Discussion

A major role of the skeleton is to support the body and also to provide a system of levers upon which muscles act to cause movement and locomotion.
The architecture of the skeleton is optimised both through evolution and in response to real time demands for energetic efficiency. Structures are designed for optimal function using both material properties and geometrical design to arrange those materials in relation to functional demands. Bone, both as a tissue and an organ systems is optimised for function. The material comprises a composite of inorganic mineral and organic protein, to maximise strength in diverse loading conditions. This material is arranged in relation to structural demands to form the specific bones of the skeleton. Some bones withstand bending, others torsion, tension and compression. The horse has evolved for speed and this has then been exploited further by training for specific elite athletic activities. The loading of the skeleton during peak athletic activity and in training presents risk of fracture.
For the racehorse the goal is for adequate strength and minimal mass at peak performance. This competitive drive leads to a high fracture risk that might be mitigated through both experience of trainers but also knowledge of the principles of adaptation of bone to mechanical loading.
In general, skeletal tissues exhibit functional adaptation and bone in particular is acutely sensitive to changes in local mechanical environment. High rates of deformation and high frequencies of loading induce an osteogenic adaptive response. The deformation or strain resulting from loads applied to the bone is the mechanical signal to which the bone cells respond. Increased bone mass required an appropriate conditioning signal over time. Too great an input may result in monotonic failure and cycles of loading over too short a period of time can cause fracture through accumulation of micro damage. Thus, the impact of mechanical input through training and athletic activity on the tissue responses may affect the competence of that skeletal component and contribute to early damage, with subsequent pain and structural failure.
As with many tissues the functional morphology is determined and maintained through tissue responses to local and systemic influences. The mechanical environment is a major factor in both determination and maintenance of efficient function. Changes in the mechanical environment occur in training and athletic competition. It is an understanding of the complex interactions of genetics, tissue adaptation, injury and repair of the component tissues in relation to the whole joint that hold the key to prevention and management of fracture risk.
The general structure of each bone is determined from a genetic template but the refinements to form the definitive skeletal element are induced by the prevailing mechanical environment. The bone geometry is also optimised for energetic efficiency with minimal mass. The diaphyses of the bones are loaded with a high component of bending and torsion; structural optimisation for this results in a tube structure. The extremities of the long bones are of a wider diameter and comprise a thin cortex supported by strategically arranged bony trabeculae to resist the compressive loading adjacent to joints with minimisation of stress at the joint surface. The ability for the area of the joint surface to be increased ceases at skeletal maturity, thus increased loading after this point leads to increased stresses at the joint surface. The subchondral bone also acts as a shock absorber and protects the overlying cartilage from high impact loads. Damage to subchondral bone may also initiate intra-articular fractures.
Recent scientific investigations reveal a complex interaction between the physiology and genetic aspects of individuals.
The morphology of the same bone in different genotypes within a species suggests differences in material properties of bone matrix. In mice and humans it has been shown that adaptation of bone to loading, differs in both increased bone mass and also loss of bone in disuse. Certain genetic polymorphisms are associated with the ability of an individual to show functional adaptation in bone. Thus, the susceptibility to injury may relate to genotype and associated response to training.
In mice and in the racehorse the material properties of bone and other skeletal tissues may differ dramatically between individuals, and this may relate to the geometry of the whole bones and morphology of joints. Potentially, this impacts on the susceptibility to injury and the need to tailor training to individuals, in not only maximising performance but also minimising injury.
Thus, the geometric optimisation of bones as structures results from a combination of the genetics, mechanical properties of the tissue matrices and the biomechanical demands.
Even within a bone it is known that the material properties are not consistent along the length of the bone the diaphyseal region is stiffer than the metaphyseal and epiphyseal regions, as a consequence of a greater mineral density of the bone matrix. Although mineral density can be used as a predictor of stiffness it does not allow assessment of strength. The collagenous phase of bone matrix provides strength and this collagenous component is invisible to clinical imaging modalities. The use of spectroscopic techniques, such as Raman spectroscopy, is now being developed to allow assessment of both organic and inorganic phases of bone matrix. These also show site-specific differences in mineralisation along individual bones.
The strategy to prevent or identify the early changes in the bone that is indicative of damage and fracture risk is challenging. However, new techniques in imaging and an increasing scientific understanding of the complex interactions between genetics, growth and development, biomechanics and pathophysiology of skeletal tissues should be aimed at clinical translation for early detection and effective management for prevention of exercise related damage to bone in individuals.