Compressive fatigue life and micromorphology of equine metacarpal subchondral bone

Abstract

Bone fatigue injuries are an important cause of lameness in racehorses and as such are an animal welfare issue and a cause of losses to the industry. The metacarpal condyles are commonly affected by stress fractures and palmar osteochondral disease, a fatigue injury of subchondral bone. Bone fatigue injuries should be preventable through training adjustments. Knowledge about the behaviour of equine bone, and particularly subchondral bone, under cyclic loading is important to inform training recommendations. Computational models have been developed to investigate the effects of training changes on stress fracture development but require equine subchondral bone material properties as an input to meaningfully model metacarpal condylar fatigue injuries.

A method for compressive fatigue testing of subchondral bone was developed and the fatigue life of equine subchondral bone determined. The fatigue life curve followed a power law, similar to cortical and cancellous bone. Subchondral bone stiffness increased during fatigue testing over hundreds to thousands of cycles, which was initially attributed to a method artefact. Initial specimen stiffness was positively associated with actual density but not with horse and training related factors.

Micro-CT was used to investigate the micromorphology of the palmar metacarpal subchondral bone. Micromorphology parameters were analysed with principal component analysis and mixed-effects linear regression models. The largest differences in micromorphology were observed in untrained horses between the age of 16 and 20 months. In racehorses in training, age and duration of a training period had no influence on micromorphology. Horses with palmar osteochondral disease had more pores in cross-section than those without. Tissue mineral density increased, and bone volume fraction decreased with increasing distance from the articular surface.

Several alterations to the fatigue testing method were explored to accommodate the curved articular surface and eliminate the stiffness increase during compression-compression cyclic loading. The stiffness increase during the first 50 cycles was demonstrated to be reversible and no microdamage or trabecular compaction was detected in specimens loaded up to 200 cycles. Stiffness increase during compression-compression fatigue testing at a physiological frequency is thus likely the result of normal viscous material properties of subchondral bone.

Finally, compressive fatigue life was positively associated with bone volume fraction in the deeper layers of subchondral bone. Initial stiffness was positively associated with tissue mineral density in the deeper layers and bone volume fraction in the superficial layer. Both maximum stiffness and cycles to maximum stiffness were positively associated with fatigue life. Cycles to 10% reduction of maximal stiffness correlated strongly with cycles to gross fracture.

The results showed that subchondral bone’s viscous material properties led to a prolonged stiffness increase during cyclic compressive loading at physiological frequencies. Further research is required to investigate the physiological implications of this finding. Subchondral bone sclerosis measured as bone volume fraction is positively associated with compressive fatigue life and thus has a protective effect on subchondral bone. Further research is required to reconcile this finding with the common colocation of fatigue damage in sclerotic subchondral bone of racehorses.