N. Aldegaither; X. Zhong; E. Saiz; S.J. Shefelbine; A.E. Porter; F. Giuliani
Biofunctional Materials 2 (2024) 1-19
Ageing-or bone-related diseases, such as osteoporosis leads to perturbations in the collagenous framework and mineralization that translate to deteriorated fracture resistance at the whole-bone level. However, bulk mechanical testing is insufficient to isolate the effect of these alterations on the mechanical response at a smaller length scale where molecular modifications manifest. Here, we combine in situ micromechanical testing using micropillars to determine elastic moduli, double cantilever beam mechanical tests to measure fracture toughness, and transmission electron microscopy (TEM) relate crack propagation at the microscale to local variations in collagen fibril organization. An osteopontin (OPN) knock out bone model with nanometer scale with regions of organised and disorganised collagen matrix and deteriorated fracture resistance at the whole-bone level was used to explore whether it is possible to propagate a crack in a transversely orientated pillar if the collagen fibrils in the pillar are disorganized. The average measured fracture energy for OPN-deficient mouse bone at this length scale, in the transverse direction was 0.94±0.67 J/m2. This value is significantly lower than wild type bone, which we found in previous studies to be approximately 20 J/m2. TEM of cross-sections of the cracked pillars showed that the lack of OPN caused disorganization of the fibrillar network, possibly leading to deteriorated fracture resistance in bones. These preliminary findings indicate that OPN may contribute to bone’s fracture resistance through collagen matrix organization. This study serves as a starting point for more in-depth investigations that use in situ micromechanical testing using micropillars to study interplay between the ultrastructure and fracture resistance in pathologic bone.