Bone fatigue and its implications for injuries in racehorses

Abstract

Musculoskeletal injuries are a common cause of lost training days and wastage in racehorses. Many bone injuries are a consequence of repeated high loading during fast work, resulting in chronic damage accumulation and material fatigue of bone. The highest joint loads occur in the fetlock, which is also the most common site of subchondral bone injury in racehorses. Microcracks in the subchondral bone at sites where intra-articular fractures and palmar osteochondral disease occur are similar to the fatigue damage detected experimentally after repeated loading of bone. Fatigue is a process that has undergone much study in material science in order to avoid catastrophic failure of engineering structures. The term 'fatigue life' refers to the numbers of cycles of loading that can be sustained before failure occurs. Fatigue life decreases exponentially with increasing load. This is important in horses as loads within the limb increase with increasing speed. Bone adapts to increased loading by modelling to maintain the strains within the bone at a safe level. Bone also repairs fatigued matrix through remodelling. Fatigue injuries develop when microdamage accumulates faster than remodelling can repair. Remodelling of the equine metacarpus is reduced during race training and accelerated during rest periods. The first phase of remodelling is bone resorption, which weakens the bone through increased porosity. A bone that is porous following a rest period may fail earlier than a fully adapted bone. Maximising bone adaptation is an important part of training young racehorses. However, even well-adapted bones accumulate microdamage and require ongoing remodelling. If remodelling inhibition at the extremes of training is unavoidable then the duration of exposure to high-speed work needs to be limited and appropriate rest periods instituted. Further research is warranted to elucidate the effect of fast-speed work and rest on bone damage accumulation and repair.

The Importance of Subchondral Bone in the Pathophysiology of Osteoarthritis

“…As more is understood about the biological behavior of subchondral bone under abnormal physiologic conditions, further clarification or consensus about these terms will likely be important. Chronic fatigue injury in the subchondral bone was initially described in clinical cases of injured racehorses (34); and validated through numerous clinical studies and experimental models (18–20, 35–37). There are three mechanisms by which damage can occur: (1) microdamage formation within the tissues; (2) an area of weakness within tissues secondary to biomechanical and tissue responses to cyclic loading, predisposing this tissue to damage; or (3) adaptive tissue responses that chronically fatigue the tissue, resulting in a change in material properties and ultimately to injury (3).…”

Musculoskeletal Pathology

“…The potential exists for fracture propagation within the area of weakened bone if high cyclic loading continues. 41 Studies have identified the presence of such microdamage in sites of spontaneous fracture in racehorses, supporting the hypothesis that these are fatigue failure injuries. 42,43 Adaptive cortical modeling is commonly seen in the third metacarpus of racehorses as increased dorsal cortical thickness and increased distal subchondral bone density.…”

Bone Radiographic Changes in Slaughter Buffalos with Low Body Condition Index

“…The bone is a tissue that provides support to the mechanical, biological and chemical functions in the animal organism and its development can be affected by age, nutrition, hormonal phase, diseases and by intense exercise [15]. Therefore, it cannot be considered a static tissue, on the contrary: it is a target tissue that undergoes modifications due to the adverse systemic conditions that affect animals, mainly those intended for production.…”

“…Among the osteopenia cases, the osteoporosis, a disease in which the nutritional deficit causes low production of osteoid tissue with consequent decrease in bone tissue and skeletal system weakening [15], is highlighted. The osteomegalias in turn is a result of multifactorial processes, with genetic, nutritional and environmental etiology.…”