A finite element study evaluating the influence of mineralization distribution and content on the tensile mechanical response of mineralized collagen fibril networks

Abstract

One of the key length scales of interest in bone's hierarchical structure is the submicroscale which has been shown to influence the fracture behavior of bone at larger length scales. At the submicroscale, the building block of bone is mineralized collagen fibrils (MCF). The mineral distribution and content of MCFs as well as the interaction between MCFs influence the mechanical response of bone at the submicroscale. However, to what extent these factors influence the submicroscale damage and failure processes in bone has not been quantified. The goal of this study is to evaluate the influence of varying mineral distribution, mineral content, and interaction between MCFs on the submicroscale mechanical and fracture response of bone using a novel finite element model incorporating a 3D network of MCFs under both transverse (representing MCF separation) and longitudinal (representing MCF rupture) tensile loading. The results showed that the apparent mechanical properties (elastic modulus, ultimate strength and fracture energy) of the MCF networks increased both with increasing uniformity of mineral distribution and with stronger interactions between MCFs under longitudinal loading whereas under transverse loading only interactions between MCFs but not the mineral distribution influenced the apparent properties of MCF networks. The mechanical properties demonstrated an exponential variation with mineral distribution under both longitudinal and transverse loading. An increase in total volume fraction of minerals at full mineralization resulted in a modest increase in the mechanical properties of MCF networks. These results provide new insights into how changes in mineral content and distribution as well as interaction between MCFs modify the submicroscale mechanical properties of bone. The unique information gained from this study cannot be directly accessible with experiments and single MCF computational models. This new information has the potential to provide a better understanding of the underlying mechanisms of damage in MCF networks which may help identify the effect of tissue modifications at the submicroscale due to disease, age-related changes, and treatments on bone fracture risk.