Читать книгу Fractures in the Horse - Группа авторов - Страница 36

There are many examples in mammalian biology of specific architectural features of bones that are ideally suited to their mechanical environment. It is generally accepted that while the basic form of each bone is genetically pre‐programmed, the shape, mass and fine structural features of bones of the appendicular skeleton are ultimately determined by a proactive response of bone cells to their mechanical environment [38, 39]. Increase in cyclical bone strains due to raised levels of activity encourages bone formation. Conversely, disuse results in net resorption. In addition, a change of activity that results in altered loading on the bone (a change in principal strain direction) stimulates a modelling response that redistributes the mass of bone about its central axis to achieve a structure that is better suited to resist the new strains. For instance, exercise at a fast gallop in the horse is associated with a shift in the neutral axis of the third metacarpal bone [36] and, presumably, this is the drive for the modelling response that occurs in this bone while young horses first adapt to fast work. Stress itself is not directly measurable, so the consequence of loading, strain or effects associated with strain, such as fluid flow or change in electrical fields throughout the tissue, must be at the root of any mechano‐sensitive mechanism. The interconnected network of osteocytes and bone surface lining cells are well placed to sense deformation, fluid flux, etc., and there is good evidence that these cells are the drivers for adaptive modelling [40]. Numerous experiments have been undertaken in an attempt to determine the precise mechanical stimulus that activates a modelling response and the biological objective of that response [40]. Intuitively, maintenance of peak strain magnitude within certain limits during routine activity would be a sensible objective, and there is evidence to support this. The concept of a thermostat‐like mechanism ‘The Mechanostat’, switching either bone resorption or formation on or off in response to decreased or increased peak bone strains, was championed by Harold Frost [41]. In all probability, there are likely to be a number of strain‐related drivers that impact the balance of cellular activity [42].

While the physiological response to a change in the mechanical environment is rapid [43] and effected after relatively few cycles of loading [44], the architectural response may take weeks or months to complete. Consequently, in the event of a sudden increase in physical activity, high bone strains associated with that activity persist for some time. This indicates the importance of ‘training’ in developing bone structure that suits needs: much as the cardiovascular system can be prepared for optimal athletic performance, then so can the skeleton. Ideal training of racehorses involves exercise programmes that are designed to stimulate an appropriate remodelling response without causing excessive damage [45].

An adaptive mechanism can only respond to strains that the bone can detect. It cannot empower the bone to resist extraordinarily high strains (monotonic overload) associated with an accident. The risk of failure due to supraphysiological loads can be mitigated by the inclusion of a margin of safety to any response: greater bone mass means stronger bones, less likely to fracture. However, the formation of bone, and, more critically, carrying an unnecessarily heavy skeleton, is metabolically costly and in its own right potentially disadvantageous, particularly in animals that rely on flight for survival. The safety factor built into any adaptive response of bone is, presumably, under genetic control. Horses ‘coded’ with light bones will have a potential speed advantage but may be more prone to accumulate fatigue damage and consequently suffer fractures. This area of skeletal physiology will inevitably receive increasing attention in the future [46, 47].

There is good evidence that cancellous bone is also modelled in response to changes in loading. Experimentally, the volume fraction of subchondral bone in the palmar aspect of the third metacarpal bone increases in response to raised levels of treadmill work [48]. There is some evidence that an increased density of subchondral bone in animals subject to increased physical activity may occur as a consequence of a response to fracture of trabecular struts [49]. It is arguable whether this can be termed ‘adaptive’ or, in fact, represents a healing response to pathology, whatever the initiating cause. Increased density is associated with reduced compliance, and this may have negative consequences for tissues, such as hyaline and calcified articular cartilage, sandwiched between the subchondral bone and point of load [49–51].