Chapter 102The Bucked-Shin Complex
Conditions of fatigue failure of bone and inadequacy of bone modeling and remodeling of the third metacarpal bone (McIII) in the racehorse are part of a condition known as bucked shins or dorsal metacarpal disease.1,2 Bucked shins start in young healthy racehorses, usually Thoroughbreds (TBs) and Quarter Horses, but occasionally Standardbreds (STBs), that undergo intense training for racing, usually as 2-year-olds, while the skeleton is still immature and in the growth phase (Figure 102-1, A). The true incidence of bucked shins is unknown and may vary geographically, but reports range from 30% to 90%. A North American questionnaire cited an incidence of 70%.1 Stress fractures (dorsal cortical or saucer fractures) usually occur some months after initial signs of bucked shins and may be a potentially life-threatening injury if a horse is raced or exercised at speed (see Figure 102-1, B). The diagnosis of bucked shins is easy and often made by the trainer or owner. The history of sudden tenderness or soreness of the left McIII (in North America) or both the McIIIs after high-speed work or the first race, or soreness developing the day after, are cardinal signs of early bucked shins. Horses with severe disease manifest acute lameness and extreme sensitivity to palpation of the dorsal cortex of the McIII and are unwilling to train or race. All gradations of pain or disability may be seen. Swelling and tenderness may suggest new bone proliferation. Radiology is helpful to determine the amount of periosteal new bone formation, which determines prognosis. Large accumulations of periosteal new bone on the dorsal or dorsomedial surface of the McIII suggest a serious imbalance between exercise and bone fatigue and may portend actual stress fractures that will be seen on the dorsolateral aspect of the McIII some months later.
Fig. 102-1 A, Dorsolateral-palmaromedial oblique radiographic image of a third metacarpal bone (McIII). Periosteal new bone formation (arrows) over the dorsomedial aspect of the McIII is evidence of bucked shins. B, Lateromedial radiographic image of the metacarpal region. This dorsal cortical fracture of the dorsolateral aspect of the McIII represents a common type of fatigue (stress) fracture (arrows) that usually occurs months after an episode of bucked shins.
An understanding of the etiology, pathomechanics, and pathogenesis of bucked shins in the TB is helpful in determining prevention and/or treatment modalities and training regimens. It was formerly suggested that bucked shins resulted from microfractures on the dorsal aspect of the McIII, caused by high-speed exercise. However, microfractures should heal without periosteal callus, which does not fit with the clinical observation of extensive periosteal new bone on the dorsomedial aspect of the McIII. Work in our laboratory led us to propose a different cause of bucked shins3 and an exercise program that significantly reduces the incidence of bucked shins and may help to eliminate catastrophic stress fractures. The following summarizes our investigations.
The McIIIs of TBs and STBs of known age were examined, and comparisons were made between breeds of a particular age group and among the age groups of a particular breed. The second moments of area relate to bending stiffness in dorsopalmar and mediolateral directions and were used to determine the minimum and maximum principal moments of inertia (Imin and Imax). The most significant changes in the bone occurred at the midsections between the ages of 1 and 2 years, but continued change occurred until age 3 or 4 years. Imin was smaller in the yearling TBs but larger in the adult TBs compared with STBs. During the first 2 to 4 years of life, Imin changed to a greater extent in TBs.4
Dumbbell-shaped specimens machined from adult McIIIs from TBs and STBs were tested in fully reversed cyclic bending experiments using a constant-strain rotating cantilever model that measured load decrement. All tests were performed at 40 Hz and continued until the specimen broke or had a 30% loss of stiffness. Three different offsets were used to establish nominal strains of 7500, 6000, or 4500 microstrain in the specimens.
Data were analyzed using a power regression model for each horse and for each breed. Statistical differences were not found among the curves for individual horses of the same breed or for the curves between breeds. Pooled data then were used to describe fatigue characteristics of cortical specimens of the McIIIs from TBs and STBs of various ages, subjected fully to reversed cyclic loading (Figure 102-2).5 The bone from young horses was much more susceptible to fatigue failure.
Fig. 102-2 In vitro fatigue data are plotted for the adult Thoroughbred (TB) and Standardbred. The regression line shows where the third metacarpal bone (McIII) will fail from repeated cycles. Superimposition of the strain levels of young TBs shows that 41,822 cycles would result in fatigue failure. The superimposition of an older TB shows that more than a million cycles would be needed before bone failure.
Because the in vitro fatigue was similar in TBs and STBs, other factors appeared to be important in the pathogenesis of fatigue failure of bone in the TB. This, together with the different inertial properties noted in STBs and TBs, led to the hypothesis that differences in training regimens or racing speeds between breeds might influence the incidence of disease.
Whole bone stiffness measurements were made from horses of 2 months to 28 years of age using an Instron testing machine (Instron, Canton, Massachusetts, United States) and a nondestructive three-point dorsopalmar bending test. The bones showed general increases in stiffness until they reached a plateau at about 6 years of age.
The material included the McIIIs from 12 2-year-old TBs, three of which had bucked shins. These three horses had differences in stiffness between the left and right McIIIs of 16% to 27%, respectively, whereas other trained or control 2-year-olds had considerably smaller left-right differences.6
Bone strain in the McIII was measured in horses of varying ages, training at or near racing speed, by placing a rosette strain gauge on the dorsolateral aspect of the McIII and recording using telemetry.7 The mean peak compressive strain in four horses 2 years of age was −4841 ± 572 microstrain, compared with −3317 in a horse 12 years of age. One 2-year-old developed bucked shins, and its strain measurements were about 6 standard deviations greater than in the other three.
After acquiring in vivo strain data, we correlated these data with in vitro fatigue data previously generated by determining the average number of cycles that a young TB would gallop in training before the onset of bucked shins. The training records of six 2-year-old TBs that developed bucked shins were analyzed to determine the total distance worked before the onset of bucked shins. Stride length at canter, gallop, and racing speed was measured in a group of TBs to determine the number of strides (cycles) per mile. The total number of gait cycles was estimated based on the distances covered at a canter, at a gallop, and at work. The six horses were trained in these gaits for 10,000 to 12,000 cycles per month and developed bucked shins at 35,284 to 53,299 training cycles. These data were compared with the in vitro data described previously and showed good correlation (see Figure 102-2).
Changing from the trot to the gallop changed the principal strain direction by more than 40 degrees on the dorsolateral surface of the McIII. Although trotting horses showed tensile strains in the long axis of the bone on the dorsal or dorsolateral surface, at racing speeds this same surface of the bone showed compressive strains.8
With the understanding that slow-speed gaits produced tensile strains on the dorsal surface of the McIII, whereas high-speed exercise induced compressive strains, a study was undertaken to determine the effects of different training regimens and track surfaces on the modeling and remodeling of the McIII in TBs.
Eight untrained 2-year-old TBs were divided into four groups of two horses each. Classical training methods were used for the horses in groups I and II. Group I horses trained on a dirt track. Group II horses trained on a wood chip track. Group III horses (control group) were not trained, but they were allowed free exercise in a large pasture. Group IV horses were trained using a modified classical training program on a dirt track.
The classical training program consisted of daily gallops (approximately 18-second furlongs or 11.2 m/sec) of 1 to 2 miles per day (1.6 to 3.2 km), followed by shorter workouts or breezes at racing speed (approximately 14-second furlongs or 14.4 m/sec) once every 7 to 10 days that increased in distance from 2 to 6 furlongs (0.4 to 1.2 km) progressively over the course of the study. The modified classical training method used similar daily gallops, but the frequency of the high-speed workouts increased to three per week, and distances increased progressively from 1 to 4 furlongs (0.2 to 0.8 km). After 5 months the McIIIs were harvested from all horses. Microradiographs of bone sections were made to determine the extent of the remodeling activity (Figure 102-3). Bone modeling on the periosteal and endosteal surfaces of the McIII changed the cross-sectional geometry differently among the experimental groups. Classically trained horses (groups I and II) responded with appositional new bone formation on the dorsomedial periosteal surface, giving the impression that the medullary cavity, although reduced in diameter, was displaced laterally. Horses in the modified training group (group IV) had bone deposition dorsally and a slightly larger medullary cavity that was not displaced laterally. Control horses (group III) had new bone formation on the medial, lateral, and dorsal surfaces. The medullary cavity remained large and centrally placed. Examination of the McIII inertial properties showed that Imin in groups I, II, and III was similar, but the Imin of group IV horses was greater and was similar to the Imin previously reported for mature racehorses.
Fig. 102-3 Fifty-percent length cross-sections of the third metacarpal bone were used to make these microradiographs. Individual photographs were taken with cross-sections magnified four times, and giant montages (approximately 50 × 70 cm) were constructed to be able to evaluate individual haversian systems of each individual bone of each horse. Lateral is to the left. A, Group I horses: classically trained on a dirt track. B, Group II horses: classically trained on a wood chip track. C, Group III horses: controls. D, Group IV horses: modified training on a dirt track. Changes in modeling, remodeling, and shape can be seen easily by comparing different groups. Group II horses appear to be earlier in the remodeling cycle than are group I horses, which already have remodeled in the medial and lateral cortices. All specimens are from the left forelimb, and increased new bone formation is seen on the medial surface of the classically trained horses (groups I and II). Modified training (group IV) and the control horses (group III) do not show this change. The lack of haversian remodeling in the dorsal-dorsolateral cortex of the classically trained horses in groups I and II is notable. In this area catastrophic stress fractures occur in racehorses.
Microradiographic sections from the middiaphysis of the McIII showed that bone remodeling occurred only medially and laterally in groups I and II. Filling of secondary haversian systems with new bone was most complete in group I specimens, indicating that the remodeling process was advanced further in horses exercised on a harder surface. A distinct lack of remodeling activity was apparent in the dorsal and dorsolateral regions in groups I and II. Horses in groups III and IV showed extensive remodeling throughout the cortex, including remodeling in the dorsal and dorsolateral aspects.