Computer model of non-Newtonian canalicular fluid flow in lacunar-canalicular system of bone tissue.

Abstract

Brittle bone diseases are a global healthcare problem for orthopaedic clinicians, that reduces bone strength and promotes bone fracture risk. In vivo studies reported that loading-induced fluid flow through the lacunar-canalicular channel (LCS) of bone tissue inhibit such bone loss and encourages osteogenesis i.e. new bone formation. Canalicular fluid flow converts mechanical signals into biological signals and regulates bone reconstruction by releasing signalling molecules responsible for mechanotransduction. In-silico model mostly considers canalicular fluid is Newtonian, however, physiological canalicular fluid may be non-Newtonian in nature as it contains nutrients and supplements. Accordingly, this study attempts to develop a two-dimensional in-silico model to compute loading-induced non-Newtonian canalicular fluid flow in a complex LCS of bone tissue. Moreover, canalicular fluid is considered as a Jeffery fluid, that can easily be reduced to Newtonian fluid as a special case. The results show that physiological loading modulates the canalicular fluid flow, wall shear stress (WSS) and streamline in bone LCS. Fluid velocity and WSS increases with increase in non-dimensional frequency and non-Newtonian parameter (Jeffery fluid parameters) and reduce with change in permeability. The outcomes of this study may provide new insights in the role of mechanical loading-induced non-Newtonian canalicular fluid flow dynamics in bone LCS. The key findings of this study can be used to improve the understanding of osteocyte mechanobiology involved inside the bone tissue.