Mini-Symposium: Osteochondrosis
CT and Micro-CT Investigations of Induced and Naturally Occurring Disease
Kristin Olstad, BVSc, PhD, CertVR
Norwegian School of Veterinary Science, Companion Animal Clinical Sciences, Equine Section,
Oslo, Norway (kristin.olstad@nvh.no)
Introduction
Investigation of early osteochondrosis lesions by micro-computed tomography (micro-CT) was
first carried out in samples from horse joints1. To provide background information and context,
the results will be presented by examining the following questions:
1. What are the clinical characteristics of osteochondrosis in horses?
2. Is the pathogenesis of osteochondrosis the same in horses as in other species?
3. Is it possible to detect early lesions of osteochondrosis in micro-CT scans, and if so; what new
information is gained?
4. Can the results of micro-CT be extrapolated to conventional CT scanning?
5. How can the results be used to further understanding of the pathogenesis and improve
diagnosis and management of osteochondrosis?
1. What Are the Clinical Characteristics of Osteochondrosis in Horses?
-Osteochondrosis in horses is, as in other species2, defined as a focal disturbance/delay in the
process of enchondral ossification3. Articular osteochondrosis in horses has been associated with
pathological fracture and the formation of hinged flaps or free-floating fragments within joints,
known as osteochondrosis dissecans (OCD), or infolding and subchondral bone cyst formation4.
-Horses diagnosed with osteochondrosis are typically young and of large horse breeds rather than
of pony breeds5. A heritable predisposition has been documented6. Horses with osteochondrosis
may therefore be the offspring of affected parents. When representative populations are screened,
gender predilection is not detectable6. A predilection has, however, been noted in that there is
variation between different horse breeds in terms of which joints are most frequently affected7.
-Horses with osteochondrosis may be asymptomatic, or present with joint effusion and lameness5.
In more than 50 % of cases, the disease affects multiple, and then often bilaterally symmetrical
pairs of joints simultaneously5.
-Diagnosis is by clinical, lameness, diagnostic analgesic and imaging examination. In
radiographs, changes tend to be located at one or more specific, recognized predilection sites
within the joint5. Radiographic changes have been followed longitudinally, and joint-specific age
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thresholds for the development and potential spontaneous resolution of changes are therefore
known8.
-Treatment is conservative or surgical. Prognosis following surgical removal of OCD fragments
is good in distal limb joints9. Prognosis in proximal limb joints is poorer5, and advanced
techniques for articular cartilage repair have therefore been attempted.
The clinical characteristics help define the disease, and should be remembered when considering
hypotheses for the pathogenesis of osteochondrosis.
2. Is the Pathogenesis of Osteochondrosis the Same in Horses as in Other Species?
The pathogenesis of osteochondrosis has been investigated most extensively in the pig and the
horse. In both species, the pathogenesis has been pursued through histological examination of
material from predilection sites prior to or during the time window when lesions are known to
develop. In horses, changes observed in such histological sentinel studies have been interpreted
in diverging directions, leading to relatively more confusion surrounding the pathogenesis of
osteochondrosis in horses, compared to in pigs.
To illustrate this, some of the major histological sentinel studies and resultant interpretations of
the pathogenesis of equine osteochondrosis may be listed chronologically, as follows:
-Pool, 198610: shear forces along the osteochondral junction disrupt capillary arcades traversing
it, leading to chondrocyte necrosis and delayed ossification, i.e. osteochondrosis.
-Carlson, 199511: focal failure of cartilage canal blood vessels leads to ischemic necrosis of
epiphyseal growth cartilage, delayed ossification and osteochondrosis.
-Grøndahl, 199612: OCD fragments represent randomly occurring accessory centers of
ossification.
-Henson, 199713 and Shingleton, 199714: accumulations of small, undifferentiated chondrocytes
are observed at predilection sites and osteochondrosis therefore represents primary
dyschondroplasia.
-Laverty, 200215 and Lecocq, 200816: changes in extra-cellular matrix staining/composition are
observed at predilection sites, thus osteochondrosis may represent a primary disorder of matrix
metabolism.
From 2007 onwards, the pathogenesis of equine osteochondrosis was re-examined in light of
new studies in piglets17. As discussed below, the results potentially unify the observations of
Pool, Carlson, Grøndahl, Laverty and Lecocq in a single pathogenetic hypothesis.
Arterial perfusion studies of cartilage canals within the epiphyseal growth cartilage of the
hock18, stifle19 and fetlock20 joints of a group of Standardbred foals confirmed that:
-Cartilage canals are present within the growth cartilage during the time window when lesions
are known to develop.
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-The canals are blind-ending and the vascular arrangement within them is glomerular, i.e. an
arteriole, its capillary bed and one or more venules course into and out of the growth cartilage
through one and the same canal, as in piglets21.
-Canals regress with increasing age through the physiological process of chondrification, and
through incorporation into the advancing ossification front, as in piglets21.
-During incorporation, vessels within cartilage canals anastomose with vessels in subchondral
bone and shift from their original perichondrial to a subchondrally located arterial source, as in
piglets17.
During repetition of histological sentinel studies, morphologically identical early lesions were
detected at predilection sites for osteochondrosis in the hock22 and stifle23. The lesions comprised
areas of chondrocyte necrosis, centered on necrotic cartilage canals, thus were compatible with
ischemic chondronecrosis and indistinguishable from osteochondrosis latens in piglets21. In both
piglets17 and foals18, the majority of lesions were located distal to a point where cartilage canal
vessels had recently been incorporated into subchondral bone. Although the exact etiology of the
vascular failure remains to be determined, the morphology of the lesions suggests that vessels are
particularly vulnerable to failure during the process of incorporation and anastomosis with
vessels in the subchondral bone17, 18.
Finally, the hypothesis of ischemic chondronecrosis as a pathogenetic mechanism for
osteochondrosis was tested through experimental induction of lesions, by surgical transection
of cartilage canal vessels supplying the epiphyseal growth cartilage of the lateral trochlear ridge
of the distal femur in a group of pony foals24. Vascular transection consistently resulted in
ischemic chondronecrosis, as previously shown in piglets25, 26. Some time after vessel transection,
the induced lesions were associated with a change in matrix staining, indicating that altered
matrix metabolism15, 16 is indeed a secondary consequence of primary ischemic chondronecrosis.
Areas of ischemic chondronecrosis were associated with a focal delay in enchondral ossification
from 21 days after vessel transection. Pathological fracture through an area of ischemic
chondronecrosis produced a hinged OCD flap in one foal, examined 42 days after surgery.
Collectively, the arterial perfusion, histological sentinel and experimentally induced lesion
studies firmly support the conclusions that:
-Osteochondrosis in horses arises through a pathogenetic mechanism of focal failure of cartilage
canal vessels, followed by ischemic chondronecrosis.
-The pathogenesis of osteochondrosis in horses is identical to the pathogenesis of
osteochondrosis in pigs.
3. Is it Possible to Detect Early Lesions of Osteochondrosis in Micro-CT Scans,
and if so; What New Information is Gained?
Cartilage-bone blocks from the tarsus of foals underwent micro-CT scanning1. The blocks
originated from the material of the aforementioned perfusion studies, thus contained permanent
barium arterial angiograms18. Micro-CT scans were viewed as multi-planar, two-dimensional
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images and as three-dimensional (3D) volume-rendered models. After scanning, blocks were
processed for histological examination.
In 3D models, early lesions were indirectly detectable as a focal absence of arterial contrast
columns. The contrast columns were observed to terminate immediately below the ossification
front, indicating that failure occurred at the point where the vessels were obliged to traverse the
ossification front following incorporation into subchondral bone17, 18.
In histological sections, lesions of ischemic chondronecrosis were associated with proliferation
of chondrocytes and cartilage canals within the adjacent, viable cartilage. Cartilage-bone blocks
were scanned before the tissue had been decalcified for sectioning. In micro-CT scans, it was
apparent that some proliferating vessels were surrounded by focal mineral opacity, compatible
with formation of separate centers of enchondral ossification. This confirms that ossification
centers occur, but represent secondary change rather than the primary disease process in
osteochondrosis 12.
In histological sections, osteoblast-like cells surrounded by osteoid-like material were present
within lesion-associated granulation tissue. Separate centers of enchondral ossification and intramembranous ossification of granulation tissue potentially explain how radiolucent defects
sometimes proceed to fill with bone opacity, i.e. undergo spontaneous resolution 8.
Early lesions of osteochondrosis were detectable in micro-CT scans. The results indicated that
failure occurred at the point where vessels traversed the ossification front, and that separate
centers of ossification may form in response to primary lesions of ischemic chondronecrosis.
4. Can the Results of Micro-CT be Extrapolated to Conventional CT Scanning?
Extrapolation of the results of micro-CT to conventional CT examination was carried out in two
stages:
-Firstly, the distal femur of pony foals with surgically induced lesions of osteochondrosis were
examined pseudo-longitudinally, i.e. by sampling different individuals at increasing time
intervals, ex vivo by micro-CT and conventional CT 27.
-Secondly, the distal femur of a cohort of hereditarily osteochondrosis-predisposed piglets was
serially scanned from 2-8 times at biweekly intervals with conventional CT, initially in vivo
under general anesthesia, but then ex vivo and coupled with post mortem examination at the last
interval for each piglet (unpublished data).
The pony femurs were normal except for the induced lesions, whereas the pig femurs contained a
range of naturally occurring skeletal lesions, including osteochondrosis.
In both studies, areas of ischemic chondronecrosis and associated delayed enchondral
ossification in histological sections corresponded to focal, radiolucent subchondral bone defects
in CT scans. Eighty-two percent of the histologically validated piglet osteochondrosis lesions
comprised multiple radiolucent lobes; a geometry that was not observed in association with other
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skeletal lesions and may prove pathognomonic for osteochondrosis in the distal femur of this
species (unpublished data).
More complete information on the correlation of histological changes with changes observed in
CT scans will be provided during the presentation associated with this abstract. Collectively, the
two studies provide a basis for the identification of early lesions of osteochondrosis by CT
examination of piglets and foals.
5. How Can the Results be Used to Further Understanding of the Pathogenesis and
Improve Diagnosis and Management of Osteochondrosis?
Suggestions for how the results can, will and already have been implemented (unpublished data)
in the management of osteochondrosis will be given in the presentation associated with this
abstract.
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