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

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  • *D/M/L = distal, medial, lateral
  • *OL/OM = osteochondrosislatens/osteochondrosismanifesta
  • *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).
  • Osteochondrosis

    1. 1. OsteochondrosisRustin Bodiker Valerie CarrilRob Bovino Katie CerulliHeather Byrnes Elena ChatcuffNin Cameron- Will ChildressBlake Brendan CloonanOmega Cantrell
    2. 2. Why did we choose thispaper? 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. 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. 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. 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. 6. Lesions (cont’d) Typically focal ◦ If presenting as multifocal lesions, they are often bilaterally symmetrical
    7. 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. 8. Proposed etiologies Rapid growth Heredity Anatomic characteristics Trauma Dietary imbalances Defect in vascular supply to epiphyseal cartilage
    9. 9. Causal diagram of etiologic factors
    10. 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. 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. 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. 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. 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. 15. Conclusions (etiologiccontributors) 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. 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. 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. 19. Ischemic necrosis of growthcartilage 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. 20. Ischemic necrosis of growthcartilage (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. 21. 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
    22. 22. 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)
    23. 23. 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