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research-article2017
VDIXXX10.1177/1040638717710238Guide to racehorse carpal diseaseEngiles et al.

Special Issue

Journal of Veterinary Diagnostic Investigation

A diagnostic pathologist’s guide to carpal 2017, Vol. 29(4) 414­–430

© 2017 The Author(s)
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DOI: 10.1177/1040638717710238
https://doi.org/10.1177/1040638717710238
jvdi.sagepub.com

Julie B. Engiles,1 Holly Stewart, Jennifer Janes, Laura A. Kennedy

Abstract. As a pathologist, postmortem examination of the equine carpus can be daunting. The anatomy is complex
and oftentimes, small or subtle lesions have significant impact on lameness and secondary lesions such as catastrophic
musculoskeletal fractures and other injuries. In performance horses, particularly racehorses, the carpus is a common site of
injury and source of lameness. Given the predisposition of racehorses to developing carpal disease, familiarity with clinically
relevant anatomy and common developmental, degenerative, traumatic, and inflammatory processes are imperative for
thorough postmortem examination. Our aim is (1) to provide a concise summary of clinically relevant anatomy and function
that serves as a guide for postmortem evaluation of the equine carpus, and (2) to review common carpal injuries and diseases in
actively training, racing, or retired racehorses, including developmental lesions (incomplete ossification, osteochondromata),
infectious and inflammatory lesions (septic arthritis and tenosynovitis), and degenerative and traumatic lesions (degenerative
and traumatic osteoarthritis, osteochondral fragmentation, and polyostotic catastrophic “breakdown” fractures). Representative
gross and histologic images are presented along with corresponding antemortem and postmortem diagnostic images, and a
review of current scientific literature pertaining to the pathogenesis of these equine carpal lesions.

Key words: Articular cartilage; bone; carpus; equine; fracture; horses; joint; orthopedic; osteochondral; racehorses;
subchondral; synovium.

Introduction impact future performance.2,5 Knowledge of functional

The carpus has complex anatomic and functional compo-
nents comprising 2 stacked rows of cuboidal bones that artic-
ulate with the distal end of the radius and proximal end of the
metacarpus, providing hinge-like movement of the proximal
2 joints,20 and planar movement of the distal joint in the dor-
sal–palmar direction.18 Carpal lameness is most common in
active and retired racehorses, where repetitive forces sus-
tained during racing and training likely exceed normal phys-
iologic stresses and strains, resulting in degenerative changes
that often lead to performance-limiting lameness and injury.81
In over 4,000 postmortem examinations on horses from Cal-
ifornia racetracks between 1991 through 2006 (84% Thor-
oughbreds, 10% Quarter Horses, and 2% Standardbreds),
carpal fractures were identified in the California Postmortem
Program initiated by the California Horse Racing Board, to
be the second and third most common cause of fatal muscu-
loskeletal injury in Quarter Horses and Thoroughbreds,
respectively.77 Moreover, surgery and iatrogenic injections
performed to manage carpal lameness and injury are associ-
ated with carpal infections (i.e., septic arthritis and tenosyno-
vitis).69
Although somewhat controversial, developmental abnor-
malities involving endochondral ossification or conforma-
tion have been reported to predispose to lameness that can
carpal anatomy and common lesions associated with carpal
lameness, traumatic injury, and inflammatory processes is
important to guide postmortem dissection and evaluation.
Our objective in this review is to provide diagnostic pathol-
ogists with a succinct reference of clinically relevant anat-
omy and review of diseases and lesions most commonly
encountered in the carpi of racehorses.
Anatomy
The equine carpus incorporates 3 joints from proximal to dis-
tal: the antebrachiocarpal (radiocarpal; Fig. 1), middle carpal
(Fig. 2A–C), and carpometacarpal joints (Fig. 2D). Carpal
Department of Pathobiology, New Bolton Center, School of Veterinary
Medicine, University of Pennsylvania, Kennett Square, PA (Engiles); Gail
Holmes Orthopaedic Research Center, Department of Clinical Studies,
College of Veterinary Medicine and Biomedical Sciences, Colorado State
University, Fort Collins, CO (Stewart); and Department of Veterinary
Science, Veterinary Diagnostic Laboratory, University of Kentucky,
Lexington, KY (Janes, Kennedy).
1
Corresponding author: Julie B. Engiles, Department of Pathobiology,
New Bolton Center, University of Pennsylvania, 382 West Street Road,
Kennett Square, PA 19348. engiles@vet.upenn.edu
 Guide to racehorse carpal disease 415

Figure 1.  A. Right antebrachiocarpal joint that shows the medial parasagittal ridge between the radial and intermediate facets of
the radius (arrow) and lateral parasagittal groove formed by fusion of the distal ulnar epiphysis (styloid process of the ulna) to the
distal radial epiphysis (arrowhead). Partial flexion of this joint highlights the distal excursion of the radial carpal bone (Cr) relative
to the intermediate carpal bone (Ci), and the ulnar carpal bone (Cu). This horse had postoperative septic arthritis that resulted in
synovial hyperplasia and a focal ulcer within the articular cartilage of the radial facet of the distal radius. B. Proximal aspects of
the proximal row of carpal bones showing, from lateral to medial: the articular facet of the accessory (Ca), ulnar (Cu), intermediate
(Ci), and radial (Cr) carpal bones.

Figure 2.  A. Middle carpal joint in partial flexion highlighting the medial palmar intercarpal ligament (arrowhead) originating from the
distolateral surface of the radial carpal bone (Cr) and inserting on both the proximal palmaromedial aspect of the third (C3) and proximal
palmarolateral aspect of the second (C2) carpal bones, and the lateral palmar intercarpal ligament (arrow) originating from the distal part of
the palmaromedial surface of the ulnar carpal bone (Cu) and inserting on the proximal palmarolateral surface of the third carpal bone (C3).
The radial (r) and intermediate (i) facets of the dorsal aspect of C3, and the distal portion of the radius (R) are also labeled. B. Middle carpal
joint disarticulated to show the distal surfaces of Cr, Ci, and Cu bones, and the palmar, non-articular portion of the accessory carpal bone Ca.
C. Middle carpal joint disarticulated to show the proximal surfaces of C2, C3, and C4, including the radial (r) and intermediate (i) facets of
C3. D. Carpometacarpal joint disarticulated to show the planar proximal articular surfaces of the second, third, and fourth metacarpal bones
(MC2, MC3, and MC4, respectively). Arrows indicate locations of transected medial and lateral intercarpal ligaments that originate between
C2 and C3, and between C3 and C4, inserting between MC2 and MC3, and MC3 and MC4, respectively.
416
Engiles et al.
bones comprise 7–9 cuboidal bones that include, from medial
to lateral: the radial (Cr), intermediate (Ci), ulnar (Cu), and
accessory (Ca) carpal bones forming the proximal row of
carpal bones; and the second (C2), third (C3), and fourth
(C4) carpal bones forming the distal row, with the first carpal
bone reported in 25–50% of horses, and the fifth carpal bone
rarely present (1–3%).51,70,71Although intercarpal articular
surfaces exist between lateral and medial, and dorsal and pal-
mar aspects of individual carpal bones, the most commonly
reported and treated lesions pertain to the dorsoproximal and
dorsodistal articular surfaces of the antebrachial and middle
carpal joints.64,70
In the standing horse, the carpus is maintained in full
extension; however, in 2-dimensional kinematic studies of
the trot, the carpus shows an average range of motion in the
sagittal plane of 89.5 ± 5°, divided into swing and stance
phases that include a large component of flexion in the
swing phase (average 83.5°) and a smaller component of
extension in the stance phase (average −6.0°).4 Three-
dimensional kinematic studies confirm the predominant
rotational motion of flexion-extension in the sagittal plane;
however, we have also identified small components of inter-
nal rotation, and dorsal displacement of the metacarpus rela-
tive to the radius, which with higher speeds could produce
larger compressive and shear forces that may increase the
risk of injury.18 The extensive attachments of the medial and
lateral collateral ligaments to the distal radius, carpal bones,
and proximal end of the metacarpus confine movement to
the sagittal plane. Overextension is prevented by the palmar
carpal ligament, formed by thickening of the palmar aspect
of the joint capsule, which, along with the flexor retinacu-
lum, extends from the palmar aspect of the accessory carpal
bone to the palmaromedial aspect of the joint.20 Together,
the palmar carpal ligament and flexor retinaculum form the
palmar annular carpal ligament that encloses the flexor ten-
dons as well as medial and lateral neurovascular structures.60
The palmar carpal ligament is also the origin of the acces-
sory ligament of the deep digital flexor tendon (inferior, or
distal, check ligament). Interosseous ligaments, including
the dorsal, transverse, and medial/lateral palmar intercarpal
ligaments maintain carpal bone alignment and prevent
hyperextension.84 Transverse intercarpal ligaments are dif-
ficult to visualize during routine postmortem examination
and carpal disarticulation. However, the medial and lateral
palmar intercarpal ligaments are easily identified by main-
taining the middle carpal joint in partial flexion while par-
tially disarticulating by incising over the dorsal joint capsule
(Fig. 2A).
Because of the anatomic complexity of the carpus, often
5–7 standard radiographic projections (dorsopalmar, latero-
medial, both dorsolateral–palmaromedial and dorsomedial
palmarolateral obliques, flexed lateromedial, and flexed
dorsoproximal–dorsodistal “skyline” views) are considered
necessary for satisfactory evaluation in the live horse.64,74
Although not necessary, in our experience, if available,
antemortem carpal radiographs or other forms of diagnostic
imaging such as computed tomography (CT), magnetic
resonance imaging (MRI), or ultrasound can prove quite
useful during postmortem evaluation by their ability to
reveal small, yet often clinically significant osteochondral
fragments or non-displaced and/or incomplete fracture
planes that may be difficult to discern on gross inspection.
Digital files of antemortem radiographs can be obtained
from the referring veterinarian via email, or good quality
radiographs can be acquired postmortem of either the intact
carpus or disarticulated rows of carpal bones to help iden-
tify lesions.
Antebrachiocarpal joint. The articulating surfaces of the
antebrachiocarpal joint allows for the greatest degree of
flexion in the carpus.20 In full extension, the medial parasag-
ittal ridge of the distal end of the radius separates the radial
and intermediate facets of the radius, and the lateral groove
formed by the fusion of the styloid process of the ulna with
the radius separates the articular facets of the Ci and Cu.33 In
flexion, a proximodistal step is formed by the distal dis-
placement of Cr relative to Ci, thus the mnemonic “i is high”
(Fig. 1). The shape of the ulnar carpal bone can vary, and
occasionally small osseous bodies are associated with the
distal palmar aspects of this bone.51,71 Findings from radiol-
ogy71, MRI, and histology51 of these small osseous bodies in
non-lame horses were compatible with clinically insignifi-
cant anatomic variation or chondro-osseous metaplasia at
the origin of the lateral palmar intercarpal ligament,51 rather
than palmar osteochondral fragments associated with frac-
tures in the dorsal aspects of the carpal bones,27 or avulsion
of the lateral palmar intercarpal ligament from the ulnar car-
pal bone.7
Middle carpal joint. The articular surface of the middle
carpal joint is different than the antebrachiocarpal joint,
with the proximal surfaces of C2, C3, and C4 having con-
cave dorsal as well as convex palmar profiles that are recip-
rocal to the distal articular surfaces of Cr, Ci, and Cu (Fig.
2A–C).73 C3 is the largest of the 3 bones in the distal row
and is “L” shaped with 3 distinct regions: the palmar por-
tion that is rarely injured, and the dorsal portion that is
divided by a distinct sagittal ridge into radial (medial) and
intermediate (lateral) facets, which are frequently injured in
racehorses.54,64 As mentioned above, the medial and lateral
palmar intercarpal ligaments that span the proximal and
distal rows of carpal bones are important structures that, in
conjunction with the collateral ligaments, prevent dorsal
displacement of the proximal row of carpal bones.84 The
medial palmar intercarpal ligament originates from the dis-
tolateral surface of the radial carpal bone and inserts on the
proximal palmaromedial surface of the third carpal bone
and the proximal palmarolateral surface of the second car-
pal bone, forming a sheet-like band divided into variably
defined fiber bundles.85 The lateral palmar intercarpal
 Guide to racehorse carpal disease
ligament typically forms a triangular band of unbundled
fibers that originates on the distal portion of the palma-
romedial surface of the ulnar carpal bone with a few fibers
attaching to the palmarolateral surface of the intermediate
carpal bone, and predominantly inserts on the proximal pal-
marolateral surface of the third carpal bone, with a few
fibers inserting on the palmaromedial surface of the fourth
carpal bone.85 Despite their relatively small size, inspection
of these intercarpal ligaments is imperative because lesions,
including avulsion fractures,7 and degeneration or partial to
complete ligamentous tears, are reported as significant
sources of carpal lameness and instability, and are often
concurrent with carpal osteochondral “chip” and bi-articu-
lar “slab” fractures.14,28,35,47,58,87
Carpometacarpal joint.  In contrast to the antebrachiocar-
pal and middle carpal joints, the carpometacarpal (CMC)
joint is considered a low motion joint, with the distal row of
carpal bones remaining in contact with the proximal
extremity of the metacarpus.72 The CMC joint is composed
of the distal surfaces of C2, C3, and C4, which articulate
with the proximal ends of the third metacarpus (MC3)
flanked medially and laterally by the second (MC2) and
fourth (MC4) metacarpi, respectively72 (Fig. 2D). In addi-
tion to the medial and lateral collateral ligaments that
extend from the distal end of the radius to the proximal part
of the metacarpi, small medial and lateral intercarpal liga-
ments originate between C2 and C3, and between C3 and
C4, inserting between the articulation of MC2 and MC3,
and between MC3 and MC4, respectively (Fig. 2D).51
Because the CMC joint communicates with the middle car-
pal joint, one should be aware that septic arthritis within the
middle carpal joint may give rise to septic arthritis in the
CMC joint. Moreover, clinical interpretation of diagnostic
analgesia performed at the proximal aspect of the metacar-
pus (e.g., high 4-point block) can be difficult because of the
medial and lateral distopalmar synovial outpouchings that
extend along the axial aspects of the proximal ends of MC2
and MC4 in the region of the origin of the suspensory liga-
ment.25 In a study of cadaver limbs, nearly all CMC joints
had a variable articulation between C3 and MC3, whereas
only 3 of 200 joints did not have a measurable articulation
between C3 and MC3.63 Lesions in the CMC region, includ-
ing desmitis of the origins of the suspensory ligament and
accessory ligament of the deep digital flexor tendon,15 syn-
desmopathies between the metacarpal bones, intercarpal
ligament, and osseous abnormalities between C2/C3 and
MC2/MC3, and lesions consistent with bone marrow edema
of the medial aspects of the carpal and metacarpal bones,59
can be difficult to identify radiographically or ultrasono-
graphically, necessitating nuclear scintigraphy and/or MRI
to diagnose.50 In our experience, the CMC joint is difficult
to disarticulate for gross examination, and unless indicated
417
in the history, is not often disarticulated during routine
postmortem examination.
Carpal canal and carpal sheath.  The carpal canal is located
along the palmar aspect of the carpus, confined by dense fas-
cia (the palmar annular carpal ligament, or carpal flexor reti-
naculum) that forms a complex subdivided tunnel-like
structure extending from the proximal margin of the acces-
sory carpal bone to the proximal metacarpus.60 The carpal
flexor tendon sheath (carpal sheath) encloses the tendons and
synovial sheaths of the flexor carpi radialis, superficial and
deep digital flexor tendons, as well as neurovascular struc-
tures including the medial and lateral palmar nerves, the pal-
mar branches of the median artery and vein, and radial artery
and vein. The sheath extends 8–10 cm proximally from the
antebrachiocarpal joint and distally to the proximal third or
middle of the metacarpus.20 Lameness associated with the
carpal sheath is often the result of compression of the soft
tissue structures contained within the lumen that can arise
from effusion caused by idiopathic synovitis or trauma-asso-
ciated intrathecal hemorrhage (e.g., accessory carpal bone
fracture), space-occupying lesions (e.g., distal radial osteo-
chondromata), diseases of tendons and ligaments contained
within the sheath, or diseases of the palmar annular carpal
ligament itself caused by orthopedic overload or hyperexten-
sion injury.21,30,60,88
Developmental lesions
In young foals (i.e., <2 mo of age), cuboidal bones of the
carpus are incompletely ossified and thus are inherently sus-
ceptible to injury.3 Although the degree of ossification at
birth varies among foals, neonatal carpal bones typically
have a rounded appearance with thick radiolucent spaces that
represent hyaline cartilage surrounding ossification centers
of the carpal bones. Ossification is often incomplete, is best
seen on a dorsopalmar radiograph (Fig. 3A), and can be dif-
ficult to discern grossly (Fig. 3B, 3C) or histologically in
demineralized specimens. Although not the focus of this
review, incomplete ossification also occurs in the cuboidal
bones of the tarsus.
In addition to leading to disrupting growth plates or
increasing loads on joints, incomplete ossification of the
cuboidal bones is one cause of angular limb deformities.
Angular limb deformities are common, with one study of
neonatal Thoroughbred foals reporting only 2 of 67 (3%)
carpi having straight conformation and valgus angular devi-
ations up to 4° considered normal.67 Although a small pro-
portion of angular deformities may “self-correct” in some
foals, many are treated with a variety of therapies including
hoof trimming, splinting, periosteal stripping, and transphy-
seal bridging, which are most effective if implemented prior
to growth cessation of the distal radial physis by 60 wk of
418
Engiles et al.

Figure 3.  Incomplete ossification of the carpus in an immature foal. A. Dorsopalmar radiograph showing rounded profiles of the distal
radial/ulnar epiphyses and carpal bones indicating incomplete ossification. In contrast to the radiographic projection, incomplete ossification
is difficult to discern grossly on transverse sections of proximal B. and distal C. rows of carpal bones.

age.62 Regardless, studies of the effect of angular limb

deformities on future musculoskeletal problems show con-
flicting results as to impact on performance,2,5,83 whereas
other carpal conformational deformities (e.g., “offset knees”
conformation) have been associated with an increased risk
of injury.2,64
Osteochondrosis is a well-documented equine develop-
mental bone disease at multiple predisposed sites as a result
of endochondral ossification. Osteochondrosis of the carpus
is rare; however, osteochondrosis dissecans of the third and
fourth carpal bones is reported in foals with angular limb
deformities,43 and subchondral cyst-like lesions (thought to
be a manifestation of osteochondrosis) have been reported in
the medial aspect of the distal radial epiphysis in 4 juvenile
horses.75 Figure 4. Osteochondroma composed hyaline cartilage (top)
As mentioned above, osteochondromata are cartilagi- that caps outer compact and inner trabecular bone. This lesion was
nous exostoses characterized by a radiolucent hyaline carti- surgically excised from a mature animal, evidenced by complete
lage cap overlying endochondral bone that communicates closure of the growth plate. Safranin-O. Bar = 500 μm.
with the medullary cavity of the parent bone.78 Osteochon-
dromata arising from defects of the perichondrial ring of lesions are often submitted for evaluation as excisional
the distal radial physis can grow and protrude into the car- biopsies (Fig. 4).
pal canal, leading to deep digital flexor tendinitis, synovitis
of the carpal sheath, and lameness that could affect current,
and potentially future, performance. Surgical removal of
Septic arthrosynovitis and tenosynovitis
the mass with debridement of the deep digital flexor tendon Septic arthrosynovitis or tenosynovitis of the carpal
results in a good prognosis,88 and although malignant trans- region can arise from hematogenous spread or introduc-
formation of these lesions is not reported in horses to date, tion of bacteria into the joint or synovial sheath through a
 Guide to racehorse carpal disease
Figure 5.  Septic carpi from a carriage horse that sustained an
accident while driving in-hand. A. Carpal bones are visible through
a large laceration in the left forelimb. B. Carpal bones are not
visible through the laceration surrounded by large abrasions in the
right carpus. C. Communication of the middle carpal joint with the
wound is evidenced by small and large foreign particulates (i.e., dirt
and gravel) associated with linear cartilage erosions (“score” lines)
and packed within the palmar recesses of the joint (arrowheads).
The third carpal bone contains a dorsal marginal fracture with
dissecting cartilage that involves the radial and intermediate facet
(arrows). The synovium is thickened and hyperemic, indicating
synovitis.
penetrating wound or iatrogenic injections and surgical
procedures (Figs. 5, 6). In a study of 192 horses diagnosed
with septic synovitis involving at least 1 synovial struc-
ture (joint or tendon sheath), 45 (18.4%) involved the car-
pus with 50% associated with surgery, 15.9% associated
with iatrogenic injection, 4.3% associated with a penetrat-
ing wound, and 8.3% idiopathic.69 In this study, the carpus
was the most frequently infected structure postopera-
tively, and the third most frequently affected structure
post-injection preceded by the tarsus and fetlock. Most
common isolates comprised gram-positive bacteria (e.g.,
nonhemolytic and hemolytic Staphylococcus spp., beta-
hemolytic and non–beta-hemolytic Streptococcus spp.)
and gram-negative bacteria (e.g., Enterobacteriaceae
family, Escherichia coli, and Pseudomonas spp.) with no
bacteria isolated in 27% of cultures.69 Septic arthrosyno-
vitis or tenosynovitis is associated with joint or tendon
sheath effusion and, with the exception of young foals,
typically manifests as stiffness and reluctance to move,
419
and severe lameness; pyrexia was observed in 54% of
adult horses.69 Synovial fluid in infected joints has reduced
viscosity with increased turbidity, coinciding with fibrin
and suppurative exudates, and can be yellow to orange-
red or brown depending on whether hemarthrosis is pres-
ent. The molecular inflammatory responses include
production of prostaglandin-E2, matrix metalloprotein-
ases, and proteoglycans that result in biochemical and
biomechanical alterations with enzymatic degradation of
the articular cartilage.44,53,66 Typical postmortem changes
to intrasynovial structures include diffuse synovial hyper-
plasia and hyperemia, often with mats or strands of fibrin
packed into synovial recesses, adhering to, or spanning
the cartilage and synovial membranes. Articular cartilage
also shows focal-to-diffuse yellowing and thinning, repre-
senting degeneration and atrophy, with ulcers and osteo-
myelitis extending into the subchondral bone (Fig. 6).
Prolonged inflammation within the carpal sheath can
result in “carpal canal syndrome,” a painful entrapment
neuropathy that results from chronic effusion, whether the
result of sepsis or trauma associated with distal radial
osteochondromata, caudal radial physeal exostoses, car-
pal hyperextension injuries (with or without accessory
carpal bone fractures), and injuries of the superficial or
deep digital flexor tendons.17
Degenerative osteoarthritis
Although inflammation from sepsis is highly destructive to
joints and synovial structures, rapidly advancing second-
ary degenerative changes can occur from prolonged non-
septic inflammatory changes. “Spontaneous” degenerative
osteoarthritis of the CMC joint (e.g., carpal spavin) pre-
dominantly occurs in older (>8 y old), non-racing Quarter
Horses and Arabian horses, and has a guarded-to-grave
prognosis given insidious yet severe, progressive narrow-
ing of the medial aspect of the CMC joint space with oste-
olysis, bridging osteophytosis, periarticular soft tissue
thickening, and effusion.56 In contrast, most cases of
degenerative carpal osteoarthritis occur in racehorses (Fig.
7). Thought to occur secondary to non-physiologic, repeti-
tive loading of the carpal bones associated with poor ana-
tomic conformation or perhaps certain training and racing
practices, this “traumatic” form of osteoarthritis may pro-
duce abnormal remodeling and function of articular carti-
lage, subchondral bone, and synovium that lead to
osteochondral fragmentation (Fig. 8) and eventual joint
failure.1,36,90 With severe joint instability, chronic degen-
eration and progressive osteophytosis can result in “end-
stage” osteoarthritis with partial-to-complete bridging
ankylosis (Fig. 9). In addition to racehorses, non-equine
athletes including humans and racing greyhounds experi-
ence repetitive post-traumatic osteoarthritis, manifesting,
420
Engiles et al.

Figure 6.  Disarticulated proximal and distal rows of carpal bones from a Thoroughbred racehorse that developed septic arthritis in the
right middle carpal joint after having bilateral arthroscopic surgery to excise osteochondral “chip” fragments (A–C, arrowheads) from the
distodorsal margins of the left A. and right B. radiocarpal bones and proximodorsal margin of the radial facet of the right third carpal bone
C. Hyperplasia and hyperemia and/or hemosiderosis of the synovium lining the joint capsule and medial palmar intercarpal ligament in
the left middle carpal joint are typical postoperative changes (A, asterisk). Postoperative infection in the contralateral right middle carpal
joint, refractory to treatment and necessitating euthanasia, shows yellowing and fissuring of the articular cartilage with fibrin adhered to
subchondral bone exposed by surgical excision of osteochondral fragments (B and C, arrowheads), fibrin packed into synovial recesses
and coating the right medial palmar intercarpal ligament (B, asterisk), and villous hyperplasia of the synovial membrane (B, arrow). D.
Parasagittal sections of the dorsal portion of the right radiocarpal bone show subchondral hyperemia and lysis (arrowheads), consistent with
osteomyelitis confirmed histologically (not shown).

in advanced cases of degenerative osteoarthritis, as joint
effusion with reduced viscosity of synovial fluid; synovial
membrane hyperplasia and joint capsule fibrosis; articular
cartilage fissures, erosions, and atrophy; and subchondral
sclerosis, lysis, fracture, and osteophytosis.1,9,16,36
A collaborative initiative developed a standardized
grading scheme, based on modified Mankin and OARSI
(Osteoarthritis Research Society International) scoring
systems, for characterization of macroscopic and micro-
scopic lesions associated with experimental or naturally
occurring osteoarthritis in horses.41 Schemes were
designed to assess all components of the joint, including
lesions identified in the synovium (inflammatory infil-
trates; hyperplasia; edema; and fibrosis), cartilage (super-
ficial, partial to full-thickness erosions; fibrillation and
fissures; chondrocyte necrosis and loss; chondrone forma-
tion; and changes to the extracellular matrix), and sub-
chondral bone (splitting of the osteochondral matrix;
subchondral bone disruption and collapse; and subchon-
dral bone remodeling).41 Although not necessary for rou-
tine postmortem exams, use of these schemes will provide
meaningful comparisons among laboratories as well as
experimental or naturally occurring osteoarthritis models.
Experimental induction of osteoarthritis has been achieved
in horses by intra-articular injection of recombinant equine
interleukin-1 beta or iatrogenic intra-articular osteochondral
fragmentation and exercise. These established models of
osteoarthritis allow the investigation of associated inflamma-
tory profiles, assessment of biomarkers related to degenera-
tion and remodeling, and better characterization of clinical
and imaging parameters.26,36,66 Studies of naturally occurring
osteoarthritic disease in racing Standardbreds did show cor-
relation between advanced gross and microscopic lesions in
the articular cartilage and subchondral bone, including ero-
sions and loss of proteoglycan content within hyaline cartilage,
cracks and collapse within mineralized cartilage, and subchon-
dral bone pits with porosity correlating with lesion-specific
increases in osteoclasts and volumetric decreases in bone den-
sity as determined by microcomputed tomography (micro-
CT).10,39 Re-examination of the original micro-CT scans
revealed acellular, high-density mineralized material that form
patches below and protrusions above the mineralizing front
 Guide to racehorse carpal disease
Figure 7.  Chronic degenerative osteoarthritis in the right carpus
of a Thoroughbred racehorse euthanized for severe intractable
lameness of 1-mo duration. Antemortem photos show a bulging
profile (arrows) seen dorsally A. and laterally B. in the right carpus
in comparison to the left that results from synovial effusion, joint
capsule thickening, and bony exostoses.
of the mineralized cartilage in osteoarthritic C3.40 These
findings, which are not visible in demineralized prepara-
tions, standard radiography, or CT, coincide with similar
high-density mineral protrusions identified within distal pal-
mar/plantar third metacarpi/metatarsi of Thoroughbred race-
horses in association with palmar/plantar osteochondral
disease, that extend through vertical cracks within the articu-
lar mineralized cartilage, and microcracks within the sub-
chondral bone and osteochondral junction in human
osteoarthritic joints.13,23,46,82 A separate study in a different
set of samples confirmed the presence of similar extruded
mineralized matrix extending from cracks in the calcified
cartilage into the deeper regions of hyaline cartilage, corre-
sponding to sites of superficial hyaline cartilage erosion and
fibrillation.31 Other studies performed in carpal bones of
both Thoroughbred and Standardbred racehorses identified
subchondral bone sclerosis with increased mineral density,
and increases in biochemical markers of bone turnover, cor-
responding to gross and histologic lesions of cartilage degen-
eration and osteoarthritis.22,79
Additional studies attempting to mimic early stages of
“naturally occurring” repetitive impact trauma induced by
conditioning exercise in 1.5–2-y-old Thoroughbred fillies
showed significantly higher bone mineral density in C3,24 as
well as mechanical and morphologic differences in the hya-
line and mineralized articular cartilage within sites that with-
stand high intermittent loads (e.g., dorsodistal Cr and Ci, and
421
Figure 8.  A. Flexed lateromedial preoperative radiograph of
the arthritic right (R) carpus in Figure 7 that shows irregularities in
the dorsodistal margin of the radiocarpal bone and an osteochondral
fragment (arrowhead) adjacent to the dorsodistal margin of the
intermediate carpal bone. B. Flexed dorsoproximal–dorsodistal,
“skyline” preoperative radiograph that shows a large osteochondral
fragment (arrowhead) adjacent to the radial facet of the third carpal
bone. C. Postmortem photograph of the partially disarticulated
middle carpal joint from the same horse 2 mo post-surgery shows
partial healing of the surgery sites in the intermediate carpal
bone (arrowheads), radial carpal bone (black arrows), and third
carpal bone (white arrows), with secondary degenerative changes
including articular cartilage fissures, synovial hyperplasia, and
thickening of the fibrous joint capsule.
dorsoproximal C3).31 48,49 Yet a different study performed in
young juvenile Thoroughbreds comparing the effects of pas-
ture exercise versus controlled, conditioning exercise insti-
tuted from birth through 18 mo of age on opposing surfaces
of cartilage and subchondral bone taken from Cr and C3
identified gross and histologic lesions involving osteochon-
dral junctions and mineralized cartilage within both exer-
cised and control groups, thus suggesting that “early”
microscopic osteochondral lesions (e.g., localized disruption
of the osteochondral junction, thickening of the mineralized
cartilage with matrix texture changes and microcracks) may
arise within sites predisposed to developing more advanced
osteoarthritis, regardless of exercise program.37,38 Although
much more is known regarding lesions associated with the
development of equine osteoarthritis, clearly the results of the
studies listed above incite additional questions necessitating
further research into the predisposition and pathogenesis of
equine osteochondral disease.
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Engiles et al.

Figure 9.  A. Postmortem photograph of a severely enlarged right carpus from a 35-y-old Quarter Horse gelding that died of natural
causes, but had a several year history of severe forelimb lameness. B. Oblique sagittal section reveals end-stage degenerative osteoarthritis
with large periarticular exostoses (osteophytes) and bridging ankylosis of the antebrachiocarpal joint (white arrowheads), a subchondral
bone cyst within the radius (black arrow), and focal ulcer in the third carpal bone (black arrowhead). C. Photograph of the dorsodistal margin
of the radial and intermediate carpal bones that shows osteophytes (arrowheads) and complete loss of articular cartilage, with subchondral
fissures and depressions (arrows). The synovial membrane (S) is hyperemic and hypertrophied.

Osteochondral fragmentation and catastrophic
carpal fractures
In conjunction with degenerative osteoarthritis, osteochon-
dral fragmentation (i.e., fracture) of the equine carpus
results from naturally occurring, repetitive impact trauma
associated with racing and training. This lesion occurs most
frequently in the middle carpal joint along the dorsodistal
margin of Cr and dorsoproximal margin C3, followed by
the antebrachiocarpal joint along the dorsolateral margin of
the distal radius and dorsoproximal margin of Ci.42,55,68,76 In
both Thoroughbred and Standardbred racehorses, early
degenerative changes (e.g., subchondral sclerosis and
lucency) associated with carpal lameness are thought to
precede cartilage damage and fractures.29,32,65,80 However,
experimental osteochondral fragmentation will induce sub-
chondral bone remodeling and changes in the mineralized
cartilage layer.52 Osteochondral fragments involve a single
articular surface of a bone (so-called “chip” fractures) or
span 2 articular surfaces of a bone (bi-articular or “slab”
fractures; Figs. 8, 10, 11). Depending on their location and
size (“large” or “small”), chip fractures can be surgically
removed, reduced with surgical implants, or treated conser-
vatively with prolonged stall rest.76 Although breed and
 Guide to racehorse carpal disease 423

Figure 10.  A. Preoperative dorsolateral–palmaromedial oblique (DLPaMO) radiograph from a 2-y-old Standardbred gelding shows a
bi-articular “slab” fracture (arrowheads) within the radial facet of the third carpal bone (C3). B. Postoperative DLPaMO radiograph shows
reduction of the C3 fracture via surgical fixation. C. Intraoperative arthroscopy photos show a semi-lunar cartilage depression (arrowheads)
corresponding to an additional large osteochondral “chip” fracture in C3 that required debridement. D. Debridement site that reveals sclerotic
bone with few superficial subchondral blood vessels. E. In addition to C3 fractures, a 70% tear in the medial palmar intercarpal ligament,
commonly associated with traumatic carpal fractures, was identified (arrowheads). F. Intraoperative arthroscopic image of a normal palmar
intercarpal ligament is provided for comparison.

activity (i.e., type of racing) does influence differences in
fracture type and predilection site, sex does not influence
lesion site or lameness.19,61,68
Recently, carpal fracture was reported to be the most com-
mon fatal musculoskeletal injury in racing Quarter Horses.8
In racehorses, most fractures occur in young (<4 y old), skel-
etally immature animals, and although fractures in Thor-
oughbreds involve the right forelimb more often than the
left, fractures in Standardbreds tend to be equally distributed
between right and left forelimbs, and are also more fre-
quently bilateral.68,76,89 The different site predispositions
between these 2 breeds may be related to differences in gait
(gallop vs. pace or trot) as well as other differences in train-
ing or racing. C3 fractures (Fig. 10) comprise incomplete or
424
Engiles et al.

Figure 11.  A. Low magnification photomicrograph of the osteochondral fragment surgically excised in Figure 10 that shows focal
degeneration and loss (arrowheads) of the hyaline articular cartilage (HAC) with superficial extension of the adjacent subchondral bone
plate through the articular–epiphyseal complex (right). There is sclerosis (S) of the deep subchondral bone in comparison to superficial
subchondral bone that shows expansion of vascular spaces by active bone remodeling. H&E. Bar = 500 μm. B. Higher magnification
photomicrograph of articular surface and subchondral bone with expanded vascular spaces (asterisk) shown in panel A. H&E. Bar =
200 μm. C. Active bone remodeling is characterized by woven bone proliferation (W) within cavities of resorbed bone containing large
vascular sinuses (asterisks) and lined by numerous multinucleate osteoclasts within resorption lacunae (arrowheads). H&E. Bar = 100 μm.
D. Sclerosis within deeper regions of subchondral bone shown in panel A is characterized by dense compact lamellar bone with many
lacunae devoid of osteocyte nuclei, few viable small vascular spaces (arrow), and numerous severely stenotic or necrotic vascular spaces
(arrowheads). H&E. Bar = 100 μm.

complete chip fractures and bi-articular slab fractures with
the vast majority occurring in the frontal plane, a few occur-
ring in the sagittal plane, and most involving the radial over
the intermediate facet.76 C3 fractures (Fig. 8) often occur in
conjunction with fractures of opposing articular surfaces
(e.g., the dorsodistal margins of the radiocarpal or intermedi-
ate carpal bones).68
Fractures in other carpal bones (Cu, C2, C4, and Ca) are
unusual, either associated with catastrophic fractures (e.g.,
“breakdown injuries”) that result in severe destabilization
of the joint necessitating euthanasia34,57,77 (Figs. 12, 13) or
occurring sporadically as the result of trauma from falls or
kicks.64 Catastrophic carpal fractures are reported in racing
Thoroughbreds and Quarter Horses, but are extremely rare
and not well reported in Standardbred racehorses (Drs. PM
Hogan and MW Ross, pers. comm., 2016), again possibly
reflecting differences in maximum racing speed and gait
differences.11 Although there are a few reports describing
palmar osteochondral fragments, they rarely occur as pri-
mary lesions, and fragments within the palmar aspect of the
antebrachiocarpal or middle carpal joint are often associ-
ated with primary lesions involving dorsal aspects of other
carpal bones (e.g., Cr, C3, Ci, Ca, Cu) or the distolateral
margin of the radius.27 Accessory carpal bone fractures are
rare (2% of all fractures) but well-recognized lesions that
often result from extreme hyperextension associated with
jumping or a fall, or other severe trauma to the palmar
aspect of the carpus.12,45 Fractures often occur as a proxi-
modistal slab in the frontal plane, and can involve the car-
pal sheath or traumatize the deep digital flexor tendon.12,45
Articular Ca fractures are often comminuted and, if not sur-
gically removed, can result in significant instability of the
antebrachiocarpal joint, and horses are at risk of secondary
osteoarthritis and intractable lameness12 (Fig. 14).
 Guide to racehorse carpal disease 425

Figure 12.  A. Subcutaneous hemorrhage corresponding to intra-articular carpal fractures associated with a catastrophic “breakdown”
injury in a 3-y-old Thoroughbred racehorse. B. Partial disarticulation of the middle carpal joint reveals complete, comminuted, displaced
fractures of the second (C2) and third (C3) carpal bones with extensive damage to the articular cartilage and rupture of palmar intercarpal
ligaments. C. Disarticulation with orientation that shows the distal portions of the proximal row of carpal bones reveals complete, displaced,
comminuted bi-articular fractures of the ulnar carpal bone (Cu) involving frontal and parasagittal planes, and osteochondral fractures of
dorsodistal margins of the intermediate (Ci) and radial (Cr) carpal bones with ulceration and dissection of the articular cartilage from the
subchondral bone. D. Disarticulation of the distal row of carpal bones reveals complete, displaced, comminuted bi-articular fractures of
the radial (r) and intermediate (i) facets of C3 involving frontal and parasagittal planes, a complete, displaced bi-articular fracture of C2
involving the sagittal plane and similar extensive damage of articular cartilage. Carpal arthrodesis was not elected, necessitating euthanasia
at the racetrack.

In addition to osteochondral fragmentation, stress-related be more severe in Standardbreds than Thoroughbreds.86

injuries to associated ligaments and tendons can occur alone,
or in conjunction with osteochondral fragmentation, leading
to further joint instability and degenerative osteoarthritis.39
Damage to the medial palmar intercarpal ligament (Fig. 10E,
10F) is common in horses >1 y of age, with tears tending to
Avulsion fractures of the lateral palmar intercarpal ligament
originating from the medial palmar aspect of the ulnar carpal
bone are described as radiographically and histologically
distinct from subchondral cystic lesions of the ulnar carpal
bone mentioned above.6
426
Engiles et al.

Figure 13.  A. Parasagittal sections of the radial (upper) and intermediate facet (lower) fractures of C3 shown in Figure 12 that
show severe subchondral sclerosis concentrated within the dorsal aspects of the bone surrounding fracture sites. B. For comparison,
parasagittal sections of the radial (upper) and intermediate (lower) facets from an age-matched Thoroughbred racehorse euthanized for
catastrophic fracture of the third metacarpus show only mild subchondral sclerosis (upper) and bruising (lower) within the dorsoproximal
aspects of the radial and intermediate facets. C. Photomicrograph corresponding to the upper frame in panel A showing abrupt cartilage
and subchondral fracture (right). The adjacent cartilage is severely fibrillated (arrowhead) and subchondral bone severely sclerotic
(S) with few viable vascular spaces. Small curvilinear microcracks (arrows) are seen within the sclerotic bone immediately adjacent
to the fracture. H&E. Bar = 500 μm. D. Photomicrograph corresponding to the lower frame in panel A showing comparatively less
sclerotic subchondral bone that merges into trabecular bone with intervening medullary spaces (M). Numerous microcracks (arrows)
are within proximal regions of subchondral bone with hemorrhage in medullary spaces (H). The articular cartilage shows degenerative
changes including hypereosinophilia with longitudinal fissures and surface fibrillation (arrowheads). H&E. E. High magnification
photomicrograph of deep articular cartilage to the immediate left of the focus of subchondral bruising shown in panels A (lower) and D
illustrates linear fissures within the mineralized cartilage (arrowheads). H&E. Bar = 100 μm. F. High magnification photomicrograph
of articular cartilage and subchondral bone from framed region in panel B shows early degenerative changes including loss and
hypereosinophilia (asterisk) of the superficial-to-transitional zones of articular cartilage and linear fissures within the mineralized
cartilage (arrowheads). H&E. Bar = 200 μm.
 Guide to racehorse carpal disease 427

Figure 14.  A. Lateromedial radiograph of an acute, complete, mildly displaced, comminuted accessory carpal bone fracture (arrowhead)
involving the proximal dorsal articular surface in a 6-y-old Thoroughbred sustained after a fall. There was marked swelling and effusion of the
antebrachiocarpal joint and carpal sheath. B. Antemortem lateromedial radiograph of the same horse 2 mo after the initial injury shows apparent
displacement of the fracture fragment (arrowhead) with lysis surrounding the fracture. The horse was euthanized due to severe intractable lameness.
C. Disarticulated antebrachiocarpal joint shows large focal cartilage ulcer (arrow) and adjacent fibrosis (asterisk) within the palmarolateral aspect
of the distal antebrachium, corresponding to the injury site, and linear depressions (i.e., “score lines”) within the articular cartilage, consistent
with secondary degenerative changes. D. Disarticulated proximal row of carpal bones shows comminuted displaced fracture fragments of the
accessory carpal bone (arrows) and osteophytosis (arrowheads) along the dorsal margin of the radiocarpal bone.

Acknowledgments
We thank Drs. Patty M. Hogan, Dean W. Richardson, and Michael
W. Ross for contributing clinical materials, images, and or con-
structive comments to this manuscript. We also thank Ms. Karie
Durynski for her excellent technical skills and efforts in producing
materials used for imaging in this manuscript.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with
respect to the research, authorship, and/or publication of this
article.
Funding
The authors received no financial support for the research, author-
ship, and/or publication of this article.
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