Osteochondrosis is a common joint disorder seen in many animal species that is caused by a failure of blood supply to growing cartilage. It occurs in focal areas of cartilage and bone, especially in weight bearing joints. While factors like heredity, rapid growth, anatomy and trauma may play a role, current evidence suggests the primary cause is ischemic necrosis of vessels in cartilage canals during adolescence. This leads to necrosis of cartilage that later fails to properly ossify. Prophylactic measures should focus on this growth period when vulnerable blood vessels are present.

1. Osteochondrosis
Rustin Bodiker Valerie Carril
Rob Bovino Katie Cerulli
Heather Byrnes Elena Chatcuff
Nin Cameron- Will Childress
Blake Brendan Cloonan
Omega Cantrell

2. Why did we choose this
paper?
 Osteochondrosis is a common
disorder that we are all likely to
encounter as practicing veterinarians
 The large scope of animals used helps
to encompass various career paths
our fellow students may consider.

3. What is osteochondrosis?
 Joint disorder
◦ “Focal disturbance of enchondral
ossification”
◦ Can be articular or physeal
 Affects multiple animal species
◦ Most commonly pigs, horses and dogs
◦ Can also be seen in cattle, cats and rats
 Multifactorial etiology
◦ Commonly cited possibilities include
heredity, rapid growth, anatomic
conformation, trauma and dietary imbalances
◦ Most likely cause is failure of blood
supply to growing cartilage

4. Stages of osteochondrosis
 Designated using modifiers
◦ Osteochondrosis latens
 Focal area of cartilage necrosis confined to
epiphyseal cartilage
◦ Osteochondrosis manifesta
 Focal failure of enchondral ossification visible
on both macroscopic and radiographic
examination
◦ Osteochondrosis dissecans
 Indicates formation of a fissure in necrotic
cartilage, extending through articular cartilage

5. Lesions
 Principle lesion is focal failure of enchondral
ossification
 Many similarities
◦ Age distribution, radiographic and macroscopic
appearance
◦ Location
 D/M/L femoral condyles
 M aspect of trochlea of talus
 D condyle of humerus
 Articular-epiphyseal cartilage lesion
◦ Characterized by cartilagenous necrosis
 Physeal plate lesion
◦ Characterized by persistence of chondrocytes with
hypertrophic morphology

6. Lesions (cont’d)
 Typically focal
◦ If presenting as multifocal lesions, they
are often bilaterally symmetrical

7. Lesions: appearance
 Pigs
◦ Commonly observed by 2 months of age
 Clinical signs of lameness most prevalent at 4-18
months
 Dogs
◦ Medium-/large-sized breeds more commonly
affected
◦ Males affected more often than females
◦ Lesions at specific sites occur at greater
frequencies in certain breeds
 Horses
◦ Frequent cause of lameness in young
athletes

8. Proposed etiologies
 Rapid growth
 Heredity
 Anatomic characteristics
 Trauma
 Dietary imbalances
 Defect in vascular supply to
epiphyseal cartilage

9. Causal diagram of etiologic factors

10. Rapid growth
 Originally thought to be related to
increased growth rate/overnutrition
◦ However, most published studies fail to
definitively prove these have a direct role
in development of osteochonrosis

11. Heredity
 Important heritable factor in pigs may
be anatomic conformation
 In horses, thought to be inherited as a
polygenetic trait, similar in dogs
 Compelling evidence seen in all
species tested, especially in relation to
late-stages of disease
(Osteochondrosis dissecans)

12. Anatomic characteristics
 Hereditary factors: exterior
conformation, joint shapes and lesions
◦ Implementation of selection based on
“better” joint shape/conformation in one
pig breeding system reduced incidence of
OD in stifle joint (from 6.7% to 1.5%)
◦ Repeat microtraumas to joints are
important factors

13. Trauma
 Areas of local biomechanical stress are
predilection sites in all species affected
◦ Increased stress (e.g., athletic activity) seems to
increase prevalence/severity of macroscopic
lesions
 Onset of clinical signs likely brought on by
trauma
◦ Usually minor, or not severe enough to cause
disease in a normal joint
◦ Major trauma may cause osteochondral fractures
 No clear evidence to support major trauma as
having a role in initiation of primary lesions
◦ Trauma alone also does not explain predilection
and bilateral symmetry of lesions

14. Dietary factors
 High vitamin D3 diet may cause
severe lesions in dogs
 Copper deficiency associated with
articular osteochondrosis
◦ In deer, bison, horses
◦ Caused by primary Cu deficiency or
exposure to factors that inhibit Cu
absorption/metabolism

15. Conclusions (etiologic
contributors)
 Strong evidence for heredity/anatomic
characteristics as etiological agents
for disease
◦ Includes exterior conformation, joint
shape
 Little/no evidence to support rapid
growth, major trauma, dietary factors
as primary causes

16. MODELS OF
PATHOGENESIS

17. Primary dyschondroplasia
 Early changes
◦ Dyschondroplasia (abnormality of chondrocyte
development and maturation)
 Leads to multifocally altered enchondral ossification
◦ Change in chondrocytic phenotype
 Causes alterations in matrix synthesis/assembly
 May be secondary to ischemia induced by necrosis of
vascular channels
 Primary lesions resist ossification  retained
cartilage  susceptible to damage
 However, no morphological evidence for this
theory
◦ Fails to account for predilection sites, bilateral
symmetry

18. Necrosis of subchondral bone
 May be caused by traumatic damage
to bone’s vascular supply
◦ Thought to be caused by formation of
osteocartilaginous flaps
 Not fully supported by current
literature

19. Ischemic necrosis of growth
cartilage
 Early (subclinical) lesions of
spontaneously occurring OL/OM in
pigs
◦ Characterized by areas of
chondronecrosis closely associated with
necrotic, non-perfused vessels in cartilage
canals
◦ Occur in highly predictable, age-
dependent locations
◦ Directly related to loss of vascular supply

20. Ischemic necrosis of growth
cartilage (con’t)
 Naturally occurring osteochondrosis may
be a consequence of necrosis to
cartilage canals
◦ Affects entire canal distal from point of
necrosis  primary lesion at cartilage-bone
interface
 In pigs, areas of articular-epiphyseal
cartilage of distal femur sustain a shift in
blood supply
◦ Loss of cartilage canal blood supply is a
result of damage to certain vessels that exist
only in animals 8-13 weeks

22. Conclusions
 Necrosis of cartilage canal vessels
initiated by vascular disturbance
during specified age window
◦ 8-13 weeks for vessels in distal femur of
pigs
 Hereditary/anatomic factors are most
important etiologic agents to
pathogenesis
◦ Other associated etiological agents can
reveal or exacerbate these issues

23. Conclusions
 Prophylactic measures
◦ Should be done in period of growth when
epiphyseal cartilage is being supplied by
vulnerable blood vessels
 Varies between species/site, but is always
during adolescence (EC becomes avascular
prior to adulthood)

24. References
 Ytrehus, B., C.S. Carlson, S. Ekman.
(2007). Etiology and Pathogenesis of
Osteochondrosis. Veterinary Pathology.
44 (4), 429-448.
 Lecocq, M., Girard, C.
A., Fogarty, U., Beauchamp, G., Richard,
H. and Laverty, S. (2008), Cartilage
matrix changes in the developing
epiphysis: Early events on the pathway
to equine osteochondrosis?. Equine
Veterinary Journal, 40: 442–454.
doi: 10.2746/042516408X297453