Susan M. Stover Stress fractures in racehorses are occupational injuries that result from repetitive activities, consistent with overuse. Repetitive motions of the limbs that occur during training and racing induce recurring high loads on the skeleton. Specific regions of the skeleton are subject to the highest stresses and strains because of the unique distribution of the loads specific to galloping at high speeds over flat race surfaces. These regions are the sites of stress fractures in racehorses. Stress fractures occur when the repetitive stresses incurred on bones cause substantial damage to be concentrated in small locations. Damage is concentrated at the sites of highest bone stresses by loads transmitted from the ground and from muscle and ligament forces during galloping at high speeds. The amount of damage that occurs in any structure is directly related to the magnitude of load with each loading cycle and the number of loading cycles. For the racehorse, this translates into racehorse speed and the number of strides, or the distance, of the gallop. Thus, longer, faster gallops induce greater bone damage for each work or race. The rate of damage acquisition is also affected by how frequently the works and races occur. The amount of damage that accumulates at a site is related not only to the rate of damage acquisition but also to the rate of damaged bone repair. Damage occurs within bones throughout a lifetime. If there were no mechanism for removal of damage, damage would accumulate, coalesce, and eventually result in fatigue failure and complete bone fracture. Fortunately, damaged bone tissue is removed and replaced throughout life, which continually renews the skeleton. At the tissue level, renewal occurs through the bone remodeling process. Microscopic regions of damaged, nonviable bone tissue are targeted for removal by osteoclasts, and resorbed bone is subsequently replaced with healthy new bone tissue by osteoblasts. However, bone remodeling is rate limited. Osteoclasts quickly remove damaged bone material within days and weeks. Osteoblasts require several months to refill the defect with new bone tissue of high quality (i.e., lamellar bone tissue). Consequently, during damage repair, porosities exist within bone tissue (Figure 202-1) that can markedly weaken the bone structure and make affected bones more susceptible to damage during normal athletic activities (i.e., activities not normally considered to be overuse). Stresses on the bone are increased for a given level of activity because the forces transmitted through the bone are distributed over a smaller amount of bone material. For stress fractures, these sites lie within the compact bone of the cortex. Another response of the bone structure to underlying weakness in the cortex is more rapid than damaged bone replacement by intracortical bone tissue remodeling. Woven bone tissue is applied to existing bone surfaces by osteoblasts in the periosteum and endosteum and by osteoblasts lining trabecular surfaces. Woven bone can be laid down rapidly. The rapid, and often exuberant, production of periosteal and endosteal callus serves to buttress the cortex during completion of intracortical remodeling. Resolution of the stress fracture includes completion of replacement of damaged intracortical bone tissue and remodeling of the callus. Woven bone tissue in the callus is replaced with stronger lamellar bone tissue. The size of the callus diminishes as the cortex regains strength. Some residual callus results in enlargement of the cortical diameter and is an adaptation to the stresses of training and racing that makes the racehorse less susceptible to recurrence of stress fracture at this location with continued training and racing. Stresses on the bone are reduced for a given level of activity because the forces transmitted through the bone are distributed over a larger amount of bone material. Risk factors are related to the magnitude, duration, and timing of loading and naivety of the skeleton to the loads associated with high-speed training and racing. High-magnitude loads induce greater bone damage and are associated with strides at faster speeds and on harder race surfaces. Longer-duration exercise induces greater bone damage and is associated with longer-distance works and races. High frequency of high-speed exercise events induces bone damage while limiting time for damage repair. Stress fractures occur when the rate of damage accumulation exceeds the rate at which the body can replace damaged bone material. Frequent training at high speeds for long distances on naive bone structures is a recipe for a stress fracture. Additional factors, like hard surfaces, may increase the likelihood of stress fractures. Skeletal adaptation to high-speed exercise reduces the likelihood of stress fracture. Stresses within the bone are lower, resulting in less damage per stride because the loads are distributed over a larger amount of bone material. Clinical signs are associated with unsoundness. Horses may be acutely lame when coming off the racetrack after exercise but appear to improve markedly within a few days. Because bilateral limbs experience similar loading circumstances, both left and right limbs are commonly affected. Consequently, some horses do not develop obvious unilateral limb lameness. Instead, bilaterally affected horses fail to perform as expected or have a change in behavior. As is typical with occupational injuries, each bone has sites that are susceptible to stress fracture. These sites are subjected to the highest stresses associated with racehorse training and racing. The ideal circumstance is to avoid development of a stress fracture. However, the skeleton is heavy and energetically expensive for locomotion. Consequently, the skeleton maintains the minimal amount of bone material to sustain the loads it has been most recently exposed to. At the initiation of training, the racehorse skeleton is not “built” for racing. Increasing the level of intensity of training, or changing training circumstances that alter loading conditions (such as changing race surface), increases stresses or changes the stress distribution on bones and induces some bone damage. A small amount of damage, or less damaging damage (some types of damage cause less cell death than other types), is needed to stimulate additional bone deposition and adaptation of the skeleton to the new loading circumstances. The challenge is to increase the level, duration, or frequency of loading during training at a rate that allows damage repair and bone adaptation to occur. There are no simple clinical diagnostic tests that indicate when a horse is ready to be taken to the next level of training. Excellent horsemanship is a key factor. Titrating the level of training to the racehorse’s response to the previous training events can be helpful in avoidance of stress fractures. Treatment of a stress fracture varies with the severity of the stress fracture. Early recognition of early stages of disease, when increasing exercise intensity is stimulating bone modeling that will result in bone adaptation, dictates modification of training. In some cases, less frequent exercise at a lower speed over shorter distances may allow resolution of inflammation and bone adaptation to the new level of exercise. Subsequent resumption of training should be gradual. Recognition of an overt stress fracture dictates stall confinement because the affected bone is markedly weakened and highly susceptible to complete fracture. Generally, 2 months of stall confinement is followed by 2 months of gradual reintroduction to exercise, and then by gradual reintroduction to race training. Periodic recheck examinations are useful for tailoring rehabilitation to the stage of resolution of the stress fracture. Hand walking, turnout in a small yard or larger pasture, ponying, and trotting may be advised depending on examination findings and the need to gradually increase bone stresses. Gradual reintroduction to race training is important because risk for some stress fractures is particularly high when horses are returning to race training after a lay-up. When stress fractures are recognized, the prognosis for healing is very good and likely related to appropriate management. Because bone tissue can regenerate and bone structures will adapt to recent loading history, the prognosis for returning to athletic performance is good, and horses can perform at their previous level. Half of affected horses that return to racing race by 7 to 8 months after diagnosis. However, in a small proportion of affected horses, stress fractures recur in the same or new locations. Recurrence is likely related to rapid increase in exercise intensity upon return to training and racing. Horses have been successfully rehabilitated and returned to racing after recurrent stress fractures. Continued training and racing in the presence of a stress fracture carries the risk of complete bone fracture. Most catastrophic, complete bone fractures in racehorses are directly related to training or racing with a preexisting stress fracture.
Stress Fracture Diagnosis in Racehorses
Stress Fracture Overview
Etiopathogenesis
Risk Factors
General Clinical Signs
Prevention, Treatment, and Rehabilitation
Prognosis
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