Cortical bone in mammals is composed of a hierarchical structure spanning macro-to nanoscales and has outstanding fracture resistance. The recent studies in the literature have shown the significant contribution of microscale features of bone on its fracture resistance. Studies have also shown that the bone morphology at the microscale is altered due to various factors such as age, bone diseases, and therapeutic treatments. One component of the bone microstructure is the lacunar-canalicular network. Osteocyte lacunae are the ellipsoidal spaces which house the osteocyte cell bodies and canaliculi are the slender long channels that include the osteocyte cell processes.
Despite extensive studies on biological function of osteocytes, there are limited studies that evaluated the structural role of lacunar-canalicular network on local mechanical properties of the bone matrix. Furthermore, changes in the osteocyte lacunar-canalicular architecture as well as in the surrounding bone matrix with age, disease, or treatment can alter the mechanical environment of the osteocytes. The modifications in the lacunar-canalicular architecture can impact both the crack initiation and propagation process as well as the mechanical stimulation of osteocytes. As a result, the goals of this study are (1) to elucidate the independent contribution of osteocyte lacunar morphology on mechanical properties and fracture behavior of the bone matrix uncoupled from its biological effects and (2) understand how the modifications in lacunar-canalicular network morphology and perilacunar region properties influence local strains around lacunae. This study utilizes computational modeling to systematically quantify the individual and combined influence of modifications in the lacunar- canalicular network and perilacunar matrix that cannot be directly evaluated by experiments. The models leverage experimental data to establish realistic models of lacunar-canalicular network to evaluate the mechanical response of bone.
The first part of this study investigated the structural influence of osteocyte lacunae on the local mechanical environment using 3D finite element models. The models were generated based on the data from the literature. A parametric study was conducted involving lacunar and perilacunar region parameters including lacunar density, volume, orientation, equancy, as well as perilacunar modulus and size.
The second part incorporated canaliculi in addition to lacunae in three-dimensional models. The objectives of this part were to understand how the modifications in the canalicular architecture including canalicular density, canalicular length, and diameter, as well as lacunae density and the perilacunar region modulus and size influence local strains around lacunae.
The third part of this study developed 2D cohesive finite element models containing multiple osteocyte lacunae based on experimental data from a lactation rat model to evaluate the influence of osteocyte lacunar porosity, density, size, axis ratio, and orientation on the elastic modulus, ultimate strength, ultimate strain of the bone matrix and on local crack formation and propagation.
The last part extended the 2D lacunar models into 3D and incorporated a continuum damage model. A case study was performed using models derived from young and aged bone specimens. The aim of this study was to further understand the influence of lacunar morphology, and perilacunar properties on the mechanical properties of local bone matrix, as well as the crack initiation and propagation.
This study presents several modeling strategies for investigating the role of lacunar-canalicular network on the local mechanical properties. It provides additional understandings and theoretical support to experimental findings.