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Osteochondrosis
Rustin Bodiker   Valerie Carril
Rob Bovino       Katie Cerulli
Heather Byrnes   Elena Chatcuff
Nin Cameron-     Will Childress
Blake            Brendan Cloonan
Omega Cantrell
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.
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
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
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
Lesions (cont’d)
   Typically focal
    ◦ If presenting as multifocal lesions, they
      are often bilaterally symmetrical
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
Proposed etiologies
 Rapid growth
 Heredity
 Anatomic characteristics
 Trauma
 Dietary imbalances
 Defect in vascular supply to
  epiphyseal cartilage
Causal diagram of etiologic factors
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
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)
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
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
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
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
MODELS OF
PATHOGENESIS
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
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
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
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
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
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)
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

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Osteochondrosis

  • 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
  • 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
  • 21.
  • 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

Editor's Notes

  1. *D/M/L = distal, medial, lateral
  2. *OL/OM = osteochondrosislatens/osteochondrosismanifesta
  3. *Faulty joint conformation is an inherited anatomic factor, but mechanical stress can reveal the problem (and thereby appears to be the cause of the issue, but is not the primary cause)Likewise, trauma or infection in a growing epiphysis may alter blood supply in the affected area, and can potentially cause ischemic necrosis. This can occur anywhere in the body (not just predilection sites), but when it occurs during a critical period of time (i.e., 8-13 weeks in pigs), it accounts for the development of osteochondrosis in these animals later in life.Trauma itself is not a major etiologic contributor to the initiation of osteochondrosis, but may cause progression of osteochondrosismanifesta (OM) to osteochondrosisdissecans (OD). Likewise, increased body weight will promote the progression of osteochondrosis to osteoarthritis due to increased joint stress. On an already weakened joint, this can be traumatic and exacerbates the underlying problem(s).