Microscopic fractures were found in the front leg bones of nearly all the euthanized racehorses used in a recent Australian study, including those whose deaths had not resulted from a catastrophic fracture.
The study team found a telling trend in the bone damage they saw in the Thoroughbreds. It was worse among the older horses and those with longer careers, which indicates accumulating injury due to chronic overload of the racehorses’ joints.
Dr Ebrahim Bani Hassan and his fellow researchers at the University of Melbourne, writing in the Australian Veterinary Journal, said the findings suggest racehorses might need longer and better-managed breaks during their careers to ward off bone fatigue, which is recognised as a common factor in catastrophic race fractures.
The scientists set out to examine the prevalence of microscopic bone fractures in the lower legs of Thoroughbreds that had been euthanised in Melbourne. They related those findings back to the training history of each animal.
Their work involved the careful examination of leg bones taken from 83 Thoroughbreds that had died or been euthanised on Melbourne metropolitan race tracks or at the University of Melbourne Equine Centre.
In all, the study team sourced bones from the lower forelimbs of 38 Thoroughbreds, and those from the lower hindlegs of a further 45 racehorses.
The bones were examined using a scanning electron microscope for evidence of microfractures, as well as undertaking an assessment of bone density.
The background of the horses, who were aged from two to 10, revealed they had careers that ranged from 0 to 66 race starts, with earnings that varied from nothing to nearly $2.7 million for one animal.
Of the 38 horses from which forelimbs were collected, 21 had been in training at the time of their deaths. Most were put down as a result of a leg fracture. Of the 17 not in training, four had died as a result of fractures. The other deaths resulted from cardiac arrest, gut problems, joint infections, ataxia, ligament problems or kidney issues. The period of time since their race training ceased ranged from 1 to 59 weeks.
Twenty-four of the 45 horses from which hindlimbs were collected had been in training at the time of death, nine of which resulted from fractures, including one pelvic fracture and one broken shoulder.
Of the 15 training horses without fractures, deaths variously resulted from exercise-induced pulmonary haemorrhage (EIPH), cardiopulmonary problems, serious gut issues, tendon injury, bleeding into the chest, and one from cancer.
This left 21 who were not in training. Eight of them suffered fractures, half of which involved the leg bones. The others died as a result of EIPH, gut problems, neurological issues, trauma, septic arthritis or lymphoma. The longest had been out of work for two years.
Palmar/plantar osteochondral disease – a degenerative condition affecting the lower leg bones – could be seen in 65.8% of the forelimb horses and 57.8% of the hindlimb group. This condition is generally considered a result of “bone fatigue”, which occurs when damage accumulates from repeated loading, also known as stress fractures.
Such fatigue injuries begin at the microscopic level and accumulate over time to become visible to the eye.
Under the microscope, microfractures were identified in the forelimbs of 97.4% of the horses. The density of these tiny front-leg fractures increased with age and the number of race starts
Changes in the subchondral bone – that’s the layer of bone just below the cartilage in a joint – were common among the Thoroughbreds in the study, the authors said, with the accumulation of damage seen in horses with longer careers being consistent with bone fatigue.
The authors acknowledged it was likely that subchondral bone damage was over-represented in the group because most had died as a result of a catastrophic bone fatigue injury.
However, the fact that the microscopic prevalence of subchondral bone injury was worse in older horses with longer racing careers was noteworthy. It was, they said, consistent with fatigue failure of the bone related to accumulated training distance.
Rest from race training may allow some degree of repair in the microscopic damage, they said. However, the burden of damage in this population suggested that, in general, the horses might need more time off from intense training than is currently the case to minimise the risk of bone injury.
Bani Hassan and his colleagues noted that plantar osteochondral disease can be seen with the naked eye in up to 80% of Thoroughbreds undergoing post mortems.
“Knowledge of the prevalence of bone fatigue is helpful for an understanding of its importance and to enable development of training strategies that will reduce the risk of injury becoming a clinical problem.”
They said small numbers of microfractures in subchondral bone are likely to be of limited significance in racehorses. “However, accumulation of numbers of microfractures in horses appears to be abnormal.”
Just how much damage needs to accrue before a clinical effect is apparent remains unknown.
“Based on the information obtained from the race records and trainer and veterinarian interviews, many of the horses in this study were performing well and were not reported to be showing signs of lameness in the weeks prior to presentation.”
Most lameness detection methods relied on detecting unevenness in the gait to identify pain in a limb, they noted. “Therefore, symmetric distribution of musculoskeletal lesions, as often occurs with plantar osteochondral disease, would mean that subchondral bone injuries may go unnoticed.”
Bilateral symmetric injuries are consistent with repetitive overload injuries in equine athletes, they said.
Bani Hassan was joined in the study by Michiko Mirams, Eleanor Mackiea and Robert Chris Whitton.
The study received backing from the Rural Industries Research and Development Corporation of the Australian Government, Racing Victoria and the University of Melbourne.
Prevalence of subchondral bone pathological changes in the distal metacarpi/metatarsi of racing Thoroughbred horses.
Bani Hassan E, Mirams M, Mackie EJ, Whitton RC.
Aust Vet J. 2017 Oct;95(10):362-369. doi: 10.1111/avj.12628