New predictive model for monitoring bone remodeling

Abstract

The aim of this article was to present a new thermodynamic-based model for bone remodeling which is able to predict the functional adaptation of bone in response to changes in both mechanical and biochemical environments. The model was based on chemical kinetics and irreversible thermodynamic principles, in which bone is considered as a self-organizing system that exchanges matter, energy and entropy with its surroundings. The governing equations of the mathematical model have been numerically solved using Matlab software and implemented in ANSYS software using the Finite Element Method. With the aid of this model, the whole inner structure of bone was elucidated. The current model suggested that bone remodeling was a dynamic process which was driven by mechanical loading, metabolic factors and other external contributions. The model clearly indicated that in the absence of mechanical stimulus, the bone was not completely resorbed and reaches a new steady state after about 50% of bone loss. This finding agreed with previous clinical studies. Furthermore, results of virtual computations of bone density in a composite femur showed the development of a dense cortical bone around the medullary canal and a dense trabeculae bone between the femoral head and the calcar region of the medial cortex due to compressive stresses. The comparison of the predicted bone density with the structure of the proximal femur obtained from X-rays and using strain energy density gave credibility to the current model.

Influence of different mechanical stimuli in a multi-scale mechanobiological isotropic model for bone remodelling

“…In the last decades, several research groups have worked in the development of new models, to describe the bone remodelling process, taking into account different stimuli in bone cell regulation, like mechanical strain, microdamage, cell biology, metabolic factors and other external contributions [8,10] . From a biochemical point of view, the first model correlated the differential activity of parathyroid hormone (PTH) as a regulator for bone resorption and formation.…”

“…Then, it was the time to demonstrate the role of hormones like autocrine and paracrine in the regulation of bone remodelling. Finally, a signalling pathway known as RANK/RANKL/OPG to regulate bone cells activities [10] . It was also found that this signalling pathway RANK-RANKL-OPG is an important regulation of the paracrine interactions between osteoblasts and osteoclast [12][13][14][15] .…”

Predicting Bone Remodeling in Response to Total Hip Arthroplasty: Computational Study Using Mechanobiochemical Model

“…In this model, the stimulus which initiates bone remodeling is formulated as proportional to the damage energy dissipation summed over all daily loading cycles. Although these models have been to some extent successful in predicting normal bone architecture, they suffer from some major drawbacks: These models use only mechanical signals to stimulate bone remodeling and fail to consider the underlying biological mechanisms that control the bone remodeling process [4,31].…”

“…If strain level is below a set point, bone is resorbed, and if it exceeds this set point, new bone is formed. The mechanostat theory is a qualitative theory because the set-point is not specified [31]. Nevertheless, several mechanobiological models have been presented so far [25,[32][33][34].…”

“…In addition, Lemaire et al [38] proposed a signaling pathway known as RANK/RANKL/OPG to regulate bone cell activities. The most noticeable defect of these cell-based models is that they do not take into account the mechanical stimulus in the bone remodeling process [31].…”