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Dairy, Veterinary & Animal Research

Review Article Volume 5 Issue 6

A review of dorsal metacarpal disease (bucked shins) in the flat racing horse: prevalence, diagnosis, pathogenesis, and associated factors

Couch S,1 Brian D Nielsen2

1Royal (Dick) School of Veterinary Studies, University of Edinburgh, United Kingdom
2Department of Animal Science, Michigan State University, USA

Correspondence: Brian D Nielsen, Michigan State University, Department of Animal Science, 474 S. Shaw Lane, East Lansing, MI 48824 1225, USA, Tel 517 432 1378, Fax 517 353 1699

Received: September 13, 2017 | Published: September 25, 2017

Citation: Couch S, Nielsen BD. A review of dorsal metacarpal disease (bucked shins) in the flat racing horse: prevalence, diagnosis, pathogenesis, and associated factors. J Dairy Vet Anim Res. 2017;5(6):228-236. DOI: 10.15406/jdvar.2017.05.00166

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Abstract

Dorsal metacarpal disease (DMD) is the most common cause of lostdays to training and racing in Thoroughbred racehorses. Colloquially termed ‘bucked’ or ‘sore’ shins, this initially painful condition commonly occurs in the first season of training and can raise welfare concerns. Clinical signs include pain with digital palpation and swelling on the dorsal, and sometimes dorso-medial, aspect of the third metacarpal (McIII). Periostitis and excessive growth of periosteal bone can be present as a response to high strain cyclic fatigue. Whilst DMD can resolve with rest or reduced exercise, it can leave bone susceptible to future catastrophic fracture at the same site, particularly saucer fractures of the lamellar bone of the diaphysis. Some trainers continue to work an animal through DMD, with the view that it will only happen once, but it can re-occur. Additionally, the animal is in discomfort and has a weakened skeletal system. In vivo studies of the effects of cyclic strain on the skeletal system of Thoroughbreds are notoriously difficult, due to the many variables involved and in vitro studies cannot mimic true training and racing conditions. Variables affecting the loading of the McIII such as exercise regimes, location, speed, direction, conformation, surfaces, farriery, and diet have all been investigated to ascertain their influence, if any, on disease predisposition and onset. In the 1990’s, it was believed that certain training methods and the young age at which Thoroughbreds commenced training were the main cause of DMD. Since then, the cause of DMD has been linked to excessive bone loading stress, with bone cell absorption exceeding replacement. Other studies have reported that lengthy periods of stabling and lack of access to short bursts of high speed exercise, results in reduced bone mineral content and strength in the equine McIII, thus predisposing it to fatigue.

Keywords: racehorse, injury, thoroughbred, bone, training

Abbreviations

McIII, third metacarpal; DMD, dorsal metacarpal disease; CT, computed tomography; MRI, magnetic resonance imaging; pQCT, peripheral quantitative CT; GRF, ground reaction forces; SMA, second moments of area; NA, neutral axis; CSA, cross sectional area; BMD, bone mineral densities; AHW, automated horse walkers; SHA, secondary haversian activity

Introduction

A Thoroughbred can gallop within hours of birth1,2 and, when trained, can sustain speeds of 56-64km/h for up to 1.6km.3The evolutionary cost has been a reduction in the size and weight of the limbs, a transition from five digits to one and an increase in muscle mass; the average weight of a racehorse being 450-550kg.4‒6 These adaptations have led to vulnerabilities in the limbs and a reduced ability of the third metacarpal (McIII) to adapt quickly to changes in ground profile.7 The McIII or cannon bone forms an integral part of the shock absorbing, weight-bearing system of the lower forelimb. Training and racing induces an increase in diaphyseal thickness of the McIII (according to Wolff’s law) to withstand strain and reduce injury.8,9 As in all mammalian bone, if repetitive high speed cyclic exercise is introduced before bone has adequately adapted, damage in the form of micro-fracture can occur – as is the case with dorsal metacarpal disease (DMD). In response to this kind of fatigue damage, excessive periostial bone growth (predominantly over the dorsal McIII) occurs. The material properties, geometry and type of bone affect the type and degree of response. Racehorses are more susceptible to fatigue fractures than other mammals, as equine bone produces higher peak strains.10

Catastrophic fractures of the scapula, tibia and pelvis in American racehorses were reported to be a corollary of previous stress-related bone injury3,11 stated that 12% of catastrophic fractures of the McIII occurred at the site of previous DMD episodes. An understanding of DMD, including how to prevent it, is important to improve animal welfare and to decrease expenses associated with veterinary care.

Prevalence

Sometimes seen bilaterally, DMD is rare in hind limbs and has been reported to have a recurrence rate of up to 40%.3,12 Norwood reported that 70% of Thoroughbreds in training and under twoyears of age experienced DMD,13 whilst Buckingham and Jeffcott reported an 80% incidence amongst young racehorses in Australia.14 A later study in the same country reported that 42% of 2-year-old racehorses were affected.15 In contradiction, Clegg stated that DMD prevalence in an Australian cohort study was 2%.16 In a survey conducted by the Japanese Racing Association, a 66% incidence of ‘bucked shin complex’ was recorded in horses during their first 8months of training,17 whilst Katayama et al. reported a 66% incidence on dirt tracks during the first 32months of training.18 Others have reported a 20-30% prevalence.19,20 The latter authors stated that their results reflected a decrease in the disease in recent times. In a sample size of 486 racehorses in Australia, 24% to 36% percent of 2yr-old horses presented with ‘shin soreness’ whilst only 7% to 12% of 3yr-olds were affected.12

Clinical signs and diagnostic techniques

  1. May be asymptomatic in the early stages
  2. Lameness of varying degrees may be visible, but is not always present in the early stages.
  3. Stride impairment, particularly at a gallop when gait can be “choppy”.21
  4. Radiography can reveal thickening of the dorsal McIII20 but cannot differentiate between cortical and trabecular bone reaction.1 At least a 30% increase in bone mineral density is needed before it will show up radiographically.22
  5. Palpation of the McIII may reveal heat, swelling over the dorsal/dorsomedial aspect of the McIII and a positive pain response.20,23,24
  6. Scintigraphy can show active bone growth over the dorsal cortex.25
  7. Computed tomography (CT) and magnetic resonance imaging (MRI) show more detailed change,26 but peripheral quantitative CT (pQCT) is currently the most accurate way of assessing in vivo bone strength and dimensions.27

Pathogenesis

Norwood stated that abnormality and periostitis over the dorsal McIII area associated with DMD were consequences of sub-periosteal haemorrhage, multiple micro-fracture and secondary callous formation.13 The haemorrhage was purported to have been caused by a tearing away of periosteum, caused by ‘concussive high speed work’, a feature of training and racing. Nunamaker contradicted that DMD was a result of the McIII’s adaptive response to exercise and the strains exerted on it at different speeds and gaits.3 He further suggested that the bending of the McIII (under stress) induced abnormal bone formation over the dorsal aspect. However, more recently, it has been suggested that a decline in bone mass associated with a lack of high speed exercise that accompanies stalling of horses may be the cause of decreased bone strength, precipitating DMD when high speed exercise is introduced into a training program.28

Wolff’s law

In 1892, Julius Wolff (a German anatomist) stated that bone will adapt to loading through modelling and remodelling and this has become known universally as ‘Wolff’s law’.29 Frost30,31 revised Wolff’s Law stating that:

  1. “It is flexing of the bone, not stress that is the principle trigger for remodelling
  2. Repetitive and not static loading triggers remodelling
  3. In flexed bone the affected surface is drawn towards the concave side”

Modelling and remodelling

Modelling is a natural process in immature mammals, altering the shape of the skeleton as it grows. It is at its most prolific stage during the growth of long bones such as the McIII and adapts bone to withstand loading.32‒34 The remodelling process (removal and replacement of bone) replaces primary bone in the juvenile vertebrate and maintains the adult skeleton through osteoclastic and osteoblastic activity.35The natural corollary of aging, weakness and/or damage to the skeleton is a remodelling response as the bone attempts to repair itself. Adaptive change is the gradual and natural response to loading forces over time, but repetitive high speed loading can lead to the rate of bone resorption exceeding bone replacement causing weakness and susceptibility to stress-induced microfracture. This non-adaptive change is a response designed to increase inertial potential.36

According to Norwood, the time between osteoclastic and osteoblastic activity is around a month, followed by a week of osteoblastic activity and approximately 3months until bone reaches previous strengths.13 During this time bone is vulnerable and the responses to stress depend on the magnitude and trajectory of the forces applied. Stated that remodelling processes are suppressed when a horse is in training.35 However, research by Hoekstra et al. showed that bone mass in the equine McIII adapts to its loading situation and can be lost during stall rest.37 Loss of bone mass due to reduction in exercise intensity, combined with the re-absorption of bone minerals in the first 50-60days of training could increase stress injuries on resumption of training,38 particularly as schedules are often ‘squeezed’ to fit racing timetables. The type of bone, as well as its properties and matrix, affect the speed at which micro-fracture, modelling and remodelling occur. For instance, cortical bone models and remodels eight times slower than trabecular bone.39 Regardless, though one must be cautious about overloading bone without allowing adequate time to modify via remodelling. Stalling of horses without access to exercise at speed may result in bone loss associated with modelling that accompanies decreased loading.

Loading and strain

Bone requires a degree of loading to maintain mass and shape in order to withstand the rigours of daily activities. During exercise, the dorsal cortex of the McIII responds to the tensile and compressive loading strains by remodelling.26,40 Bending rigidity is assumed to reflect the orientation of bending forces.41 Whilst strain increases with speed and fatigue,42,43 no studies to date have been able to identify levels of loading-induced strain on the McIII during normal maintenance activities, e.g. standing, walking and sleeping.44 Speeds of 10 metres per second (m/s) can elicit >2,000 microstrains (µstrains) on the dorsal cortex of the McIII43,45 and 3,000 µstrains (at 16-19m/s) was insufficient to stimulate an adequate remodelling response in a study by Davies.46 An in vivo strain gauge study found that McIII’s of young Thoroughbreds withstood compressive microstrains (µstrains) of up to 5,670 dorsally at galloping speeds.3 Slow speeds increase peak strains over the medial cortex.47

The cross-sectional shape of the McIII (ellipse) both inhibits and equalises directional load and Les et al. stated that the McIII serves to “augment and regulate” the sagittal bending of bone when a horse is racing.7 During locomotion, loading of the equine McIII comes from opposing directions. Body mass exerts compression downwards whilst ground reaction forces (GRF) generate load upwards. The degree of bending or stress to the bone is complex and depends on the magnitude and orientation of the force and also the shape, condition, and constituents of the bone.41 Metacarpals bend mainly in the saggital plane during life.23 Moreira et al. stated that the lateral and medial cortices of the McIII have almost the same biomechanical properties and elastic modulus and that a correlation exists between bone density and biomechanical properties.48 They also noted that bone widths in the dorsal, palmar, lateral, and medial aspects of the diaphysis are varied. However, data were floored, as training histories were unknown, making it impossible to assess how far differing bone geometry was due to adaptive change.

Bone area is distributed in such a way that it minimises loading strain.41,49,50 The diaphysis is generally the stiffest part of the McIII, resisting bending or failure through energy absorption.7 Gibson et al. reported that the dorsal surface is less stiff than the lateral surface.10 Loading of the McIII during training is maximal in the mid-diaphyseal region.51 Compressive strains peak over the medial cortex during mid-stance and are probably a response to body mass.52 Strain is intermittent and variable over the lateral cortex suggesting a possible role in balance and body mass support.52 When a Thoroughbred gallops, the neutral axis rotates slightly and peak strains switch from the medial cortex to the dorso-medial cortex.47 Davies and McCarthy stated that peak strains on the dorsal cortex of the McIII in Thoroughbred yearlings occurred immediately after hoof impact when decelerating and/or turning.53 Strain increases on the trailing forelimb and dorsal aspect of the MCIII when a horse is racing despite weights, surface, or farriery.43 Strain levels were found to drop by 42% during the transition from trot to canter in an experiment by Rubin & Lanyon42 whilst Rubin et al.54 argued that peak strains occur at canter.54 However, their sample (3 Thoroughbreds) was small and results for cortical strain densities were disparate. The authors proposed that the disparity could be evidence of an “internal homeostatic” response not linked to strain, or that only a brief period of stimuli is needed to maintain bone integrity. Uniformity in reaction to peak strain observed in other mammals was attributed to a “safety margin” between peak strain and failure.42

Aetiology

Breed: Whilst DMD is predominant in Thoroughbreds, while Goodman reported an incidence of 5-50% in twoyear-old Quarter horses in training.55 Nunamaker stated that DMD is occasionally diagnosed in Standardbreds.56 Nunamaker et al.24 found no difference between the McIII bones of Thoroughbreds and Standardbreds in a reversed cyclic bending study.24

Age: DMD is rarely seen in the mature equine skeleton (age 4 and over) in Thoroughbreds.23,57 Whilst cases have been reported between the ages of 8months and 3years,58 it usually affects two-year-olds in their first year of training.18,20,23,59 It should be noted that National Hunt Horses in Northern Ireland have been reported to experience DMD as five-year-olds, particularly when stalled for significant amounts of time after weaning and when not raced until that age.

Young mammals show strong modelling and remodelling responses to mechanical loading, whilst older adults produce a small and/or limited response.41,60,61 The skeleton of a young horse is capable of more rapid remodeling than that of mature horses. Whilst it is generally accepted that cross sectional area (CSA) and cortical thickness of the mammalian McIII increases with age,62 the McIII’s of young horses were more susceptible to fatigue in a study by Nunamaker et al.24 Primary bone is stronger than remodelled bone, so the latter can lead to inferior mechanical properties in the skeleton of juvenile horses.63 Nunamaker et al.57 stated that changes to the midshaft of the McIII occurred mainly between ages 2 and 3 in Thoroughbreds and Standardbreds, occasionally continuing until age 4.57 In another study, minimal changes occurred in yearling Thoroughbreds, was less in adults, and greater in Thoroughbreds than in Standardbreds.57 This study used second moments of area (SMA) and assumed that cross sectional properties link to cross sectional strength and did not take into account the shift in the neutral axis (NA) brought about by axial compression. Leiberman et al.41 later identified this shift in NA in an in-vivo treadmill experiment using rosette strain gauges on sheep metatarsals.41 Bone tissue in 1- and 2year-old horses is more porous and less mineralised than older horses. Secondary osteon formation throughout the cortex of older horses reduces the likelihood of microfracture and therefore predisposition to DMD.64

Back et al.65,66 stated that age has little effect on kinematics.65,66 In contrast, Butcher and Ashley-Ross found that 2year-olds had a faster and greater rate of fetlock joint dorsi-flexion and a shorter time from hoof impact to mid-stance.67 The longer the impact force lasts, the more opportunity there is for GRF dissipation. Whilst Butcher and Ashley-Ross proposed that the results were probably due to immaturity of the suspensory apparatus,67 this has significant implications regarding bone fatique of the McIII.

Gender: Lemazurier et al.68 stated that ossification occurs earlier in fillies and this can affect bone strength and maturity.68 In contrast, an ultrasound study of cortical bone showed that geldings in training had larger CSA’s and strength in their McIII’s than fillies or entire colts, but lower bone mineral densities (BMD).62 Whilst osteopenia has been reported in other castrated animals,69 no research has indicated a predisposition to exercise-related fractures in Thoroughbred geldings. Little difference in loading strains was found on the dorsal cortex of Thoroughbred fillies and geldings that had been exercised identically.70

Genetics and Epigenetics: Research from the 21st century highlights the interaction between environment and genotype.29 Up to 50% of differences in limb bone geometry within certain human populations are attributed to genetics.71,72 Bone morphology is also under genetic control.73 Wallace et al.74 stated that genetics significantly affected cortical bone geometry in the femoral diaphyses of wheel-exercised mice, where periosteal enlargement and endo-cortical expansion occurred independently of the amount of exercise.74 In human bone, genetics have been shown to play a major part in the aetiology of osteoporosis.75,76 In a study of McIII bones taken from 6 yearling and 6 mature Thoroughbred racehorses, Davies found a relationship between peak strains and bone geometry.77 Furthermore, the longer the McIII bone, the higher the load is at flexion of the dorsal cortex.48

Racecourse surfaces: Limb bones remodel when GRF is both high and vertical41 and vibration at a level of 30-40 Hertz is sufficient to trigger fatigue injury in bone.78 The materials used on racing and training surfaces affect the acceleration rates of hoof impact and GRF, both of which increase with speed. A synthetic track creates lower hoof acceleration and GRF than turf and dirt and also alters the angle at which the hoof enters the surface.79 Dirt surfaces are known to be the hardest and the incidence of DMD is reported as being higher in the United States where dirt is most commonly used for racing.80 Setterbo et al.81 stated that a synthetic race surface (made of sand, rubber, and polypropylene) caused less impact and hoof shock at landing and take-off than turf and dirt, with 26 to 73% less impact and loading force than dirt.81 However, these data came from a simulated ‘track-in-a-box’ experiment, where laboratory conditions and track testing devices vary. Laboratory tests cannot replicate natural hoof impact velocities accurately and studies using racehorses on the track with accelerometers/force plates are fraught with numerous confounding factors and variables, for example:

  1. Weather, temperature and humidity82
  2. Human opinion re: the ‘going’79
  3. Differing equipment
  4. Differing surface constituents
  5. Surface maintenance during trial e.g. harrowing
  6. Kinematics affected by equipment79
  7. Horse body mass
  8. Small sample79,80
  9. Age of synthetic surface

Crevier-Denoix et al.79 noted that hoof angle in relation to the track on landing was larger when cantering on turf than on synthetic.79 Hoof angles vary between forelimbs and hind-limbs, but with only a limited number of studies of fore-limb kinematics on racing surfaces,21,79 there are insufficient data to compare hoof angle with the incidence of strain pathology on the McIII. The onset of DMD occurred after 51 fast kilometres on dirt and 138 fast kilometres on wood fibre in a study of 171 similarly-trained Thoroughbreds racehorses in a study by Moyer et al.83 However, variables regarding training regimes were not included. In contrast, a study by Davies found that track surface had no effect on the incidence of DMD in 16 to 19month-old Thoroughbreds in training.43

Speed: One difficulty when reviewing global literature on racing speeds is the variance in terminology and speed descriptions. A ‘gallop’ in the United States = a European ‘canter’ and is usually somewhere between 24 and 48km/hr. In Australia, a ‘gallop’ is sometimes described as anything over 48km/hr. In a United States study, Rubin et al.54 stated that a slow trot was 2.3 to 3.3metres per second (m/s), a fast trot 3.5 to 6.0m/s, and a canter 6.0 to 8.8m/s.54 In a New Zealand study, a canter was described as 13.3m/s.84 A gallop in the United States has been described as around 11m/s and breezing as 15 to 16m/s.85 The leading forelimb experiences highest loading on entering the suspension stage of a gallop86 and thickening of the dorso-medial cortex occurs as a response to high-speed exercise.46 Several studies have shown that training increases the CSA (and therefore bone strength) of the McIII.87,88 A huge decrease (98%) in risk of DMD occurred with every extra mile worked at high speed and increases in distances cantered raised risks by 33%.85 A study by Verheyen et al.20 contradicts Boston and Nunamaker’s85 findings by showing that hazard ratios increased with short periods (<1month) of high speed work (≥15seconds/furlong).

Direction: Thoroughbreds will swap leading legs several times during a race with the inside forelimb normally leading around turns, with a switch to the outer fore when running on the straight. Lead changes are common in the final furlong, possibly to enable the horse to take an extra breath, or perhaps due to muscle fatigue in the leading limb. Track direction varies both globally and regionally. For instance, United States tracks always run counter-clockwise and, in Australia, track directions vary from state to state. Studies examining the effects of track direction on forelimbs have had varied results. In one Australian study it was stated that the reason for larger cortical CSA and McIII diameters in the right forelegs of an entire sample was partly due to the use of counter-clockwise tracks.62 In contrast, another Australian study stated that dorsal cortical size increased more in the left leg than the right.46 However, as radiographic views were taken from only one side of each McIII and failed to account for geometric unsharpness (penumbra), the results of this study should be questioned. In bilateral cases of DMD in the United States, the left McIII was affected before the right and Nunamaker attributed this to counter-clockwise racing.3 In other United States, United Kingdom, and Australian studies, Thoroughbred forelimb injuries to racehorses were equally distributed,89‒91 whilst Clanton et al.92 noted that catastrophic fractures commonly occur on the last turn of a race.92

Camber: Tracks in the United States are flat, whilst in Europe, where turf is the prevalent surface, racecourse design and direction vary. Slopes, cambers, uphill sections, twists and turns are often included in the layout and are more weather-dependant. Races may be run clockwise, counter-clockwise, or straight. Characteristics of a track can alter gait93 and increase strain, but how far this and other track variables affect skeletal adaptation of the McIII or the incidence of saucer fractures as a corollary of DMD is unknown. Davies concluded that camber does not affect the prevalence of DMD.43 In a study using externally fixed markers by Hobbs et al.94 six horses (of unstated breed) were walked, trotted, and cantered on flat and banked curves in a 10-m lunging circle.94 The McIII and MtIII angles of inclination were significantly greater on the flat curve than the banked and increased in line with speed. The accuracy of external markers is questionable, due to the fact that tissues and underlying anatomy can move and tape and gadgetry may affect limb proprio-reception and therefore gait.95

Breeding and foal management: Exercise is essential for maintaining bone strength and increasing bone mass.96 Allowing foals to exercise freely with their dams should be adequate to ensure normal bone development. The amount of exercise a Thoroughbred foal receives during early life can depend on many factors including stabling, illness, and herd dynamics. Forced exercise of foals is rare on Thoroughbred breeding establishments. Studies into the effects of forced exercise in foals prior to commencement of training have reported no incidents of musculo-skeletal damage and show a positive effect on cartilage.97,98 In animals, BMD plays a role in bone strength.99 Immobility in both humans and horses can cause osteoporosity. In a study by Cornelissen et al.100 BMD and CSA in the McIII’s of Dutch Warmblood foals (0 to 5months) were lower when boxed for long periods, compared to those kept on pasture, or in training.100 When the same three groups of foals were exercised for a further 6months, differences in CSA disappeared and BMD decreased, particularly in the dorsal cortex. A higher bone density in this area is known from previous studies.64 In an 8week study of 20week-old foals,28 radiographic bone aluminium equivalence (an indicator of bone mineral content) showed increased cortical size and BMD in exercised foals (82-m daily sprints for 5 d/week) in comparison with a boxed control group and a group contained within a 992-square metre yard. Studies of this kind are problematic due to difficulties assessing all physical movements of free or confined horses.

Foal and yearling sales preparation: In Northern Europe, Thoroughbred foal and yearling sales occur around the beginning of November. To enhance the overall appearance of the animal, the development of a winter coat is kept at bay. As rugging of foals is problematic, they are usually boxed at night and during cold spells, reducing their access to exercise. Some foals are boxed for long periods to avoid getting cuts and bruises which are considered by some to detract from saleability. For conditioning, at least 6weeks preparation is required whilst 3 to 4months pre-sale confinement is not unusual.96,101 During this time, foals are usually walked in-hand, lunged for short periods, and potentially turned out for a few hours and brought in at night. In an experiment by Buckingham and Jeffcott, Standardbred yearlings experiencing long periods of sub-maximal exercise lost BMD (n=5).101 During yearling sales preparation, colts tend to get more exercise than fillies84-possibly due to colts being generally harder to train and condition. Colts are generally more valuable which may suggest that more time is spent on conditioning colts through exercise to enhance their saleability.

Pre-training: Bolwell et al.101 reported that in a study of 114 New Zealand Thoroughbreds, 24 horses spent only 11-15days in pre-training.102 A horse in the earlydays of pre-training normally does no fast work and spends long periods in a box stall where strain is reduced due to lack of free exercise.103 This could follow previous immobility due to sales preparation. Higher strains on the dorsal McIII have been observed in yearlings53 and re-absorption of bone minerals has been reported in the first 50 to 60days of training.38 Nielsen et al.103 reported a marked decrease in BMD in 18-month-old Quarter Horses betweendays 0 and 60 of training.103 Automated horse walkers (AHW) are a common way to control exercise and Keller and Spengler stated that there will be positive bone change if the loading threshold on the AHW is around 25% of the maximum loading effort.104 However, Hoekstra et al.37 observed that boxed horses still lost bone mass when walked for an hour each day.37 Bolwell et al.102 reported an association between increased hand walking or time spent on an AHW for yearlings and the incidence of later training interruptions, of which 9 out of 17 were due to DMD.102 This study lacked statistical power and variables such as turn-out time, herd dynamic, and paddock size were not included. Additionally, speeds on AHW have been omitted in past studies making results difficult to interpret.

Training: In humans it has been shown that 10 minutes of bone loading per day causes a training response.105 The McIII of a young Thoroughbred adapts to training in different ways according to the type of training. How long it takes for bone to respond to various training regimes is not known.106 Thoroughbred training methods are individualist with ‘Traditional’ and ‘Classical’ regimes involving daily long slow work, (perhaps 1.5 to 2.5km per day) at a “gallop” (United States) or “canter” (Europe), with a “breeze” (United States) or “racing gallop “(Europe) of perhaps 0.8km every two or more weeks.85 Interval training is practised by some yards where the horse is either walked or trotted between bouts of exercise.

Strain rates need to be high (2,000 to 3,500 microstrains) to induce and maintain maximum peak strain levels over the McIII.45 In a New Zealand study, the left diaphyses of two-year-old Thoroughbreds from three different groups (pasture only, medium exercise, and intensive exercise) were analysed in vivo using double-calcein labelling and post-mortem CT scanning.107 Whilst Firth et al.107 were able to create benchmarks for future studies, the point at which changes to bone size and density occurred could not be isolated, though BMD did increase ahead of bone size.107Primary haversian activity was highest in the intensively exercised horse, but no secondary haversian activity (SHA) was identified. Whether this was due to the early stages of sub-periostial microdamage is unknown. Such SHA would be expected during remodelling and/or during active microdamaging.40

Boston and Nunamaker stated, in accordance with Wolff’s Law, that training must mimic racing (regular high speeds), so that the bone adapts to racing.85 Trotting was found to have no effect on McIII adaptations in their study of 226 two-year-olds. Contrary to this, Cogger et al.12 stated that the incidence of DMD was higher in Thoroughbreds who covered more distance at speeds of >890 m/min in the first ten weeks of training.12 Cogger et al.12 also stated that different distances galloped at speeds of 800-890m/min made no difference to the incidence of DMD.12 Clegg argued that risk of DMD is reduced when distances fast cantered begin to accumulate over time and that high speed exercise introduced quickly (in 1month) was detrimental.16 Jackson et al.108 stated that fast work should be avoided in the early stages of training.108 Cogger et al.12 Clegg,16 and Jackson108 reported that short bursts of high intensity training, introduced slowly, leads to more controlled adaptive change and a reduction in the risk of microfracture. Hence, the regular use of high speed breezes reduces the incidence of DMD.

Furosemide: Furosemide, a loop diuretic, has been controversially used in horseracing in the United States for over 50years to reduce incidences of exercise-induced pulmonary haemorrhage. In humans, Furosemide has been linked to bone mass loss and osteoporotic fractures.109 It also raises urinary calcium loss that can lead to secondary hyperparathyroidism.110 In the United States, 98% of racehorses receive Furosemide.111 Data on how this drug acts on osteoblastic cells are limited and Kim et al.112 finding that it had no direct effect on osteocalcin levels or human bone marrow stromal osteoprogenitor cells, suggested that Furosemide may be affecting calcium metabolism indirectly.112 However, their data may have been flawed due to the use of second passage cells, limited osteoblast function data, and non-inclusion of the effects of Furosemide on osteoclasts. More research into the effects of Furosemide on equine bone is needed. However, given that DMD often occurs in horses prior to their first racing start, it is unlikely to play a role in the development of this problem though it could possibly have an influence on bone health once racing, though it is likely the effects are minor compared to other factors.

Precursor to catastrophic bone failure

In a study of 1,178 flat racing Thoroughbreds from 13 yards in the United Kingdom, stress fractures were the most common (57%), with the McIII being affected most often. Of the five fatal fractures, one was a mid-shaft McIII. Over three-quarters of fractures occurred in training, whilst 22.3% occurred in racing.90

Micro-fractures, left unchecked, can predispose bone fatigue and ultimate catastrophic fracture113 due to an accumulation of cyclic loading of the McIII, rather than just one single traumatic event.114 In a study of Californian racehorses, 89% of horses with catastrophic fractures were found to have underlying stress-related bone pathology.11 On racetracks in the United States, 10 to 12% of all fatal injuries have been compound fractures of the diaphyseal dorso-lateral cortex of the McIII in horses with a history of DMD.23

Incomplete, longitudinal, and proximo-palmar fractures of the McIII have also been reported as being caused by micro-fracture as a corollary of cyclic loading.114‒117 Dallap et al.114 reported a predominance of dorso-lateral stress fractures in the left McIII’s of male 3year-olds.114 Nunamaker reported that “saucer” fractures tend to only be found in horses that previously experienced DMD.3

Biomarkers

Several studies have been conducted to show how biomechanical markers of bone metabolism reflect skeletal response to exercise in horses.118‒120 In a study by Inoue et al., biomarker response to exercise intensity was measured in 4year-old Thoroughbred stallions exercised on a treadmill for 3weeks.121 Exercise was increased weekly and serum and urinary biomarkers were analysed at the end of each week. Low speed exercise had no influence on OC but it was suppressed at high speeds. As exercise increased, HYP and DPD diminished. The results suggest that high speed exercise leads to a reduction in bone resorption. However, the sample was small and 1week of exercise is short.

Nielsen et al.38 in a longer experiment (16weeks), found an initial rise and then decline in serum OC betweendays 14 and 42 in 2year-old Quarter Horses entering training.38 Interestingly, Price et al.118 found that indicators of bone formation (PICP and BAP) were raised in 2year-old Thoroughbreds immediately after commencing exercise regimes, suggesting an increase in bone turnover from the onset of training.118 Such varied results suggest that, as an indicator of bone metabolism, biomarker data should be used in conjunction with other analytical techniques such as x-ray or scintigraphy for more meaningful results.

Conclusion

Data and study results in this review are varied and often contradictory, reflecting the difficulties involved in Thoroughbred exercise research. Costs, logistics, multiple variables, and a lack of specialised technology are problematic. Global variations in racehorse management, racing practices, and terminology add to the research variables and make comparisons difficult. Most available data are still predominantly from the United States, where DMD is common. Experiments examining load and strain in control versus treatment groups are problematic due to the inability to accurately record all movements that affect bone homeostasis. In vitro studies are cheaper and easier than in vivo but less informative due to an inability to fully replicate natural horse movements under laboratory conditions whilst longitudinal in vitro experiments often present with recording biases. There is a paucity of relevant training data which would increase understanding of the predisposition and earlier stages of DMD. Most research into musculo-skeletal problems of the racehorse use racing data, yet a horse spends more time training than racing and most injuries occur during training.

There are still conflicting views regarding the effects of racing horses before skeletal maturity and also when and how high speed exercise should be implemented to avoid skeletal damage. Research to date suggests that speed and distance should be increased gradually and should include some high speed work at full racing speed (according to Wolff’s Law). Recent technological advances in GPS, gait analysis, nuclear medicine and equine genetics have led to improvements in data retrieval and should lead to an eventual increase in in vivo research and understanding of DMD. Biochemistry may help predict predisposition to DMD at an earlier stage so that prophylactic changes to training methods can be effected.

More research into human bone fatigue exists and is often heavily relied upon by the equine researcher. Horses experiencing DMD appear to be in pain so there is a welfare concern – a concern that esculates when the incidence of related catastrophic fractures of the McIII is taken into consideration. Changes to training regimes steeped in historical ritual will be hard to implement and is an on-going challenge for the scientific researcher. Extensive ‘box time’ is a major feature of training and has an impact on BMD and strength. A need exists for more education amongst racing professionals to raise awareness regarding bone health – particularly when research has clearly shown bone loss associated with stalling of horses without access to high-speed exercise. There is reason to believe that the problem with DMD can be virtually eliminated if horses are afforded short bouts of high-speed exercise – either free-choice or forced – to maintain bone integrity and mitigate bone loss associated with stalling. Quite possibly it is the lack of high-speed exercise traditionally experienced during preparation for sales and during the early training under saddle that causes bone loss and the predisposition to DMD.

Acknowledgements

None.

Conflict of interest

Author declares that there is no conflict of interest.

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