Mini-Symposium: Osteochondrosis
Current Understanding of the Pathogenesis and Risk Factors
Stina Ekman, DVM, PhD, Diplomate of ECVP
Department of Biomedicine and Veterinary Public Health, Swedish University of Agricultural
Sciences, Uppsala, Swede, (stina.ekman@slu.se)
Osteochondrosis (OC) is a common skeletal disease in domestic animals and has also been
reported in humans. OC is seen in predilection sites that are variable among species.
It is defined as a disease of growth cartilage that causes focal failure in endochondral
ossification. The pathogenesis of OC involves vascular failure leading to necrosis of growth
cartilage, focal ossification failure and, later, osteochondral fragmentation (OCD). It is
suggested that the vascular failure is influenced by local dynamic processes within the joints.
Repeated and/or high mechanical load on the articular cartilage and the underlying growth
cartilage may cause vascular damage which results in ischemia and subsequent
chondronecrosis1.
It is important to keep in mind that OC is a dynamic process that changes morphologically
with time. The early changes will not cause any pain and, thus, cause no clinical signs. The
chronic form of OC – OCD, however, includes secondary joint inflammation causing pain and
discomfort that is accompanied by lameness.
The early characteristic lesion of OC is a focal area of necrotic epiphyseal growth cartilage,
adjacent to non-perfused necrotic vessels, within a cartilage canal2, 3, 4. These early lesions,
caused by local ischemia to epiphyseal cartilage of the articular/epiphyseal cartilage (AEC)complex, are strikingly similar in different species, suggesting a common pathogenesis. This
early lesion, defined as OC latens, can develop into OC manifesta1, which is seen as cartilage
retention due to focal failure of the endochondral ossification. The necrotic cartilage fails to
undergo mineralization or vascular penetration and is subsequently surrounded by normal
growth cartilage undergoing ossification; hence retention of dead cartilage is seen in the
subchondral bone.
Local ischemia of epiphyseal cartilage secondary to impaired blood supply from cartilage
canals vessels is the key factor in the initiation of OC and explains many of the different
features of the OC process. These include the development of the disease during skeletal
growth, primary involvement of epiphyseal but not articular cartilage, and the fact that lesions
are seen in multiple and predictable focal locations that may vary among species. For
example, the predilection site in the stifle joint is the lateral femoral trochlea in the horse,
whereas the medial femoral condyle is affected in the pig. These predilection site differences
may reflect variation in mechanical load within the stifle of these two species. Because
cartilage canal blood vessels only are present in epiphyseal cartilage during a limited period
of time during growth, the early/subclinical lesions of OC can only develop during a narrow
window of time in growing animals, during which the epiphyseal cartilage is dependent on
this blood supply. Clinical signs due to osteochondral fragmentation may, however, be
evident in adults.
The vessels in the cartilage canals of the growth cartilages are more vulnerable to load and
prone to compression when the canals cross between bone and cartilage3. Also mechanical
loading of the overlying articular cartilage can cause cleft formation with osteochondral
fragmentation i.e. osteochondritis dissecans (OCD) causing joint pain with clinical signs and
eventual osteoarthritis. Environmental and genetic factors are involved in the pathogenesis of
OC, and the disease is considered having a multifactorial etiology1. Frequent repeated micro
trauma to cartilage canals and later to necrotic areas of epiphyseal growth cartilage can occur
as a result of joint conformation with more mechanical load to certain areas within the joint.
Also, animal weight (growth rate), conformation (joint shape) as well as environmental
factors such as fighting, obstacles (e.g. high stair steps), and transportation by truck may
increase mechanical loading of the joints. Mechanical load is most likely a key factor in both
the early ischemic event5 and the later development of an osteochondral flap (OCD).
References:
1. Ytrehus B, Carlson CS, Ekman S. Review Article: Etiology and pathogenesis on
2.
3.
4.
5.
osteochondrosis. Vet Pathol 44: 429-448, 2007.
Ytrehus B, Ekman S, Carlson CS, Teige J, Reinholt FP. Focal changes in blood supply during
normal epiphyseal growth are central in the pathogenesis of osteochondrosis in pigs. Bone
35:1294-1306, 2004.
Olstad K, Ytrehus B, Ekman S, Carlson CS, Dolvik NI . Epiphyseal cartilage canal blood
supply to tarsus of foals and relationship to osteochondrosis. Equine Vet J 40:30-39, 2008.
Olstad K, Ytrehus B, Ekman S, Carlson CS, Dolvik NI. Early lesions of osteochondrosis in the
distal tibia in foals. J Orthop. Res. 25:1094-1105, 2007.
Björnar Ytrehus B, Carlson CS, Lundeheim N. Mathisen L, Reinholt FP, Teige J, Ekman, S.
Vascularisation and osteochondrosis of the epiphyseal growth cartilage of the distal femur in
pigs – development with age, growth rate, weight and joint shape. Bone 34:454-465, 2004.