Repetitive strain injuries of the skeleton in high performance equine athletes

Repetitive strain injuries of the skeleton in high performance equine athletes

Christopher M. Riggs and Rob Pilsworth


Bone injuries are common among racehorses. Catastrophic fractures account for over 80% of all racecourse fatalities.1 Stress fractures lead to significant loss of training days and disease of subchondral bone affects a high proportion of horses, often leading to permanent impairment of joint function and consequent loss of performance and premature retirement.2 A large body of evidence has accumulated over the last 20 years to demonstrate that the majority of these injuries are the end result of a progressive process associated with fatigue damage of the bone.

The vital nature of bone, including its ability to undergo repair and stimulate an adaptive response to changes in its mechanical environment, are widely documented. Under ideal circumstances, the size and shape of bones will perfectly match ambient conditions of loading and any damage that may be incurred will soon be repaired through the coordinated action of bone cells. The fact that injuries are so common indicates that circumstances are frequently not ideal; we expect too much of the skeleton or, simply, we fail to understand the mechanisms of adaptation and repair, and to modify training regimes to suit their natural response rates.

Increasingly, fatigue-related injuries are referred to in the literature as examples of ‘maladaptation’, or by some other, equally unfortunate, term. ‘Adaptation’ suggests a physiological process that confers some advantage, which is, presumably, why it has endured the processes of natural selection. That this process should become a ‘disease’ in its own right confuses the simple fact that the limits of adaptation or repair are frequently overwhelmed through over-demanding training schedules. It also overlooks that bone undergoes pathological processes, such as infarction, necrosis etc., like any other tissue.

The very fact that many skeletal injuries in high-performing horses are the end result of a progressive process can be viewed as potentially very encouraging. Once we learn to detect damage early enough in the process, we can recommend intervention strategies to allow healing to occur before serious harm is done; many more racing fractures will be prevented and the incidence of joint disease will be greatly reduced. Equally, through understanding the pathophysiological mechanisms of failure that lead to stress fractures, training regimes can be modified to reduce the risks. For instance, the introduction of nuclear scintigraphy to Thoroughbred racehorse practice in the mid 1980s was a great advance in the detection of early bone pathology and led to a significant reduction in the incidence of catastrophic fractures associated with certain common stress fractures.

Clinical signs associated with early fatigue damage of bone are often minimal and can easily be mistaken for other, less significant, injuries. In addition, associated changes in bone structure are often so subtle as to be difficult or impossible to detect by radiography and ultrasonography. The application of specialized techniques, such as nuclear scintigraphy, computed tomography or magnetic resonance imaging, can successfully indicate the presence of or visualize these injuries but these techniques are not suitable as routine screening tools. The application of knowledge from epidemiological studies to the analysis of training and race records, or by performing routine testing for biomarkers in serum or urine, could be used to identify ‘at risk individuals’. This would facilitate the selective application of higher level imaging to these animals. However, it is likely that much better outcomes could probably be achieved than at present, simply by using the current routine techniques more effectively. This would require better application of existing knowledge and skills, and a greater awareness of the possibility of fatigue injury and the lesions that could develop from it, in order to encourage owner, trainer and veterinary surgeon to take mild but significant signs seriously. It could also involve active screening of horses known to be at higher risk, e.g. those returning from a period of rest. It would involve education to help veterinary surgeons to recognize the anatomical predilection sites for injuries, and encourage them to routinely use ‘specialist’ radiographic projections and ultrasonographic views that are most effective at showing up subtle early signs of bone damage and to recognize these signs on images acquired.

In order to achieve the best outcomes for racehorses, clinicians need to have a good understanding of bone physiology and pathology and the reader is encouraged to study Chapter 8 for a review of relevant information. In addition, clinicians must have a working knowledge of the types of lesion that arise, their specific anatomical locations and the subtle radiographic and ultrasonographic features that may be associated with them.

Clinical syndromes associated with repetitive strain injury of bone

Recurrent strain injury of subchondral bone associated with synovial articulations

A growing body of work convincingly demonstrates the progressive nature of many of the injuries associated with joints in Thoroughbred racehorses, which are presumed to arise as a consequence of repetitive, high strains experienced by these tissues while horses train and race. A significant proportion of common, severe racing fractures (e.g. parasagittal fractures of the distal condyles of the third metacarpal bone, frontal slab fractures of the third carpal bone) originate from pre-existing pathology in subchondral bone. In addition, osteochondral chip fractures arise in areas of diseased subchondral bone and degenerative change of hyaline articular cartilage is often preceded by primary disease of underlying subchondral bone.

While pathological changes in subchondral bone have been characterized in numerous studies, there is no unifying hypothesis to explain how they culminate in clinical lesions. We speculate the following may happen: Increased volume fraction of subchondral bone (due to infilling of trabecular spaces with new bone and which may be apparent radiographically as ‘sclerosis’) in response to higher loads associated with greater exercise, reflects an adaptive response. The resultant structure will be stronger but the more dense bone will be less compliant and, therefore, more prone to injury during impact loading. In the face of a continued cyclical burden, injury may manifest in the form of microdamage and/or osteocyte necrosis. The matrix will become hypermineralized following osteonecrosis, making it more brittle and, therefore, further prone to damage. Disruption of blood supply following more extensive matrix damage exacerbates the rate of osteonecrosis. At some stage (e.g. following a period of reduced loading) a remodeling response to remove damaged or necrotic bone is initiated. This may result in a focal defect in subchondral bone that acts as a stress-riser, which predisposes to fracture. Alternatively, if a relatively large volume of subchondral bone is affected, a void may be created between vital and necrotic tissue during the initial resorptive phase of remodeling. On resumption of loading the superficial, necrotic tissue may collapse into the void, resulting in a depression in the joint surface or may fracture away from the parent bone, leaving a deep ulcer in the joint surface (Fig. 22.1). Longitudinal studies with suitable imaging techniques are required to substantiate this hypothesis.

There are specific anatomical predilection sites in joints for repetitive strain injury in the Thoroughbred racehorse. The reasons why particular animals appear more prone to these injuries than others remain obscure. Attempts to demonstrate material abnormalities of bone, which may predispose to injury, have been unrewarding. Conformational abnormalities or fine variations in neuromuscular control, both of which lead to altered loads on the skeleton, are more likely to be involved. These would affect all limbs symmetrically, and would be consistent with the observed injuries, which are frequently bilateral or quadrilateral. The progressive nature of the disease process results in a continuum of clinical signs and associated findings on diagnostic imaging and the severity of lameness often show poor correlation with extent of structural changes identified.

Subchondral bone disease in the third carpal bone



It is vital that a properly positioned third carpal skyline projection (flexed dorsal 60° proximal-dorsodistal oblique) is included in radiographic examination of the carpus to demonstrate structural changes associated with this syndrome. While easy to accomplish with practice, this projection is often poorly executed and, therefore, significant abnormalities are overlooked. The lesions are most commonly visualized in the radial articular facet of the third carpal bone but can also occur in the intermediate facet. The radiographic appearance of the bone progressively changes as the inter-trabecular spaces are filled with new bone, resulting in an amorphous radiopaque ‘haze’ as the normal trabeculated pattern of the bone is steadily lost. As the disease advances, focal areas of resorption, often associated with nutrient foraminae, appear within the sclerosis3 (Fig. 22.2). Fissure fracture of the dorsal cortex may become visible and in advanced cases, sagittal or curvilinear slab fracture lines may be visualized. On scintigraphic examination, moderate increased radiopharmaceutical uptake (IRU) is visualized over the entire outline of the third carpal bone and this will become more intense and focal in the event of fracture (Fig. 22.3).


On first diagnosis of third carpal bone disease in youngsters, the speed, intensity and duration of the horse’s training workload should be rapidly reduced to avoid irreversible injury. A period of one month of stable rest will usually result in significant reduction in radiopacity of the third carpal bone. Full training should be heldup until the radiographic appearance of third carpal bone approaches normality. This may take two to three months removed from full speed work, the remainder of which can be walking, trotting and slow canter work, or pasture turnout if available and practical.

Marked sclerosis of the third carpal bone in the older horse often reflects conformational abnormalities rather than inappropriate training strategies, but can also be present when the warning signs in the two year old are ignored, and training is continued. Consequently, these horses are more difficult to manage; long periods of rest from training might result in partial resolution of the sclerosis, but there is a degree of bone change in some horses which appears to be irreversible, irrespective of the length of time off. In some horses, lameness returns as soon as high speed training is resumed, presumably due to abnormal forces as a result of the conformational defect. Corrective shoeing to help balance loads on the limb, particularly with carpal valgus and ‘offset’ knees, may help. Careful selection of training surface and avoidance of firm ground can help in some cases also.

Subchondral bone disease of the distal condyles of the third metacarpal and third metatarsal bones



Progressive disease of the bone underlying the articular surface of the mid palmar/plantar aspect of the condyles of the third metacarpal and third metatarsal bones is extremely common in Thoroughbred racehorses.2,4,5 Originally termed ‘traumatic osteonecrosis’, it has more recently been referred to as ‘palmar osteochondral disease’.2 Lesions arise at the point of articulation with the basilar half of the proximal sesamoid bones when the joint is at full extension and are presumed to be due to excessive, repetitive stress at these points. A spectrum of pathology is seen, from faint bruising of subchondral bone, visible through the articular cartilage, to deep ulcers associated with saucer-shaped complete, displaced fractures of a 2–3 mm depth of articular cartilage and subchondral bone5,6 (Fig. 22.4). It is assumed that the different degrees of pathology represent varying stages of the same process. In addition, lameness in which the only related findings are pain localized to the distal condyles of the third metacarpal or metatarsal bone, associated with IRU in the palmar/plantar condyles of these bones is extremely common. It is likely that this is part of the same syndrome.

Fig 22.4 Gross images of the palmar aspect of the distal condyles of the third metatarsal (22.4a, b) and third metacarpal (22.4c, d, e, f) bones of Thoroughbred racehorses illustrating a spectrum of pathology associated with osteonecrosis of subchondral bone in the palmar aspect of the condyles.
(A) Six-year-old gelding; lateral to the right. Normal appearance to subchondral bone in both condyles but faint linear fissures visible in medial and lateral condylar grooves. (B) Seven-year-old gelding; lateral to the right. Bruising of subchondral bone visible through intact overlying articular cartilage. Grade I palmar osteochondral disease (POD) lesion medial condyle, Grade II POD, lateral. There is a small linear fissure in the medial condylar groove. (C) Seven-year-old gelding, lateral to the right. Grade II POD lateral condyle and Grade I POD medially. There is localized fibrillation of articular cartilage in the region of the transverse ridge in both condyles. There are multiple, marked wear lines in the articular cartilage overlying both condyles and the sagittal ridge. (D) Seven-year-old gelding, lateral to the left. Grade III POD medial condyle associated with severe disruption of the articular surface with complete ulceration of articular cartilage and a deep cavity in the underlying subchondral bone, which is filled with fibrin. Focal erosion and tearing of articular cartilage overlying the transverse ridge in the lateral condyle. There are multiple, marked wear lines in the articular cartilage overlying both condyles and the sagittal ridge.
(E) Five-year-old gelding, lateral to right. Grade III POD medial condyle associated with incomplete saucer fracture of superficial bone and articular cartilage overlying a large defect deeper in the subchondral bone (note that the articular cartilage overlying the fracture fragment is intact). Grade I POD lateral condyle. There are multiple, marked wear lines in the articular cartilage overlying both condyles and the sagittal ridge. (F) Four-year-old gelding. Lateral to the left. Complete lateral condylar fracture (one month after surgical repair) associated with a Grade III POD lesion lateral condyle. There are multiple, marked wear lines in the articular cartilage overlying both condyles and the sagittal ridge.

Lesions are more common and progress to a greater extent in the medial condyles of the third metacarpal bone and lateral condyle of the third metatarsal bone.7 However, the clinical condition commonly occurs bilaterally or quadrilaterally and this is reflected in the pattern of gait abnormality seen. Associated lameness is typified by a shortened protraction of each limb at the trot, a low limb flight and a lack of animation or ‘bounce’ in the gait. Low limb flight and increased pelvic excursion seen with bilateral metatarsal disease often leads to the horse catching its toes, giving a characteristic wear pattern to the feet.

Riders often report that affected horses feel ‘wrong’ behind and describe that they are not pushing during exercise. These horses also have a characteristic gait at the canter where they will often ‘bunny hop’ for the first few steps as they break into that gait.

Occasionally a severe bone injury occurs unilaterally causing single leg lameness, although some form of unilateral angular limb deformity almost always accompanies this.


Early stages of the disease are associated with few clinical signs other than lameness and there is little heat or effusion of the affected joint. Sometimes a mild pain response on flexion can be elicited. Perineural anesthesia will localize pain to the fetlock region: a four- or six-point block above the fetlock joint will usually give partial or complete resolution of the lameness. Intra-articular anesthesia often improves but does not abolish lameness. Deeper subchondral bone may be partially innervated by nerves leaving the bone at the nutrient foramen. This may explain why some horses, which improve to low 4- or 6- point blocks, are only rendered sound by sub-carpal or sub-tarsal anesthesia.

In horses showing bilateral lameness, very often blocking the medial and lateral palmar metacarpal/tarsal nerves alone, adjacent to the ‘button’ of the splint (two point block) will abolish most of the pain from the condyles and reveal a marked to moderate degree of lameness in the contralateral limb.

Radiography is unrewarding at early stages of the disease. Attempts to demonstrate sclerosis of subchondral bone in the palmar or plantar aspect of the condyles is hampered by superimposition of other radiopaque structures. Dorsal 45° proximal 45° lateral-plantarodistomedial oblique and the opposite oblique projections8 provide a relatively unobscured image of a small area of each respective condyle and can demonstrate structural changes associated with increased bone volume fraction in some cases (Fig. 22.5). In more advanced cases of disease that are associated with defects in the subchondral bone plate created by collapse or ulceration of the subchondral bone, crescent shaped radiolucent defects can be identified on lateromedial or flexed dorsopalmar/plantar projections (Fig. 22.6). In these end stages of palmar osteochondral disease the joint surface can collapse or sustain a saucer fracture, leading to severe pathology of articular cartilage (Fig. 22.4). This almost always results in obvious signs of inflammation of the affected joint and is associated with profound lameness.

Jun 18, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Repetitive strain injuries of the skeleton in high performance equine athletes
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