Applied mechanical loading to mouse hindlimb acutely increases skeletal perfusion and chronically enhanced vascular porosity

Gohin, S and Javaheri, B and Hopkinson, M and Pitsillides, A A and Arnett, T R and Chenu, Chantal (2020) Applied mechanical loading to mouse hindlimb acutely increases skeletal perfusion and chronically enhanced vascular porosity. Journal of Applied Physiology. ISSN 8750-7587

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Official URL: https://doi.org/10.1152/japplphysiol.00416.2019

Abstract

Blood supply is essential for osteogenesis, yet its relationship to load-related increases in bone mass is poorly defined. Herein, we aim to investigate the link between load-induced osteogenesis and the blood supply (bone perfusion and vascular porosity) using an established osteogenic non-invasive model of axial loading. Accordingly, 12N mechanical loads were applied to the right tibiae of six male C57BL6 mice at 10-12 weeks of age, 3 times/week for two weeks. Skeletal perfusion was measured acutely (post-loading) and chronically in loaded and contralateral, non-loaded hindlimbs by Laser Doppler imaging. Vascular and lacunar porosity of the cortical bone and tibia load-related changes in trabecular and cortical bone were measured by nanoCT and micro-CT, respectively. We found that the mean skeletal perfusion (loaded: non-loaded limb ratio) increased by 56% immediately following the first loading episode (versus baseline, P<0.01) and a similar increase was observed after all loading episodes demonstrating that these acute responses were conserved for 2 weeks of loading. Loading failed however to engender any significant chronic changes in mean perfusion between the beginning and the end of the experiment. In contrast, two weeks of loading engendered increased vascular canal number in the tibial cortical compartment (midshaft) and, as expected, also increased trabecular and cortical bone volumes and modified tibial architecture in the loaded limb. Our results indicate that each episode of loading both generates acute enhancement in skeletal blood perfusion and also stimulates chronic vascular architectural changes in the bone cortices which coincide with load-induced increases in bone mass.