Group presentation on osteochondrosis for pathology II (VPA 5443) at RUSVM.

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