Tissue-Level Mechanical Properties of Bone Contributing to Fracture Risk.

Tissue-level mechanical properties characterize mechanical behavior independently of microscopic porosity. Specifically, quasi-static nanoindentation provides measurements of modulus (stiffness) and hardness (resistance to yielding) of tissue at the length scale of the lamella, while dynamic nanoindentation assesses time-dependent behavior in the form of storage modulus (stiffness), loss modulus (dampening), and loss factor (ratio of the two). While these properties are useful in establishing how a gene, signaling pathway, or disease of interest affects bone tissue, they generally do not vary with aging after skeletal maturation or with osteoporosis. Heterogeneity in tissue-level mechanical properties or in compositional properties may contribute to fracture risk, but a consensus on whether the contribution is negative or positive has not emerged. In vivo indentation of bone tissue is now possible, and the mechanical resistance to microindentation has the potential for improving fracture risk assessment, though determinants are currently unknown.

Increased tissue-level storage modulus and hardness with age in male cortical bone and its association with decreased fracture toughness.

The incidence of bone fracture increases with age, due to both declining bone quantity and quality. Toward the goal of an improved understanding of the causes of the age-related decline in the fracture toughness of male cortical bone, nanoindentation experiments were performed on femoral diaphysis specimens from men aged 21-98 years. Because aged bone has less matrix-bound water and dry bone is less viscoelastic, we used a nanoindentation method that is sensitive to changes in viscoelasticity. Given the anisotropy of bone stiffness, longitudinal (n = 26) and transverse (n = 25) specimens relative to the long axis of the femur diaphysis were tested both dry in air and immersed in phosphate buffered saline solution. Indentation stiffness (storage modulus) and hardness increased with age, while viscoelasticity (loss modulus) was independent of donor age. The increases in indentation stiffness and hardness with age were best explained by increased mineralization with age. Indentation stiffness and hardness were negatively correlated with previously acquired fracture toughness parameters, which is consistent with a tradeoff between material strength and toughness. In keeping with the complex structure of bone, a combination of tissue-level storage modulus or hardness, bound water, and osteonal area in regression models best explained the variance in the fracture toughness of male human cortical bone. On the other hand, viscoelasticity was unchanged with age and was not associated with fracture toughness. In conclusion, the age-related increase in stiffness and hardness of male cortical bone may be one of the multiple tissue-level characteristics that contributes to decreased fracture toughness.