  Age-related bone loss and postmenopausal osteoporosis are disorders of bone
remodelling, in which less bone is reformed than resorbed. Yet, this
dysregulation of bone remodelling does not occur equally in all bone regions.
Loss of bone is more pronounced near and at the endocortex, leading to cortical
wall thinning and medullary cavity expansion, a process sometimes referred to
as "trabecularisation" or "cancellisation". Cortical wall thinning is of
primary concern in osteoporosis due to the strong deterioration of bone
mechanical properties that it is associated with. In this paper, we examine the
possibility that the non-uniformity of microscopic bone surface availability
could explain the non-uniformity of bone loss in osteoporosis. We use a
computational model of bone remodelling in which microscopic bone surface
availability influences bone turnover rate and simulate the evolution of the
bone volume fraction profile across the midshaft of a long bone. We find that
bone loss is accelerated near the endocortical wall where the specific surface
is highest. Over time, this leads to a substantial reduction of cortical wall
thickness from the endosteum. The associated expansion of the medullary cavity
can be made to match experimentally observed cross-sectional data from the
Melbourne Femur Collection. Finally, we calculate the redistribution of the
mechanical stresses in this evolving bone structure and show that mechanical
load becomes critically transferred to the periosteal cortical bone.
