Endocortical bone loss in osteoporosis: The role of bone surface availability

TL;DR

This study uses a computational model to show that microscopic bone surface availability influences localized bone loss in osteoporosis, especially near the endocortical wall, leading to cortical thinning and altered stress distribution.

Contribution

The paper demonstrates that non-uniform microscopic surface availability can explain the regional bone loss patterns observed in osteoporosis through a computational simulation.

Findings

Bone loss accelerates near the endocortical wall where surface availability is highest.

Cortical wall thinning and medullary cavity expansion match experimental data.

Mechanical stress redistributes to the periosteal surface as bone structure evolves.

Abstract

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.