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Updated: May 10, 2026

Trabecular Bone Microarchitecture Evaluation in an Osteoporosis Mouse Model
Published on: September 8, 2023
Endocortical bone loss in osteoporosis: the role of bone surface availability
Pascal R Buenzli1, C David L Thomas, John G Clement
1School of Mathematical Sciences, Monash University, VIC 3800, Australia; Engineering Computational Biology Group, The University of Western Australia, WA 6009, Australia.
Abstract:
Age-related bone loss and postmenopausal osteoporosis are due to a dysregulation of bone remodelling in which less bone is reformed than resorbed. This dysregulation of bone remodelling does not occur with equal strength in all bone regions. Loss of bone is more pronounced near the endocortical surface. This leads to thinning of the cortical wall proceeding from the endosteum, a process sometimes called 'trabecularisation'. In this paper, we investigate the influence of the nonuniform distribution of bone surface within bone tissue for osteoporotic bone losses. We use a spatio-temporal computational model of bone remodelling in which microstructural changes of bone tissue are represented by a phenomenological relationship between bone specific surface and bone porosity. The simulation of an osteoporotic condition by our model shows that the evolution of bone porosity within a bone cross section is significantly influenced by the nonuniform availability of bone surface. Greater bone loss occurs near the endocortical wall, leading to cortical wall thinning and to an expansion of the medullary cavity similar to cross-sectional observations from human femur midshafts. Our model suggests that the rate of cortical wall thinning is fast/slow in the presence/absence of an adjacent trabecular or trabecularised bone compartment.
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