The Multiscale Origins of Fracture Resistance in Human Bone and Its Biological Degradation

Abstract

Akin to other mineralized tissues, human cortical bone can resist deformation and fracture due to the nature of its hierarchical structure, which spans the molecular to macroscopic length scales. Deformation at the smallest scales, mainly through the composite action of the mineral and collagen, contributes to bone’s strength or intrinsic fracture resistance, while crack-tip shielding mechanisms active on the microstructural scale contribute to the extrinsic fracture resistance once cracking begins. The efficiency with which these structural features can resist fracture at both small and large length scales becomes severely degraded with such factors as aging, irradiation, and disease. Indeed, aging and irradiation can cause changes to the cross-link profile at fibrillar length scales as well as changes at the three orders of magnitude larger scale of the osteonal structures, both of which combine to inhibit the bone’s overall resistance to initiation and growth of cracks.