0000000000407608
AUTHOR
José Ramón Caeiro
Cortical bone thickening in Type A posterior atlas arch defects: experimental report.
Abstract Background Context To date, no information about the cortical bone microstructural properties in atlas vertebrae with posterior arch defects has been reported. Purpose To test if there is an increased cortical bone thickening in atlases with Type A posterior atlas arch defects in an experimental model. Study Design Micro-computed tomography (CT) study on cadaveric atlas vertebrae. Methods We analyzed the cortical bone thickness, the cortical volume, and the medullary volume (SkyScan 1172 Bruker micro-CT NV, Kontich, Belgium) in cadaveric dry vertebrae with a Type A atlas arch defect and normal control vertebrae. Results The micro-CT study revealed significant differences in cortica…
Atlases with Arcuate Foramen Present Cortical Bone Thickening That May Contribute to Lower Fracture Risk.
To date, no information about the cortical bone microstructural properties in atlas vertebrae with arcuate foramen has been reported. As a result, we aimed to test in an experimental model if there is a cortical bone thickening in an atlas vertebra which has an arcuate foramen that may play a protective role against bone fracture.We analyzed by means of micro-computed tomography the cortical bone thickness, the cortical volume, and the medullary volume (SkyScan 1172 Bruker micro-CT NV, Kontich, Belgium) in cadaveric dry atlas vertebrae with arcuate foramen and without arcuate foramen. We also reviewed a case series of 31 posterior atlas arch fractures to correlate the possible presence in t…
Impact of estrogens on atherosclerosis and bone in the apolipoprotein E-deficient mouse model.
Objective The common inflammatory pathophysiology has nourished the hypothesis of a relationship between osteoporosis and cardiovascular disease. Estrogens are key agents in the modulation of both processes. We investigated whether induction of atherosclerosis affects bone and whether estrogens modulate both processes. Methods Female apolipoprotein E-deficient mice (a well-established model of atherogenesis) were ovariectomized or falsely operated and fed either standard diet or high-fat diet (HFD). Six animals were included in each of the four groups. To clarify mechanisms, we treated preosteoblastic MC3T3-E1 cells with mouse serum. Results Physiological levels of estrogens in falsely oper…