Fresh research in California has reinforced the central role of bone microdamage and tissue remodeling in predisposing racehorses to a common leg fracture.
A recent study by Sarah Shaffer, Dr Susan Stover and colleagues at the J.D. Wheat Veterinary Orthopedic Research Laboratory at the University of California, Davis, School of Veterinary Medicine sought to characterize bone abnormalities that precede proximal sesamoid bone fractures and determine if pre-existing abnormalities are associated with these fractures.
The group retrospectively studied cases from California Thoroughbred racehorses that died from proximal sesamoid bone fractures, and controls that died for other reasons.
These fractures are the most common fatal injury in racehorses in the United States. They account for 45 to 50 percent of such injuries in Thoroughbreds, and 37 to 40 percent in racing Quarter Horses.
The proximal sesamoid bones are two comparatively small bones located in the fetlock that act as part of the suspensory apparatus. Fractures in these bones are likely because of the accumulation of repeated, stress-related processes. This is supported by evidence that racehorses in intensive training are at higher risk for such fractures, but the exact causes are not well understood.
Other repetitive overuse injuries in horses are known to be bilateral in nature, meaning that they are similar on both sides of the horse, with the more severely affected limb usually incurring the fracture.
With this in mind, the study looked at both the fractured proximal sesamoid bones and the intact one from the opposing limb of the same horse for all of the cases.
The researchers hypothesized that horses with fractures of this bone would also show evidence of stress in the bone in the opposite limb, and that the bone that sustained the break would show more severe changes than the intact bone.
The results showed that 90 percent of fractured proximal sesamoid bones from the cases had visible discoloration on the surface of the fracture, most commonly in a characteristic crescent pattern (70 percent of the time).
Directly below the cartilage, evidence of bone loss was noted in 70 percent of cases. This bone loss was located in the same region as the discolorations. The fractured proximal sesamoid bones had lower bone volume fraction and tissue mineral density within the lesion sites than comparable locations in opposing limbs and controls. These regions were contiguous with the fracture lines. Evidence of microdamage was also observed in the fractured bones.
Overall, changes identified in the bones were more numerous in case horses than control horses and more severe in the fractured limbs than the opposing limbs in cases. Sampling from areas of bone distant from the lesions noted no significant differences in bones from case and control horses other than the presence of a lesion.
This data supports the role of microdamage and tissue remodeling in the formation of lesions in proximal sesamoid bones. It is important to note that all of the horses in this study were California racehorses, so it is currently unknown if the results will apply equally to racehorses in other areas. Future studies with larger sample sizes may provide further information.
Understanding the mechanism of such fractures is necessary in order to determine risk factors and prevent them from occurring. Combining this information with advanced technology, such as the recent introduction of positron emission tomography (PET scan), may facilitate the identification of horses at risk for such fracture and inform management alterations to avoid injury.