A theory for bone resorption based on the local rupture of osteocytes cells connections: A finite element study

Abstract

In this work, a bone damage resorption finite element model based on the disruption of the inhibitory signal transmitted between osteocytes cells in bone due to damage accumulation is developed and discussed. A strain-based stimulus function coupled to a damage-dependent spatial function is proposed to represent the connection between two osteocytes embedded in the bone tissue. The signal is transmitted to the bone surface to activate bone resorption. The proposed model is based on the idea that the osteocyte signal reduction is not related to the reduction of the stimulus sensed locally by osteocytes due to damage, but to the difficulties for the signal in travelling along a disrupted area due to microcracks that can destroy connections of the intercellular network between osteocytes and bone-lining cells. To check the potential of the proposed model to predict the damage resorption process, two bone resorption mechano-regulation rules corresponding to two mechanotransduction approaches have been implemented and tested: 1) Bone resorption based on a coupled strain-damage stimulus function without ruptured osteocyte connections (NROC); and 2) Bone resorption based on a strain stimulus function with ruptured osteocyte connections (ROC).The comparison between the results obtained by both models, shows that the proposed model based on ruptured osteocytes connections predicts realistic results in conformity with previously published findings concerning the fatigue damage repair in bone.

High-resolution 3D imaging of osteocytes and computational modelling in mechanobiology: insights on bone development, ageing, health and disease

“…One such study has suggested that there is a damage threshold below which osteocyte processes can sense changes in strain and fluid flow, above which osteocyte signalling is disrupted and apoptosis occurs (McNamara and Prendergast, 2007). In line with that, a FE model based on ruptured osteocyte connections suggests that microcracks inhibit transmission of signals through the osteocyte network (Ridha et al, 2015).…”

“…In a FE modelling study for a simplified Haversian system, where strain-induced interstitial fluid velocities in osteons have been evaluated, Nguyen and colleagues showed that the presence of a microcrack would reduce the fluid velocity, modifying the cellular environment and thus mechanobiological mechanisms (Nguyen et al, 2011). It is also suggested that microcracks do not cause a reduction in local signal sensation but a reduction in transduction (Ridha et al, 2015). Computational studies incorporating both mechanical strain and microdamage have been carried out.…”

Finite Element Models of Osteocytes and Their Load-Induced Activation

“…While local stressing of osteocytes may be enhanced by microdamage, the major effect may be that the transport of nutrients, waste products and signalling is disturbed. Ridha modelled osteocyte signalling and its inhibition by microcracks and found that such a mechanism could explain the activation of osteoclasts and osteoblasts on the bone surface [ 140 ]. Reduction in the number and connectivity of canaliculi affects diffusion and convection of fluid flow, nutrients and waste products.…”

Mechanical Stimuli in the Local In Vivo Environment in Bone: Computational Approaches Linking Organ-Scale Loads to Cellular Signals

“…For now, one accessible building block could be the lacuna-canalicular system, which acts as a communication pathway, chemically, as shown by osteocyte calcium signalling correlations to dynamic loading magnitude (54) and frequency (55), and physically, via gap junctions. Ridha et al (56) captured elements of these features by applying FEA to simulate rupturing of osteocyte cell connections, showing how the loss of connection leads to bone resorption, while Jahani et al (57) used network simulations to model osteocyte apoptosis and its effect on bone lining cells, showing that only a 3% decrease in osteocytes was needed to have a significant reduction in peak signal to the bone lining cells. These types of studies begin to shed light on the interlinked, mechanosensitive biochemical relationship between osteocytes, osteoclasts and osteoblasts which collectively governs bone (re)modelling.…”