress Fracture Etiology as Dependent on Mechanically Induced Fluid Flow

摘要

Bone fluid flow is hypothesized to initiate aberrant remodeling which can ultimately compromise bone quantity and quality. Thus, pathologic response of load-induced fluid flow can potentially damage tissue viability, and initiate bone's remodeling process, ultimately leading to the stress fracture syndrome. Results from this year's study have shown that fluid flow stimuli in bone has potentials not only in initiating bone's remodeling, but also in vasculature adaptation. Within the physiological range, bone formation is proportional to applied fluid flow stimulation. While the pressure exceeds the physiological intensity or falls within the pathologic range, i.e., addition to normal physical loading, it triggers extensive remodeling and thus even weaken the quality of bone, i.e., increase intracortical porosity and induce lesions. Repetitive cyclic fluid flow in bone has shown an effect on the nutrient vessel remodeling inducing vessel wall thickening and smooth muscle cell proliferation, which may potentially contribute to pathological remodeling in bone. These results may provide insight of fluid flow in physiological and pathological remodeling and its role in stress fracture. To understand the etiologic factors of stress fracture is extremely important. As a short-term goal, this study is aimed to acquire an improved understanding of the patho- physiology of stress fractures at the tissue level such as fluid flow alone triggers the osteopenia and lesion. As a long-range goal, if we can identify these osteogenic signals, this may help to design or alter specific training regimes to reduce the risk factors of stress fractures.