The influence of bone surface availability in bone remodelling - A mathematical model including coupled geometrical and biomechanical regulations of bone cells

TL;DR

This paper presents a mathematical model integrating biochemical, biomechanical, and geometrical factors to understand how bone surface availability influences bone remodelling, with implications for osteoporosis development.

Contribution

It introduces a novel mathematical model that incorporates microstructural geometry into bone cell regulation mechanisms, expanding understanding of bone remodelling processes.

Findings

Geometrical regulation significantly affects bone porosity and stiffness.

Late-stage osteoblast and osteoclast differentiation are less influenced by geometry.

Osteoporosis development may be accelerated by geometrical regulation in cortical bone.

Abstract

Bone is a biomaterial undergoing continuous renewal. The renewal process is known as bone remodelling and is operated by bone-resorbing cells (osteoclasts) and bone-forming cells (osteoblasts). Both biochemical and biomechanical regulatory mechanisms have been identified in the interaction between osteoclasts and osteoblasts. Here we focus on an additional and poorly understood potential regulatory mechanism of bone cells, that involves the morphology of the microstructure of bone. Bone cells can only remove and replace bone at a bone surface. However, the microscopic availability of bone surface depends in turn on the ever-changing bone microstructure. The importance of this geometrical dependence is unknown and difficult to quantify experimentally. Therefore, we develop a sophisticated mathematical model of bone cell interactions that takes into account biochemical, biomechanical and geometrical regulations. We then investigate numerically the influence of bone surface availability in bone remodelling within a representative bone tissue sample. The interdependence between the bone cells' activity, which modifies the bone microstructure, and changes in the microscopic bone surface availability, which in turn influences bone cell development and activity, is implemented using a remarkable experimental relationship between bone specific surface and bone porosity. Our model suggests that geometrical regulation of the activation of new remodelling events could have a significant effect on bone porosity and bone stiffness. On the other hand, geometrical regulation of late stages of osteoblast and osteoclast differentiation seems less significant. We conclude that the development of osteoporosis is probably accelerated by this geometrical regulation in cortical bone, but probably slowed down in trabecular bone.