Fatigue Fracture Interaction Mechanisms In Cortical Bone

Abstract

The skeletal system accumulates microscale fatigue damage with everyday use. Bone has the ability to repair fatigue damage; however, the effectiveness of the repair mechanism can deteriorate with age and disease leading to an accumulation of damage. An increase in fatigue microdamage with age is thought to contribute to the occurrence of fragility fractures in the elderly. However, the mechanisms that are responsible for the interaction of fatigue damage and the fracture resistance of bone are not well understood. Therefore this thesis aims to analyse the mechanisms of interaction between accumulated fatigue damage and the fracture resistance of cortical bone (i.e. fatigue fracture interaction mechanisms). This aim is achieved by the application of engineering fracture mechanics theory to investigate the effects of accumulated fatigue damage on the fracture resistance of cortical bone. This thesis consists of two main components: 1) experimental studies and 2) numerical modelling. The experimental component is separated into three separate experiments, each designed to analyse the effects of fatigue damage on the fracture resistance of cortical bone. The first experiment analysed the effects of tensile fatigue damage on the longitudinal fracture resistance of cortical bone; the second experiment analysed the effects of tensile fatigue damage on the longitudinal and transverse fracture resistance of cortical bone; and the third experiment analysed the effects of tensile and compressive fatigue damage on the transverse fracture resistance of cortical bone. The general methodology used for these experiments included splitting specimens into control and damaged groups then ex-vivo fatigue loading the damaged group specimens. All specimens were then fracture resistance tested and the fracture behaviour of the control and damaged groups was compared. The results of these experiments were used to propose conceptual models of fatigue fracture interaction. In general the results showed that fatigue microdamage in the form of linear microcracks is detrimental to the fracture resistance of cortical bone. The second component of this thesis was the numerical modelling of the toughening mechanisms in cortical bone and their contribution to the overall fracture resistance behaviour. The specific mechanisms that were modelled include: uncracked ligament bridging, crack deflection and microcracking. The results from the numerical modelling were then combined with the experimental data to develop a model of toughening behaviour in bone. Overall, the results of this thesis show that fatigue microdamage is detrimental to the fracture resistance of cortical bone. In addition to this, microstructural changes with age or disease may exacerbate the detrimental effects of fatigue microdamage on the fracture resistance of cortical bone. Therefore the results of this thesis suggest that fatigue microdamage may be a contributing factor to clinical fractures.