Articular Fetlock Injuries in ExercisingHorses

Elizabeth M. Santschi, DVMDepartment of Veterinary Clinical Sciences, College of Veterinary Medicine,

The Ohio State University, 601 Vernon L. Tharp Street, Columbus, OH 43210-1089, USA

The fetlock joint is a high motion joint that consists of two long bones(third metacarpus/metatarsus [MC/T3] and first phalanx) and two sesamoidbones. The joint accommodates rotation in the sagittal plane around thecenter of the distal aspect of the MC/T3. The fetlock joint flexes duringlimb protraction, which is accomplished by muscle contraction and passiveenergy return from elastic structures, largely tendons and ligaments [1,2].The passive energy return is critical to efficient locomotion, and reducesthe work of galloping horses by 50% because of the contribution of elasticstrain energy stored in the tendons and ligaments [1]. The fetlock joint is thecritical component of the elastic system because its long lever arm duringfetlock extension stretches the palmar/plantar soft tissues. When the limbis unloaded, the return of energy stored in the palmar/plantar soft tissuesduring loading assists in limb advancement and forward motion [1].

As the load applied to the fetlock increases, the joint extends farther [3]and increases load transfer to the first phalanx [4] and to the suspensoryapparatus (suspensory ligament, proximal sesamoid bones, and distal sesa-moidean ligaments). At maximal weight-bearing at racing speed or uponlanding after a jump, the fetlock hyperextends and, from a lateral or sagittalperspective, the long bones approach a right angle (Fig. 1). At full stance,the dorsal surface of the first phalanx is compressed by the dorsal articularsurface of MC/T3, and the palmar/plantar apical region of the MC/T3 con-tacts the proximal sesamoids and intersesamoidean ligament (Fig. 2) [4],producing compression and shear [5] and dorso-palmar bending in theMC/T3 [6].

To accommodate the exercise-associated loads, the entire skeleton, andparticularly MC/T3, must undergo remodeling during early life and duringrace training [5–11]. This remodeling occurs even in young horses, and

Vet Clin Equine 24 (2008) 117–132

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Fig. 1. Computer rendering of the lateral view of the fetlock in midstance. Note close apposition

of theMC/T3 to the proximal sesamoid bones and stretching of the soft tissues of the suspensory

apparatus. (Courtesy of The Ohio State University College of Medicine, Columbus, OH; with

permission.)

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a load path based on bone sclerosis is proposed that runs obliquely from thepalmar/plantar apical region of the MC/T3 to the dorsal proximal aspect ofthe distal epiphysis [9–11]. This pattern of sclerosis can also be seen in activeracing horses (Fig. 3), and corresponds to a route linking the sesamoids, thepalmar/plantar apical region, and the dorsal cortex of MC/T3. Because the

Fig. 2. Close-up computer rendering of the fetlock in midstance demonstrating the articulation

of the sesamoid at the palmar/plantar apical region of the MC/T3. (Courtesy of The Ohio State

University College of Medicine, Columbus, OH; with permission.)

Fig. 3. A T1-weighted parasagittal MRI of the fetlock joint in a 4-year-old Thoroughbred race

mare. Note the presence of sclerosis (dark areas) on the articular surface of the proximal sesa-

moid bones, the palmar apical region of the metacarpus, and proximal oblique course to the

dorsal aspect of the metaphysis of the metacarpus. The MRI was obtained with the horse se-

dated and standing (Hallmarq Veterinary Imaging, Acton, Massachusetts).

119ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

palmar apical region of MC/T3 and the sesamoid bones are very commonareas of arthrosis and fracture in racing horses, excessive load and nonadap-tive remodeling are proposed as contributing factors to injury [5,6,8,12–16].

It is necessary also to consider the anatomy of the fetlock joint in thetransverse plane, particularly the articulation of the sesamoids on the pal-mar/plantar apical aspect of MC/T3 (Fig. 4). The articular surface of theproximal sesamoid bone is not flat, but presents two surfaces, a longer ab-axial and shorter axial. The axial surface is angled about 50� palmar/plantarto the abaxial surface, forming a wedge that fits in the sagittal groove of theMC/T3. The condylar groove on MC/T3 is the site of many injuries and iswhere many condylar fractures originate (Figs 5 and 6) [6–8,12–15]. Duringfetlock extension, tensile forces in the suspensory apparatus compress theproximal sesamoids and the intersesamoidean ligament onto the palmar-plantar MC/T3. As load increases, the sesamoids may even carry a largerpercentage of the load over a smaller area than that carried by the first pha-lanx [17]. This force is transmitted through the MC/T3 condyle in a dorsaldirection, perhaps concentrated by the sesamoid angle. This anatomy maybe the fulcrum that causes dorso-palmar/plantar bending of the MC/T3implicated in condylar fracture [3].

The predominant features of the frontal plane of the fetlock joint are (1)the MC/T3 condyles and their articulation with the first phalanx, (2) theMC/T3 median sagittal ridge, and (3) the corresponding sagittal groove inthe articular surface of the first phalanx. The condyles of MC/T3 serve to

Fig. 4. Computer rendering of the palmar articular surface of the fetlock joint illustrating

anatomic features of the fetlock joint. (Courtesy of The Ohio State University College of Med-

icine, Columbus, OH; with permission.)

Fig. 5. A T1-weighted transverse MRI of the distal fetlock joint in a 4-year-old Thoroughbred

race mare. An incomplete (dorso-palmar) condylar fracture is present. This horse, the same as

in Fig. 3, had lameness referable to her fetlock joint with equivocal radiographic signs. Note

close approximation of the sesamoid angle of the lateral sesamoid and the palmar aspect of

the incomplete condylar fracture. (Courtesy of Elizabeth M. Santschi, DVM, Columbus, OH.)

Fig. 6. A dorso-palmar radiographic projection of an incomplete (proximal-distal) lateral con-

dylar fracture. Note articular location of fracture in condylar groove.

121ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

transmit load to the articular surface of the proximal first phalanx [4,17].The median sagittal ridge and the groove in the proximal first phalanx serveto limit any forces other than flexion and extension in one plane.

Bone remodeling and injury

Most fetlock injuries in racing horses occur in predictable locations andconfigurations. A growing body of evidence indicates that musculoskeletalinjury in racing horses, particularly that affecting the fetlock joint (eg, frac-ture, osteochondral fragmentation), is the result of excessive stress from over-use. Chronic repetitive small injury leads to accumulated microdamage. Inbone, there is usually evidence of an attempt to respond to injury by remod-eling [15,18,19]. It is unclear why repair is so often ineffectual, but continuedtrauma, alteration of blood supply, and the severity of damage are probablecontributing factors [18]. There also is a lag period between bone removal andbone formation when the repairing bone has reduced strength [18]. Mono-tonic fractures (those resulting from a single supraphysiologic loading event),such as a ‘‘bad step,’’ are less common than those due to accumulated dam-age. Fractures probably occur as a combination of accumulated damagesuperimposed onto excessive or irregular loading as a result of missteps,irregular surfaces, soft tissue injury [20], and muscular fatigue.

Fetlock arthrosis in racing horses is due to chronic mechanical overload[15–19] and is characterized by cartilage damage, subchondral bone sclero-sis, and necrosis of subchondral bone. It occurs in a highly predictable site,the palmar/plantar apical region of the condyles of the MC/T3 [6,8,12–19].

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While damage to the MC/T3 sagittal ridge and axial aspect of the sesamoidis rare, injuries to the sagittal groove and adjacent bone of the first phalanxare relatively common, but damage to the MC/T3 sagittal ridge and axialaspect of the sesamoid are less frequent (Fig. 7).

There is considerable debate about the initiating event in equine joint dis-ease, but it is clear that both cartilage and subchondral bone damage be-come involved at some point. Many of the individual events are knownand probably occur simultaneously in a given area of damage. The sequenceof events in the bone and calcified cartilage starts with sclerosis of subchon-dral bone (trabeculae and matrix), osteocyte death, and plugging of canal-iculi with debris. The impact of loss of perfusion and osteocytecommunication at this time is unknown, but presumed to be contributory.The next event is the appearance of microcracks in the subchondral boneand bone matrix followed by small, then larger and branching cracks inthe calcified cartilage [21], which has bone fragmentation at its margins[6]. Bone modeling and remodeling occur throughout a horse’s life and inresponse to exercise [9–11], but at some point become maladaptive [15].The final event is bone and cartilage collapse due to continued loading.

Fig. 7. A dorso-palmar radiographic projection of an incomplete (proximal-distal) sagittal

proximal first phalangeal fracture. Essentially all of these sagittal fractures originate in the cen-

ter of the sagittal groove.

123ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

Traumatic osteochondrosis, an example of the end result of this process inracing horses, occurs in the fetlock in the palmar apical region of the MC/T3[9,10,12,13]. In nonracing horses, the location is less uniform and, whilemore common in the MC/T3, can also occur in the first phalanx (Fig. 8).

This maladaptive remodeling can also lead to severe life-threatening mac-rofractures in racing horses. The most common severe bone injury to the fet-lock of racing horses is the condylar fracture, which may be the result ofcoalescence of branching arrays of cracks in the condyle and condylargroove [8,19,21]. The severity of injury depends, to an extent, on howsoon the horse is stopped after the small cracks become bone fractures.The fractures begin at the palmar/plantar articular surface at the condylargroove or slightly abaxial to it, where the cracks predominate. Comminu-tion at this palmar/plantar apical location suggests that dorso-palmar bend-ing is acting on the MC/T3, perhaps because of the fulcrum presented by thearticular angle of the ipsilateral sesamoid. If the horse continues to load thelimb after the palmar/plantar fracture originates, dorsal fracture propaga-tion continues because of the compression of the sesamoid on the condyleabaxial to the fracture. The condyle bends further in the dorso-palmar planeunder sesamoid pressure with further strides until the dorsal surface in themetaphysis fractures and the fracture becomes complete (Fig. 9). The switchfrom bending palmar/plantar to bending at the dorsal surface is the result ofthe instability of the fracture and the cyclic loading by the lateral sesamoid.Bending at the dorsal metaphysis is supported by the frequent occurrence of

Fig. 8. A dorso-palmar radiographic projection of a horse used for barrel racing that presented

for worsening lameness referable to the fetlock. A subchondral bone cyst is present in the prox-

imal first phalanx. Radiography 3 months previously had revealed a normal appearance to the

subchondral plate of the first phalanx.

Fig. 9. A CT transverse slice of the proximal first phalanx of the horse in Fig. 8. Note the

irregular lucency in the subchondral bone plate adjacent to the condylar groove.

124 SANTSCHI

comminution at the dorsal metaphysis [6]. Further damage to the limboccurs with more strides. After a complete lateral condylar fracture, the me-dial suspensory branch and sesamoid are overloaded, and those structuresfail, usually through the body of the medial sesamoid. Occurring simulta-neously is asymmetric load of the first phalanx, which is trapped by thesoft tissues between the damaged MC/T3 and the intact second phalanx.At the proximal aspect of the first phalanx, instability of the median sagittalridge in the sagittal groove results in subtle obliquity of the sagittal ridge inthe groove and asymmetric loading. The dorsal and palmar/plantar aspectsof the median sagittal ridge act as oblique destructive wedges generating ad-ditional fracture planes that originate in or near the groove and divide theproximal aspect of the first phalanx into rough quadrants (Figs.10 and11). If the proximal first phalangeal fracture planes result in a larger (usuallymedial) fragment, a column of bone in the first phalanx will remain intactbetween the metacarpo-phalangeal and proximal interphalangeal joints.However, if the proximal first phalangeal fragments are of similar cross-sec-tional area, they are not large enough to maintain an intact diaphysis of thefirst phalanx. Further damage distal on the first phalanx occurs as a sagittalfracture appears between the distal condyles, probably generated by the me-dian sagittal ridge of the proximal second phalanx. When the first phalanxfails, the horse usually falls, ending the injury cascade. This general scenariofully takes into account the possibility of other injuries, such as diaphysealfractures of MC/T3, lateral sesamoid fractures, and further comminution ofthe first phalanx.

Fig. 10. A dorso-palmar radiographic projection of a complete and slightly displaced lateral

condylar fracture. This fracture has an articular component slightly lateral to the condylar

groove. A fracture in this location is less common than a fracture involving the groove.

125ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

Palmar/plantar osteochondral disease

While long bone fractures are the most dramatic injuries to the fetlock,less serious bony injuries are more common in both racing and other

Fig. 11. The indistinct oval in the middle of the image is the most distal aspect of the median

sagittal ridge. Medial is to the left, and this horse had an intact medial strut from fetlock

to pastern joint. All fracture planes involve the condylar groove. (Courtesy of Elizabeth M.

Santschi, DVM, Columbus, OH.)

126 SANTSCHI

performance horses. More horses are lost to performance because of theseless serious injuries than because of long bone fractures. Subchondralbone inflammation (‘‘bone bruising’’) that results in lameness is usuallyapparent in the distal MC/T3. Subchondral bone inflammation usuallyoccurs in high performing individuals and it is a use or trauma injury. Itcan be a frustrating condition to diagnose because it is difficult to documentwith conventional means, such as local anesthesia and radiography. In itsworst manifestation, focal subchondral bone inflammation can result inthe formation of a subchondral bone void (Fig. 12) that further inflamesthe joint by shedding debris and causing mechanical cartilage damage.Nuclear scintigraphy can be helpful in the diagnosis of horses with radio-graphically silent inflammation and less obvious subchondral bone pain.However, because these horses are often undergoing bone turnover due toage or occupation, scintigraphy can be equivocal unless markedly asymmet-ric. MRI shows great potential in the diagnosis of radiographically silentbone inflammation or early bone destruction [22,23], but has the disadvan-tages of expense and limited availability. Future investigations using newlyavailable modalities should improve our ability to diagnose this conditionearlier and prevent further deterioration.

Sesamoiditis

Anadditional condition probably caused by bone inflammation is sesamoi-ditis, a condition characterized by proximal sesamoid bone lucencies.

Fig. 12. Transverse CT image of a Standardbred horse with a comminuted first phalangeal frac-

ture. This first phalanx was left without an intact medial strut, possibly because the fractures

roughly divide the proximal aspect of the first phalanx equally. (Courtesy of Elizabeth M.

Santschi, DVM, Columbus, OH.)

127ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

Sesamoiditis is a radiographic diagnosis based on observing lucencies anda change in shape to the palmar/plantar border of the sesamoid (Fig. 13)[24]. Little hard evidence supports the contention of local inflammation, butscintigraphic evaluation reveals evidence of strong bone activity, and therecan be local pain in addition to lameness referable to the fetlock. Sesamoiditisis believed to be the result of local inflammation in the proximal sesamoidbones and sesamoid branch attachments.Again, hyperextension of the fetlockjoint is implicated in the pathogenesis, with focal tearing of the suspensoryligament as the proximate cause of the inflammation. Sesamoiditis can some-times precede sesamoid fracture, but more often presents as fetlock lameness.

Osteochondral (‘‘chip’’) fractures

Smaller fractures to themargin of the bones of the fetlock are also commonin performance horses. These fractures are most common at the proximaldorsal aspect of the first phalanx and at the apical and abaxial aspects ofthe proximal sesamoid bones. Proximal-dorsal fractures of the first phalanxoccur because of fetlock hyperextension and direct trauma to the first phalanxby the dorsal aspect of theMC/T3 (Fig.14). The dorsal aspect of the proximalarticular surface of the first phalanx is subjected to MC/T3 contact only atvery high loads and experiences very high peak pressures [4]. Small dorsalproximal first phalangeal fractures can be clinically irrelevant, but larger frac-tures can result in joint inflammation and cartilage damage. Proximal sesa-moid fractures (Fig. 15) are also the result of fetlock hyperextension, as

Fig. 13. A dorso-palmar lateral to medial radiographic projection of the fetlock joint in

a 4-year-old Standardbred with severe lateral sesamoiditis. The proximal sesamoid bone has

multiple large widened linear lucencies and marked remodeling in its palmar border.

Fig. 14. A lateral to medial radiographic projection of a Thoroughbred yearling with a large

dorsal first phalangeal fracture in a hind fetlock.

128 SANTSCHI

these bones probably fail because of tension from the branch of the sesamoidligament [25] and bending forces generated by the palmar/plantar aspect ofthe MC/T3. Proximal sesamoid fractures do not heal except in very youngfoals and can cause continued local inflammation of the joint and suspensory

Fig. 15. A lateral to medial-lateral radiographic projection of a Thoroughbred yearling with

a small apical sesamoid fracture in a hind fetlock. Oblique projections should be taken to

determine the sesamoid affected.

129ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

ligament and fetlock lameness. Fractures to the distal aspect of the proximalsesamoid bone, where the bone fails at the attachment of the distal sesamoi-dean ligaments (Fig. 16), are also thought to be the result of fetlock hyperex-tension.Diagnosis of these fractures is usually achieved easily by conventionalradiography, although occasionally specialized views are required.

Soft tissue injury

Inflammation of the fetlock joint soft tissues (capsulitis and synovitis) isvery common and is also the result of trauma. Persistent joint inflammationcan result in degenerative changes in the soft tissues, cartilage, and bone of thefetlock joint. Cartilage damage begins with the release of cytokines that causedegradation of cartilage matrix and degradation of collagen. After matrixand collagen depletion, the cartilage is less effective at absorbing concussion,and continued exercise continues the traumatic insult. Synovial changesresulting from continued inflammation include hyperplasia and fibrosis.Bony changes include formation of osteophytes and loss of periarticularbone, such as supracondylar lysis (Fig. 17). Diagnosis of soft tissue injuryis often made by clinical observations, such as lameness, joint effusion, a re-duced range of motion, and pain on joint manipulation. Further diagnostics,such as ultrasound and MRI, can provide additional information.

Treatment principles

It is not the intention here to describe specific treatments for all condi-tions of the equine fetlock. That information can be found in several texts.

Fig. 16. A dorso-palmar medial to lateral radiographic projection of a front fetlock of a 3-year-

old Thoroughbred with a modulatory sized fracture of the base of the sesamoid.

Fig. 17. A flexed lateral radiographic projection of a front fetlock in a 6-year-old Thorough-

bred. The horse was used as a hunter, but had been purchased from the racetrack 6 months pre-

viously without a prepurchase examination. The horse was lame on this limb, and local

anesthesia localized the lameness to the fetlock joint. A chronic apical-abaxial sesamoid fracture

of the medial sesamoid is present. The dorso-palmar thickness of the metacarpus at point B is

5mm less than thickness at point A, indicating moderate supracondylar lysis. The loss of bone

on the palmar aspect of the metacarpus at the palmar fetlock joint pouch is the result of chronic

fetlock joint synovial inflammation.

130 SANTSCHI

However, general precepts regarding treatment can be summarized. The firstis controlling inflammation, which is achieved by rest; compressive bandag-ing; topical therapies, including application of cold therapy, various topicaldrawing and cooling agents, and systemic and topical nonsteroidal agents;and intra-articular medications, such as hyaluronic acid and corticosteroids.Surgical procedures, such as joint flushing to remove cytokines, cartilagedebris, and osteochondral fragments, also can reduce inflammation andlimit further damage. For larger fractures that involve the joint, internalfixation to re-establish the joint surface is critical to resuming function. Itis impossible to overemphasize the importance of adequate rest and rehabil-itation, the cornerstone of treatment. However, the equine clinician is oftencaught in the conflict between joint health and the realities of equine athleticcommitments. Owners should be counseled on the necessity of rest if a long-term career is the goal for their horse.

Prevention

Much work needs to be done on several fronts if the performance horseindustries are to adequately address the issue of injury prevention. For rac-ing, much more information is needed about the contributing causes to

131ARTICULAR FETLOCK INJURIES IN EXERCISING HORSES

injury, the early diagnosis of predisposing factors to injury, and the predic-tion of injury risk so that racetracks, trainers, regulatory and private prac-tice veterinarians, and horse owners can make informed decisions thatbalance racing goals with the need to protect horses. Prospective multiyearand multivariable analyses that include data on exercise schedules, trackquality, and individual horse characteristics, are essential to make reason-able and useful conclusions. While sufficient data are still lacking, recom-mendations for injury prevention for Thoroughbred racing horses includeproper trimming and shoeing (eg, avoidance of long toe-grabs), minimizingthe accumulation of high-speed works, and stressing the importance of earlyintervention when injury is mild [18].

As an extreme athlete, the racing horse can provide information helpfulin injury prevention for horses in other athletic disciplines. Early interven-tion in cases of injury, maintenance of appropriate hoof balance, and pro-visions for appropriate footing are all common-sense approaches to theprevention of career-threatening injury. What are less clear are the idealtraining and exercise regimens for individual disciplines and horses.

Summary

The fetlock joint is the essential joint to the performance horse. Withoutthe specialized anatomy of the fetlock, horses would be unable to so effi-ciently convert muscular activity to athletic prowess. Loss of an effectivefetlock joint ends most equine athletic careers, so understanding thedemands placed on the fetlock in the equine athlete is essential to optimaljoint health. Injury prevention and early detection of injury are essentialto preserve athletic capability.

References

[1] Wilson AM,McGuiganMP, Su A, et al. Horses damp the spring in their step. Nature 2001;

414:895–9.

[2] Wilson AM, Watson JC. A catapult action for rapid limb protraction. Nature 2003;421:

35–6.

[3] Wilson AM, McGuigan MP. The effect of gait and digital flexor muscle activation on

limb compliance in the forelimb of the horse Equus caballus. J Exp Biol 2003;206:

1325–36.

[4] Brama PAJ, Karssenberg D, Barneveld A, et al. Contact areas and pressure distribution on

the proximal articular surface of the proximal phalanx under sagittal plane loading. Equine

Vet J 2001;33:26–32.

[5] Norrdin RW, Kawcak CE, Capwell BA, et al. Subchondral bone failure in an equine model

of overload arthrosis. Bone 1998;22:133–9.

[6] Radtke CL, Danova NA, Scollay MC, et al. Macroscopic changes in the distal ends of the

thirdmetacarpal andmetatarsal bones of Thoroughbred racehorses with condylar fractures.

Am J Vet Res 2003;64:1110–6.

[7] Stover SM, Johnson BJ, Daft BM, et al. An association between complete and incomplete

stress fractures of the humerus in racehorses. Equine Vet J 1992;24:260–3.

132 SANTSCHI

[8] Riggs CM. Aetiopathogenesis of parasagittal fractures of the distal condyles of the third

metacarpal and third metatarsal bonesdreview of the literature. Equine Vet J 1999;31:

116–20.

[9] Firth EC, Rogers CW. Musculoskeletal responses of 2-year-old Thoroughbred horses to

early training. Conclusions. N Z Vet J 2005;53:377–83.

[10] Reilly GC, Currey JD, Goodship AE. Exercise of young Thoroughbred horses increases

impact strength of the third metacarpal bone. J Orthop Res 1997;15:862–8.

[11] Murray RC, Vedi S, Birch HL, et al. Subchondral bone thickness, hardness and remodeling

are influenced by short-term exercise in a site-specific manner. J Orthop Res 2001;19:

1035–42.

[12] Pool RR,MeagherDM. Pathologic findings and pathogenesis of racetrack injuries. Vet Clin

North Am Equine Pract 1990;6:1–30.

[13] Krook L, Maylin GA. Fractures in Thoroughbred race horses. Cornell Vet 1988;78(Suppl):

1–33.

[14] KawcakCE, Bramlage LR, EmbertsonRM.Diagnosis andmanagement of incomplete frac-

ture of the distal palmar aspect of the third metacarpal bone in five horses. J Am Vet Med

Assoc 1995;206:335–7.

[15] Riggs CM,Whitehouse GH, BoydeA. Pathology of the distal condyles of the thirdmetacar-

pal and third metatarsal bones of the horse. Equine Vet J 1999;31:140–8.

[16] Norrdin RW, Stover SM. Subchondral bone failure in overload arthrosis: a scanning elec-

tron microscopic study in horses. J Musculoskelet Neuronal Interact 2006;6:251–7.

[17] Easton KL, Kawcak CE. Evaluation of increased subchondral bone density in areas of con-

tact in the metacarpophalangeal joint during joint loading in horses. Am J Vet Res 2007;

68(8):816–21.

[18] Stover SM. The epidemiology of Thoroughbred racehorse injuries. Clinical Techniques in

Equine Practice 2003;2:312–22.

[19] Stepnik MW, Radtke CL, Scollay MC, et al. Scanning electron microscopic examination of

third metacarpal/metatarsal bone failure surfaces in Thoroughbred racehorses with condy-

lar fractures. Vet Surg 2004;33:2–10.

[20] Hill AE, Gardner IA, Carpenter TE, et al. Effects of injury to the suspensory appara-

tus, exercise, and horseshoe features on the risk of lateral condylar fracture and suspen-

sory apparatus failure in forelimbs of thoroughbred racehorses. Am J Vet Res 2004;65:

1508–17.

[21] Muir P, McCarthy J, Radtke CL, et al. Role of endochondral ossification of articular carti-

lage and functional adaptation of the subchondral plate in the development of fatiguemicro-

cracking of joints. Bone 2006;38:342–9.

[22] Dyson S, Murray R.Magnetic resonance imaging of the equine fetlock. Clinical Techniques

in Equine Practice 2007;3:389–98.

[23] Zubrod CJ, Schneider RK, Tucker RL, et al. Use of magnetic resonance imaging for iden-

tifying subchondral bone damage in horses: 11 cases (1999–2003). J Am Vet Med Assoc

2004;224:411–8.

[24] Spike-Pierce DL, Bramlage LR. Correlation of racing performance with radiographic

changes in the proximal sesamoid bones of 487 Thoroughbred yearlings. Equine Vet J

2003;35:350–3.

[25] Woodie JB,RugglesAJ, BertoneAL, et al. Apical fractures of the proximal sesamoid bone in

Standardbred horses: 43 cases (1990–1996). J Am Vet Med Assoc 1999;214:1653–6.