Equine osteoarthritis: a brief review
of the disease and its causes
Angela E Schlueter and Michael W Orth*
Department of Animal Science, Michigan State University, 2209F Anthony Hall,
East Lansing, MI 48824, USA
*Corresponding author: email@example.com
Submitted 20 October 2003: Accepted 17 June 2004 Review Article
Degenerative joint diseases, such as osteoarthritis, adversely impact the health of the equine athlete as well as the
economics of the equine industry. Our understanding of the aetiology of osteoarthritis, although not nearly
exhaustive, has increased substantially in recent years. Molecules, including cytokines, inﬂammatory mediators,
and metalloproteinases, have been identiﬁed and associated with the progression of joint disease. Several factors,
including trauma to the joint, immobilization, conformation, shoeing, and ageing, have been linked with osteo-
arthritis. Our continued efforts into elucidating critical biological mediators and risk factors, coupled with
better chondroprotective therapies and diagnostic tools, should facilitate our ability to maintain the skeletal
health of the equine athlete
Keywords: cytokines; metalloproteinases; joint disease; risk factors
Impact of osteoarthritis in the equine
The equine industry is a growing industry that encom-
passes diverse disciplines ranging from sport horse to
work horse, and has a sizeable share in the US econ-
omy. The American Horse Council Foundation
(Barents Group LLC, 1996) reported that there were
6.9 million horses in the USA in 1996; 725 000
horses were involved in racing, 1 974 000 in showing,
2 970 000 in recreation and 1 262 000 in other activi-
ties. In addition, the equine industry directly provided
338 500 full-time jobs. The report also determined that
in 1996 the equine industry produced goods and ser-
vices valued at $25.3 billion, and the total contribution
to the US gross domestic product was $112.1 billion.
Lameness is a major cause of wastage in horses and
adversely affects the horse industry because one of the
main factors determining a horse’s value is soundness,
especially in athletic horses
. Jeffcott and Kold
assessed the wastage in Thoroughbred racehorses
from conception to 4 years of age, and determined
that lameness was the most signiﬁcant factor respon-
sible for failure to race, outweighing respiratory
problems, colic or limited racing ability
study also indicated that, among 140 Thoroughbred
two-year-olds evaluated, only 34 (24%) did not show
any signs of lameness. Similar results were found in a
study determining the wastage of racehorses between
1982 and 1983
. The greatest number of days lost to
training was caused by lameness (68%); among 314
horses examined, 53% were lame at some period
during the racing season.
Osteoarthritis (OA) is one of the most common
causes of lameness, and is of particular concern in
horses because their value is closely tied to their
soundness. Lameness that results from OA is a
major cause of poor performance and early retire-
ment of equine athletes
. A survey performed at a
veterinary school found that 33% of all equine
patients had intra-articular lesions related to OA
Tew and Hackett
randomly evaluated 72 equine
joints at necropsy and discovered that 35% of them
had evidence of grossly visible cartilage damage.
Not only is this degenerative disease found in dom-
estic horses, but it also occurs naturally in the
joints of wild horses
. Despite the huge economic
importance of joint disease and OA in horses, our
understanding of the pathophysiological mechanisms
involved in joint degeneration in this species is lim-
. Whether OA is a single disease or is caused
by several disorders with a similar ﬁnal common
pathway remains unclear
Equine and Comparative Exercise Physiology 1(4); 221 – 231 DOI: 10.1079/ECEP200428
qCAB International 2004
Aetiology of OA
OA, often referred to as degenerative joint disease
(DJD) in the horse, is characterized by deterioration
of articular cartilage, accompanied by changes in the
bone and soft tissues of the joint. The end stage of
OA results in a net loss of articular cartilage, causing
pain, deformity, loss of motion, and decreased func-
tion. Horses have naturally occurring OA, which is
similar to that of humans, and are often used as
models to investigate the pathogenesis and treatment
Synovial joints are the joints usually associated with
lameness in the horse. These joints have two major
functions: to enable movement and to transfer load.
Synovial joints consist of the articulating surfaces of
bone, covered by articular cartilage, secured by a
joint capsule and ligaments, and have a cavity contain-
ing synovial ﬂuid. Articular cartilage is an avascular
tissue, which serves as a shock absorber for bone
and has a frictionless surface bathed in synovial ﬂuid.
This tissue consists of sparsely scattered chondrocytes
(cartilage cells). The extracellular matrix (ECM) pro-
vides cartilage with its compressive strength and is pri-
marily composed of type II collagen and proteoglycans
(PGs). Collagen forms a ﬁbrous network giving carti-
lage its tensile strength. Large aggregating PGs (aggre-
cans), composed of a protein core with several
glycosaminoglycan (GAG) side-chains attached to it,
hydrate the collagen network and provide the tissue
with viscoelastic properties and the ability to resist
. When the joint capsule is
disrupted, proteolytic enzymes are secreted into the
synovial ﬂuid and can facilitate PG and collagen degra-
. In an attempt to repair structural changes
in the ECM, chondrocytes proliferate and stimulate
synthesis of these components. However, over time,
the metabolic activity of chondrocytes shifts towards
a state where the breakdown of matrix constituents
outweighs new matrix synthesis
, beginning the
gradual process of ECM degeneration and thus the
loss of articular cartilage.
Subchondral bone, the bone underlying the articular
cartilage, can also be affected by OA. Because it remo-
dels rapidly, subchondral bone is responsible for chan-
ging the shape and congruity of the joint. Mechanical
stimulation of subchondral bone often leads to
micro-damage, which may result in (1) normal remo-
delling; (2) excessive remodelling, leading to bone
sclerosis; or (3) accumulation of micro-damage, leading
to gross fracture
. Subchondral bone thickening is a
normal response in exercising horses. However, an
increase in the degree of subchondral bone sclerosis
corresponds to greater degrees of generalized OA in
joints (i.e. fetlock)
. Sclerosis of the subchondral
bone can lead to the development of chip fractures,
focal lesions of traumatic osteochondritis dissecans
and slab fractures. Articular cartilage covering sites of
subchondral bone sclerosis is predisposed to the devel-
opment of OA
Soft tissues of the joint include the intra-articular liga-
ments, joint capsule, menisci and synovial membrane.
Damage to intra-articular ligaments, which provide sup-
port for the joints and distribute normal surface stresses,
can stimulate an inﬂammatory response and change the
loading characteristics of the joint surface. An example
of this phenomenon is shown by mechanical instability
of the joint after transection of the cranial cruciate
ligament. This surgical procedure produces joint laxity,
loss of joint congruency, and abnormal cartilage
weight-bearing forces and trauma that can directly and
indirectly induce abnormal cartilage wear
17 – 20
erative joint disease often develops in humans following
. Increased stress across the knee joint
induced by performing surgical meniscectomy stimu-
lates OA in humans, rabbits and guinea pigs
18,21 – 23
Chronic disease of the equine joint capsule, capsulitis,
can lead to the formation of scar tissue and increased
stiffness, leading to instability of the joint by changing
its surface stresses
. Acute synovitis and capsulitis
may cause signiﬁcant clinical compromise of the joint,
and also contribute to the degenerative process by the
release of cytokines, inﬂammatory mediators and
. While the cause of acute primary synovitis
has never been determined, the development of an
acutely inﬂamed joint is prevalent in trained Thorough-
breds and Standardbreds
Molecules associated with OA
Interleukin (IL)-1 induces and augments the pathologi-
cal processes involved in inﬂammatory joint disease.
Morris et al. were the ﬁrst to identify IL-1 in the
equine osteoarthritic joint, and found that equine IL-1
has many of the characteristics of IL-1 isolated from
. IL-1 stimulates chondrocytes and syno-
vial cells to release enhanced amounts of prostaglandin
), PGs and matrix metalloproteinases (MMPs)
such as collagenases and stromelysin, and increases
nitric oxide (NO) production
. Stimulation by IL-1
creates an inﬂammatory response that is similar to natu-
rally occurring OA. As a result, IL-1 is often used to
stimulate an inﬂammatory response in chondrocytes.
Equine explants stimulated with IL-1 have demon-
strated an increase in the release of GAGs from the
29 – 32
. Decreased PG synthesis and increased
MMP-3 activity have been reported in equine explants
following stimulation with IL-1
, while recombinant
human interleukin-1b(rhIL-1b) induces the expression
of MMP-13 in equine chondrocytes in monolayer
culture and explants
. IL-1 also induces IL-6
AE Schlueter and MW Orth222
synthesis in human cartilage from normal controls,
patients with OA and patients with rheumatoid arthri-
. Increased PGE
and IL-6 concentrations were
found in the synovial ﬂuid of equine joints injected
. In a subsequent study by Simmons et al.
in which rhIL-1bwas injected into the metacarpopha-
langeal (MCP) joints of horses, an increased concen-
tration of IL-6 was also found
. Other interleukins,
such as IL-6, -8, -10 and -18, have been studied in
arthritic cartilage as well, although the link to OA is
not as clear for these cytokines as it is with IL-1.
Tumour necrosis factor-b(TNF-a) exerts many of
the same catabolic effects as IL-1 since it activates simi-
lar cell signalling pathways
. As an example, like IL-1
it upregulates both MMP-13 and ADAMTS (a disintegrin
and metalloproteinase with thrombospondin motif)
. In equine chondrocytes, it greatly
increased the gene expression of MMP-1, -3 and -13
while only mildly increasing the expression of tissue
inhibitor of MMP-1 (TIMP-1)
. Models of inﬂammation
in horses demonstrate an increase in TNF-a
TNF-aconcentrations in synovial ﬂuid are not con-
sidered reliable indicators of the severity of joint
damage in horses
Prostaglandins are widely distributed in the body and
mediate or modulate a variety of physiological and
pathophysiological processes in many organ systems
and tissues, including the haematopoietic, cardiovascu-
lar and reproductive systems. They are believed to
bind to receptors on the sensory nerve endings, pro-
moting the discharge of impulses and consequently
causing an increase in pain
Prostaglandins (primarily E group) are produced in
inﬂamed joints and can cause a decrease in the PG
content of the cartilage matrix
. Actions of PGE
joints include vasodilation, enhancement of pain per-
ception, degradation of PGs and inhibition of PG syn-
thesis from cartilage, bone demineralization and
promotion of plasminogen activator secretion.
Cyclooxygenase-2 (COX-2) is one of the rate-limiting
enzymes responsible for the production of PGE
from cell membrane phospholipids. IL-1 stimulates
the synthesis of PGE
, and increased concentrations
in affected joints suggest a causal link of this
inﬂammatory mediator to the pathophysiological
events of OA
. Equine synovial cells and chondro-
cytes increased PGE
production after stimulation
with recombinant equine interleukin-1b(reIL-1b) and
lipopolysaccharide (LPS). Exposure of equine synovial
explants to reIL-1benhanced expression of COX–2
In addition, equine articular cartilage explants incu-
bated with LPS or IL-1 had an increase of PGE
into the culture medium
. Signiﬁcantly higher
production has been reported in the medium
of explants originating from horses with moderate
OA, compared with normal joints
. The PGE
in the synovial ﬂuid of equine osteoarthritic joints was
increased relative to levels in asymptomatic joints
The generation of speciﬁc COX-2 inhibitors for joint
pain in humans demonstrates the signiﬁcance of inhi-
NO may also be involved in the pathogenesis of OA.
This uncharged free radical is released from various tis-
sues and cells, and is the product of a reaction between
L-arginine and oxygen. NO has one unpaired electron
and readily reacts with oxygen, superoxide radicals
and transition metals, which may generate further
. Stadler et al. ﬁrst showed
that articular chondrocytes have the ability to generate
large amounts of NO
. NO is a major component of the
inﬂammatory response, and may mediate the suppres-
sion of cartilage matrix synthesis occurring in response
to intra-articular cytokines
. NO activates MMPs
suppresses PG synthesis
and induces apoptosis in
human articular chondrocytes
. The death of chondro-
cytes from NO occurs under conditions where other
reactive oxygen species are generated
Although NO is generally thought to be an important
mediator of the inﬂammatory response, it may have an
anabolic function in inhibiting articular cartilage cata-
bolism. NO inhibited degradation of aggrecan in
equine explant cultures, suggesting that NO has an
anticatabolic role in PG degradation
. However, the
majority of research suggests that its overproduction
has negative consequences in horses. Explant cultures
of equine synovial membrane and articular cartilage
released signiﬁcantly higher amounts of NO when the
explants originated from horses with OA
et al. injected rhIL-1bintra-articularly into the MCP
joints of six horses, and measured nitric oxide synthase
(NOS) in the synovial ﬂuid of injected joints 6 h post
. Although the intensity and extent of
inﬂammation were signiﬁcantly greater in the IL-1b-
exposed specimens compared with healthy specimens,
no signiﬁcant increase in the inducible isoform of NOS
(iNOS) was found between the control joints and the
joints exposed to IL-1. However, this might not be
the case if different concentrations of IL-1 are tested.
Increased NO synthesis occurs in chondrocytes and
synoviocytes in response to LPS and IL-1 within a
48 h incubation period. In addition, LPS or IL-1 dramati-
cally increased NO synthesis relative to non-stimulated
controls in equine explants
. An NOS inhibitor pre-
vented cartilage degeneration in dogs with induced
. Thus, inhibiting or minimizing NO production
in the joints of horses would probably be beneﬁcial.
Although all classes of proteinases may be involved in
the degeneration of the ECM, the MMPs may play the
Equine osteoarthritis 223
pivotal role in cartilage destruction. These enzymes are
characterized by a requirement for Zn
in their active
site. Calcium is also required for the expression of full
activity but does not reside in the active site. Overall,
the MMPs are capable of degrading ECM components
such as collagen, aggrecan, link protein and cartilage
. This growing family of proteo-
lytic enzymes has been divided into four main classes:
collagenases (MMP-1, -8 and -13), gelatinases (MMP-2
and -9), stromelysins (MMP-3 and -10) and mem-
brane-type (MMP-14, -15 and -17). MMPs are inhibited
by a group of endogenously produced tissue inhibitors
MMP activity increases in equine osteoarthritic
. Speciﬁcally, MMP-2 and MMP-9 have been
found in synovial ﬂuid from diseased equine
. The activity of both of these MMPs was
upregulated in normal equine cartilage and synovial
ﬂuid following stimulation with IL-1b
. In fact, MMP-
9 in synovial ﬂuid could potentially be an indicator
of joint damage
. Stimulation of cartilage explants
with IL-1 also induced the synthesis of MMP-3 in
young and adult horses
. rhIL-1 and LPS stimulated
MMP-13 expression in equine chondrocytes and carti-
. An exciting area of research is the
development of assays to quantify the protein frag-
ments of type II collagen degradation by MMPs such
as MMP-13 in biological ﬂuids
Causes of OA
Cartilage damage due to trauma, impact injuries, abnor-
mal joint loading, excessive wear or as part of an ageing
process can lead to changes in the composition, struc-
ture and material properties of the tissue
changes can compromise cartilage function in the stren-
uous mechanical environment normally found in
weight-bearing joints. Regardless of the speciﬁc cause,
the initial injury is usually mechanical in nature, with
an imbalance between the load applied and the tissues’
capacity to withstand that load
. Trauma to the joint,
immobilization of the joint, poor conformation, impro-
per shoeing and age are often preliminary factors that
contribute to the onset of OA in the horse.
Trauma to the joint is believed to be the primary cause
of OA in the horse. Mackay-Smith
referred to use-
trauma, or trauma occurring from normal use of the
joint, as a percurrent factor of OA. Very strenuous
exercise injures articular cartilage by increasing ﬁbrilla-
tion of the cartilage and reducing PG content and qual-
ity. Cartilage no longer responds with improved
biomechanical properties, and overload results from
such factors as extensive and intensive exercise, fati-
gue, speed, and poor conformation or footing
example, a racehorse’s pace generates millions of
foot-pounds of force per mile, and the wear and tear
produced on the joints during a race can be severe
Also, in a rabbit trauma-induced model for studying
OA, regular exercise accelerated subchondral bone
thickening and cartilage damage after injury
could be a quite relevant model for the equine athlete.
Most lameness occurs in the forelimbs, because they
carry 60 – 65% of the horse’s weight and are subjected
to higher load rates than the hind limbs
74 – 76
. The hind
limbs propel the horse, while the forelimbs receive the
shock of landing. However, this may vary among breed
and performance event. Different areas of joints and
joint surfaces in both the forelimb and hind limb are
subjected to different types of loading, such as low-
level constant loading during weight-bearing, intermit-
tent loading during locomotion, and very high and
sudden loading during training or racing
carpal, fetlock, proximal interphalangeal and distal
intertarsal/tarsometatarsal joints are most frequently
affected by OA.
The fetlock joint of the foreleg has the largest
number of unique degenerative and traumatic lesions
of any limb joint in racing horses
. Brama et al.
graphically mapped contact areas and pressure distri-
butions on the proximal articular surface (PAS) of the
proximal phalanx (P1) under various clinically relevant
loading conditions in the forelimbs of 13 horses. These
authors found that certain areas of the PAS of the P1
are permanently loaded in the standing horse, and as
the load was increased to mimic the walk or trot, the
contact area enlarged in the dorsal, dorsolateral and
dorsomedial directions. The joint pressures in the con-
tinuously loaded central area of the equine fetlock joint
are relatively low in the standing horse, but may
increase up to six-fold when loads are applied that
can be expected during athletic performance.
Articular cartilage degeneration of the dorsal joint
margins of the carpal bones in racehorses may be the
direct result of trauma
. Repetitive exercise may
induce the replacement of normal subchondral bone
by sclerotic bone, therefore contributing to the patho-
genesis of OA. Research into the effects of exercise on
PG metabolism in the carpal joints has produced con-
ﬂicting results. Palmer et al.
assessed the relevance
of site and the inﬂuence of exercise on articular cartilage
PG synthesis and metabolism on third carpal articular
cartilage in 16 horses. PG synthesis was increased
in exercised horses relative to non-exercised horses at
the end of a 6-week period. However, the increase in
newly synthesized PG was not reﬂected in endogenous
PG within the matrix at different sites on the third
carpal bone. A signiﬁcant correlation of site on endogen-
ous PG was evident, with a greater concentration of PG
located in the palmar aspect of the radial facet compared
with the sites located on the dorsal aspect of the radial
AE Schlueter and MW Orth224
facet or all sites on the intermediate facet. Total PG con-
tent on sites of the middle carpal joint increased in
untrained Thoroughbreds with short-term exercise
PG content was greater at palmar sites overall, and
dorsal sites of the high-intensity trained group had 12%
higher PG compared with those of the low-intensity
trained group. A contradictory study to those previously
described evaluated the effect of strenuous versus
moderate exercise on the metabolism of PGs in the
articular cartilage from different weight-bearing regions
in the equine third carpal bone
. PG synthesis was
reduced in both exercise groups and greater PG loss
was found in the different joint regions of the strenu-
ously trained animals. No change in PG size or ability
to aggregate in different regions of any articular cartilage
site was found in this study. The differences in the
studies cited could be due to the use or non-use of seden-
tary controls and different exercise programmes. For
example, Palmer et al.
trained horses for 6 weeks,
Murray et al.
for 19 weeks, and Little et al.
weeks. The fact that the longest exercise programme
had decreased PG synthesis may be signiﬁcant.
Low-motion joints such as the proximal interphalan-
geal, distal intertarsal and tarsometatarsal are vulner-
able to the development of OA because they have a
relatively smaller area of joint surface that must sustain
the same weight-bearing load for a relatively longer
period of time during joint movement
. Both ring-
bone and bone spavin can produce crippling lameness
in horses. Although the aetiology of ring-bone and
bone spavin is undetermined, the cause could be
trauma to the periarticular soft tissues including the
joint capsule insertions and periosteum
Ring-bone is a term used to describe DJD of the
proximal and distal interphalangeal joint. This disorder
most commonly occurs in horses forced to make quick
turns and abrupt stops, such as Western performance
horses, polo ponies and jumpers
. Ellis and Green-
evaluated six cases of ring-bone in young Thor-
oughbreds ranging from the age of 3 months to 4
years. All cases except one had other pre-existing or
concurrent bone disease, which could have conse-
quently placed abnormal weight on the interphalan-
geal joint resulting in DJD. Ring-bone was the most
serious cause of wasting in Norwegian Do¨le horses
over 30 years ago
Bone spavin is the most common cause of hind-limb
lameness of athletic horses, and involves the distal
intertarsal, tarsometatarsal and occasionally the proxi-
mal intertarsal joints
76,86 – 88
. This degenerative dis-
order has been found in a variety of breeds including
Quarter Horses, Thoroughbreds, Standardbreds and
Icelandic horses. Wyn-Jones and May
horses and ponies for lameness due to bone spavin,
ﬁnding that 25 of the 30 horses were lame in both
hind legs and that lameness varied from slight to
severe. Twenty-three per cent of Icelandic horses eval-
uated radiographically (379 total) had signs of bone
spavin, suggesting a predisposition to the disease
Reduced loading or immobilization, due to lack of
exercise, can lead to atrophy or degeneration of articular
cartilage. While excessive forces may lead to articular
cartilage loss, removal of all mechanical stimulation
leads to atrophy. When cartilage is subjected to high-
pressure loads, PGs are compressed and water is
expressed from the cartilage
. Cartilage then expands
as it is rehydrated upon alleviation of pressure. Physio-
logical loading and motion are therefore essential to
maintain the normal nutrition and metabolism of articu-
lar cartilage provided by exchange with synovial ﬂuid.
Although several immobilization studies have been
conducted, few have been done on horses. An early
study investigating changes in the metabolism of PGs
in immobilized limbs of sheep showed a decrease in
GAG content of the non-load-bearing joint
. PGs iso-
lated from the immobilized limb were smaller than
those isolated from load-bearing joints. Instability of
the MCP joint was performed surgically in six horses
by transecting the collateral and lateral sesamoidean
. This procedure induced OA in all
horses, which resulted in lameness, increased joint cir-
cumference, decreased joint range of motion and
increased new synthesis of PG production. Horses
immobilized with ﬁbreglass casts from the proximal
portion of the metacarpus down to the hoof tended
to have lower hexosamine concentrations in articular
cartilage biopsied from their cast joints
. The contral-
ateral limbs of each horse served as a mobilized con-
trol, and the control articular cartilage tended to gain
hexosamine during the 30-day trial. These researchers
saw little change in GAG synthesis in the cast joints,
while the largest signiﬁcant change occurred in the
control. Similar results have been found in the
. Thus, contralateral limbs are unsuitable for
controls in immobilization studies because of their bio-
logical response to increased weight-bearing. Palmer
found a lower concentration of newly syn-
thesized PGs in non-exercised horses than in exercised
horses. Exercised horses had a noticeable increase in
the early PG peak of newly synthesized PGs, while
this did not occur in the sites of the non-exercised
group. Immobilization studies performed with canine
and rabbit limbs have indicated a depletion of PGs,
defective aggregation of PGs and accumulation of
water in the tissue
92 – 94
. These problems may be
reversed after remobilization.
Conformation is deﬁned by the physical appearance
and outline of a horse, which is dictated primarily
Equine osteoarthritis 225
by bone and muscle structures. Certain conformational
traits can predispose the horse to lameness. Confor-
mation defects such as ‘calf knees’, ‘knocked knees’
(carpus valgus), ‘bowed knees’ (carpus varus) and
‘bench knees’ cause the animal to load its carpus
abnormally, and OA can result
. In the rear legs,
horses that are extremely straight in angulation of
the stiﬂe and hock, or are obviously sickle- or
cow-hocked, are predisposed to conformationally
. Certain breeds’ characteristic con-
formation magniﬁes their risk of developing OA. For
example, Icelandic horses with sickle hocks had a
prevalence of radiographic signs of bone spavin of
42%, which was signiﬁcantly higher than that of
horses with straight (20%) or normal (19%) confor-
. In addition, the prevalence of bone spavin
was 19% in horses with a light skeletal type, whereas
lesions were identiﬁed in 23% of those with intermedi-
ate and in 24% of those with heavy skeletal type. A
more recent study conﬁrmed this ﬁnding, and indi-
cated that the prevalence of radiographic signs of
DJD in the distal tarsus of Icelandic horses increased
in horses with a smaller tarsal angle
. Upright pas-
terns, base-narrow front limbs and a rectangular-
shaped P1 in the Norwegian Do¨le horse are confor-
mation defects that contributed to the development
. Quarter Horses can be prone to OA
because they have a relatively large body mass,
poor carpal conformation, small feet and short upright
Since the hoof capsule is malleable, the manner in
which it is trimmed and shod can have a marked
effect on the performance and soundness of the
equine athlete. The hoof of the horse must be
balanced to absorb high-impact vibrations when it is
exposed to the repetitive trauma incurred during per-
formance events and normal use. Maximum energy dis-
sipation depends on proper hoof preparation and
. Good shoeing is an art and maintenance
of the natural angle and balance of the hoof is critical.
Improper shoeing can change the limb conﬁgur-
ation of the horse, resulting in a modiﬁcation of the
forces placed on the joint surfaces
. Increased abnor-
mal wear and loading on the joint surface due to
improper shoeing can contribute to degeneration
of articular cartilage. The typical long toe/low heel
conformation commonly seen in Thoroughbred race-
horses can accentuate hyperextension-type injuries in
the fetlock and carpus and cause direct injury to the
foot in the form of OA in the distal interphalangeal
Corrective trimming and shoeing alters the hoof
shape or angle to affect stance or stride and breakover,
in order to help the horse achieve a more normal
movement. Altered foot orientation, which could
result from trimming and shoeing, inﬂuences intra-
articular pressure in the articular contact area of the
. When a hoof is being actively re-formed,
the change in shape during one trimming may be dra-
matic. Types of shoes and shoeing devices can alter the
traction of the hoof. For instance, sliding plates and
wide web shoes are often used on reining horses.
These types of shoe provide inadequate traction for
the horse, and can result in strained tendons or
sprained ligaments. Traction devices, such as toe
grabs, heel calks and borium, can provide too much
traction. Excess torque on the limb and joints resulting
from using these devices can lead to strain or sprain
and may contribute to the development of OA.
Horses shod with hoof caulks had altered joint
angles, which could change the forces placed on the
joint surfaces or the soft tissue structures in the
. A study evaluating the effects of shoeing
horses with wedges (angle 3.7 and 58) showed that an
increased elevation of the heel delayed unloading of
the heel and an increased elevation of the toe
. These results suggest that the
horse does not compensate for an acute foot imbalance
by redistributing the load under the foot. Increased
joint pressure has been implicated in the progression
.Anin vitro study evaluating the intra-articu-
lar pressure in the DIP joint showed that elevating the
heels by 58signiﬁcantly increased DIP pressure
Advancing age is the most signiﬁcant risk factor for OA
in humans. In horses, however, OA is known to
develop in animals as young as 2 years of age. Young
performance horses are most likely to develop OA
early in life, because of the emphasis on racing and
showing young horses in futurities and other events.
Training horses at a young age may precipitate
damage to joints unable to withstand the extreme
forces they are subjected to during training and com-
. Racing and training may accelerate the
naturally occurring age-related changes. In addition,
some horses may be genetically predisposed to devel-
oping OA due to either age or training, while other
horses may never be prone to the disease
Pathological and arthroscopic examinations have
shown that OA is commonly observed in the joints
of older horses
and in speciﬁc locations
within a joint
. Naturally occurring OA also becomes
more severe with age in untrained wild horses
Increased severity of lesions is correlated with sub-
chondral bone sclerosis and ossicles with increasing
age. Age is also a signiﬁcant cause for the prevalence
of OA in Icelandic horses
. Many studies have
described surgical treatment of horses diagnosed with
OA ranging from the age of 1 year up to the age of 21.
AE Schlueter and MW Orth226
Similar to humans, as the horse ages, the biochemi-
cal properties of articular cartilage change. Several
recent studies have investigated the effect of age on
the biochemical characteristics of equine articular
cartilage. Variations in biochemical characteristics of
cartilage in relation to site and age showed no
signiﬁcant change in cartilage collagen between
horses ranging from 4 to 30 years old, but indicated
that non-enzymatic cross-linking was higher in older
horses and was linearly related to age
. A steady
increase in pentosidine cross-linking increased with
age from 5 years onward, resulting in a 10-fold increase
up to the age of 30 years. Cross-linking of articular car-
tilage by non-enzymatic glycation is expected to result
in stiffer, more brittle tissue that is more vulnerable to
damage by mechanical loading. Non-enzymatic cross-
linking during ageing may predispose older horses to
development of OA.
The biochemical characteristics of articular cartilage
in mature cartilage differ from those of immature carti-
lage at different sites on the joint surface. No signiﬁ-
cant differences in water content and
hydroxylysylpyridinoline cross-links were found at
two different sites of the MCP joint in neonatal, 5-
month-old and 1-year-old horses. However, differences
in DNA, GAG, collagen and hydroxylysine content
between sites paralleled those shown in the mature
. In a more recent study, the same researchers
investigated the inﬂuences of age and exercise on the
biochemical characteristics of articular cartilage
Neonatal foals showed no site-speciﬁc biochemical het-
erogeneity, in contrast to mature horses. The process
of formation of site differences was almost completed
in exercised foals at age 5 months, but was delayed in
those deprived of exercise. They concluded that the
functional adaptation of articular cartilage to mechan-
ical loading occurs during the ﬁrst 5 months postpar-
tum, and that a certain amount of exercise is
required to sustain this adaptation. Joints of horses
less than 2 years of age had signiﬁcantly higher cell
numbers, total collagen and DNA content, and lower
PG content, relative to mature horses ranging in age
from 2 to 20 years old
. No signiﬁcant difference in
these measurements was found within the mature
age groups. Another study has reported no signiﬁcant
difference in collagen or GAG content in cartilage
derived from horses aged 2 – 5 years
Chondroitin sulphate (CS), the most abundant GAG
in aggrecan, and keratan sulphate (KS), the most
widely distributed GAG in aggrecan, have both been
reported to change with age. The sulphation patterns
in CS chains affect the speciﬁc properties and func-
tions of these molecules. Cartilage degeneration in
the MCP joints of racehorses was accompanied by
deposition of CS chains with altered sulphation pat-
. Six-sulphation of internal and terminal CS
residues increased with age. The same phenomenon
has been reported in human studies
High KS concentrations were reported in foals from
1 week after birth to 3 months of age
. These values
decreased rapidly from 3 to 5 months, and gradually
reached adult values between the ages of 5 and 18
months. This pattern also has been reported in chil-
. Todhunter et al.
had a simi-
lar ﬁnding, and reported a signiﬁcant relationship
between age of foals and plasma KS concentration.
Mean plasma KS concentration peaked when foals
were 10 weeks old. Age affected KS concentration in
the synovial ﬂuid of 32 clinically normal horses. How-
ever, no signiﬁcant effect of age on plasma KS concen-
tration was seen in normal adult horses with a mean
age of 65 months. An earlier study also reported no
age-related changes in synovial ﬂuid KS concentrations
in mature horses ranging in age from 8 to 30 years
Based on explant studies, ageing equine cartilage is
not as sensitive to stimulation of PG synthesis by link
. In humans, the concentration of osteo-
genic protein-1, a growth factor found in cartilage,
decreases dramatically with age
. Thus, although
some gross measurements might stay relatively con-
stant, subtle changes in the metabolism of chondro-
cytes over time may facilitate degenerative changes.
The focus of this brief review was to provide updated
information concerning equine OA and factors associ-
ated with it. Exercise is essential to the horse’s well-
being. Although we do not know unequivocally how
to prevent OA, our molecular understanding of it and
how to monitor it are improving quickly. In the near
future, intensive research efforts should identify
better markers for monitoring cartilage loss and pro-
vide more information regarding how chondrocytes
adapt to stress and ageing. Using relatively non-inva-
sive measures to monitor the effects of training regi-
mens and management on joint health should
facilitate the care of the equine athlete. This strategy
is currently being used to monitor bone health in
horses under various conditions
119 – 122
chondroprotective nutraceuticals, diagnostic tools
and therapeutic strategies will improve and expand.
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