Bovis ISSN 2398-2993

Osteochondrosis

Synonym(s): OCD, Osteochondritis dissecans

Contributor(s): Sophie Mahendran , Paul Wood

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Introduction

  • A skeletal disorder of growing calves that affects the physis or articular-epiphyseal cartilage complex.
  • Cause: defective endochondral ossification + accelerated growth rate.
    • Cartilage canal blood vessel necrosis theory.
    • Damage to cartilage and subchondral bone, causing osteochondritis dissecans, osteochondral fragments or subchondral bone cysts.
  • Signs: lameness, effusion; sites affected:
    • Stifle (femoropatellar joint: lateral and medial trochlear ridges of the femur, lateral facet of patella, medial femoral condyle).
    • Tarsus (tarsocrural joint: distal intermediate ridge of the tibia, lateral and medial trochlear ridges of talus, medial malleolus of tibia, central and third tarsal bones).
    • Shoulder, elbow, carpus, hip, fetlock and cervical spine are less commonly affected.
  • Diagnosis: radiography, arthroscopy, scintigraphy.
  • Treatment: box rest, nutritional management, intra-articular medication, arthroscopic surgery.
  • Prognosis: guarded for return to productivity depending on site, location, extent of lesion(s) and secondary pathology.

Pathogenesis

Etiology

  • Osteochondrosis is a multifactorial disease -  a complex interaction of environmental influences and genetic susceptibility.
  • It occurs due to abnormal differentiation of cells in growing cartilage.
  • Lesions occur in sites of high biomechanical loading, thick cartilage and limited blood supply, so trauma and vascular insults may be involved in etiology:
    • Biomechanical forces → shearing of cartilage canals in immature cartilage → loss of blood supply.
    • Direct trauma or excessive loading of growth plate over time.
    • Nutritional or other systemic factors, affecting collagen stability or increasing connective tissue fragility → microfractures in cartilage → disruption of metaphyseal vasculature → osteochondral fragmentation, e.g. copper deficiency Copper: overview, excess phosphorous.
    • Congenital deformities - abnormal joint surface → excessive biomechanical loading.
  • As a consequence to osteochondrosis, Osteochondrosis Dissecans (OCD) may occur.
    • This is when impaired vascularization of the articular cartilage develops, leading to the necrosis and fragmentation of articular cartilage.
  • The following factors may have a primary or contributory role in the etiopathogenesis

Growth rate

  • Large, rapidly growing animals are typically associated with osteochondrosis, but a clear association between body size/growth rate and disease incidence has not been shown.

Nutrition

  • Excess energy (carbohydrate and/or fat) may → cause abnormal development of cartilage.
  • Mineral homeostasis - excess phosphorus, excess calcium Calcium and phosphorous: overview and copper deficiency Copper: overview are implicated.
  • Excess carbohydrate can influence endocrine factors in cartilage development, e.g. hyperinsulinemia/hyperglycemia, hypothyroxemia → chondrocyte maturation → endochondral ossification.
  • High dietary phosphorus can → abnormal endochondral ossification.

Hereditary

  • Several studies suggest an influence of genetics on the development of connective tissue disorders.
  • No appropriate program for screening dams, sires or progeny has been developed.

Exercise

  • Biomechanical factors have not been investigated fully:
    • Excessive force on normal growth cartilage.
    • Normal forces on abnormal cartilage.
    • A relationship appears to exist between the intensity of exercise, the level of nutrition and the incidence of osteochondrosis.

Predisposing factors

General

Pathophysiology

  • The pathophysiology of osteochondrosis has not been fully resolved, although it is most commonly regarded as a developmental condition with a focal disturbance of endochondral ossification.
  • Normal endochondral ossification:
    • Cartilage canals nourish the chondrocytes, with the blood supply initially coming from the perichondral vasculature, but then switching to the metaphyseal vasculature.
    • This healthy blood supply allows capillary buds and osteophytes to invade the mineralized cartilage matrix and chondrocytes to disappear.
    • Osteoblasts secrete osteoid and form woven bone to later be replaced by mature bone.
  • However, in animals with osteochondrosis:
    • Damage to the blood vessels will deprive the cartilage of its blood supply, so capillary buds fail to penetrate hypertrophic zone → failure of final cartilage maturation and modification of matrix.
    • Failure of mineralization → necrosis of basal layers → thickening and retention of growth cartilage → osteochondrosis lesion.
    • This is the cartilage canal blood vessel necrosis theory.
  • Development is split into 2 phases:
    • Chondrocytes fail to differentiate and mineralize → failure of bone formation.
    • Causes abnormal cartilage thickening → cartilage retention.
  • The thickened cartilage causes reduced absorption of nutrients from the synovial fluid, leading to cartilage degeneration and necrosis.
  • Primary lesion is rarely recognized before cycles of repair, remodelling and re-injury have occurred → degenerative joint disease.
  • Progression of the lesion depends on the type of biomechanical forces applied:
    • Fissures or fractures of the cartilage occur with shear forces.
      • Complete separation of the cartilage from the underlying subchondral bone forms an osteochondritis dissecans (OCD) lesion.
        • Known as a 'joint mouse' if the cartilage is released into the joint.
    • High compressive loading on dysplastic cartilage areas creates cartilage mis-folding and resorption.
      • Forms a subchondral bone cyst.
  • Multiple sites and types of lesions are possible due to the variation in types of bone surfaces and the three areas in which endochondral ossification takes place (epiphysis, metaphyseal growth plate, secondary centers of ossification).

Classification

  • Attempts to classify osteochondrosis have been based on the lesion and etiology.
  • Lesion classification:
    • Type 1 - cartilage fragmentation in a typical site(s).
    • Type 2 - fragmentation of cartilage and subchondral bone in a typical site(s).
    • Type 3 - thickened cartilage (delayed ossification) in a typical site(s).
    • Type 4 - multiple lesions in typical and atypical sites including growth plates and secondary centers of ossification.
  • In cattle, the stifle and tarsus are most commonly affected, but other joints may be affected:
Stifle
  • Lateral trochlea ridge of femur.
  • Lateral facet of patella.
  • Medial femoral condyle.
  • Medial trochlear ridge - lesions may occur at any age.
Tarsus
  • Distal intermediate ridge of tibia.
  • Medial malleolus of tibia.
  • Lateral and medial trochlear ridge of talus.
  • Central tarsal and third tarsal bones.
Fetlock
  • Palmar/plantar eminence third metatarsal or metacarpal bones.
  • Mid-sagittal ridge and condyles of MC3/MT3.
  • Medial condyle proximal phalanx.
Carpus
  • Rare.
  • Intermediate, ulnar, third and fourth carpal bones.
  • Distal medial radius.
  • Distal medial radial carpal bone.
  • Proximal third carpal bone.
Distal interphalangeal joint
  • Dorsoproximal aspect of extensor process of distal phalanx.
Proximal interphalangeal joint
  • Lysis of the distal end of the proximal phalanx.
Elbow
  • Rare.
  • Medial humeral condyle.
  • Proximal radius.
Shoulder
  • Glenoid fossa of scapula.
  • Humeral head.
Other
  • Areas uncommonly affected:
    • Hip.
    • Cervical vertebra joints, especially the atlanto-occipital joint in feedlot cattle.
  • Atypical pattern:
    • Multiple lesions.
    • Physeal lesions.
    • Uncommonly bilaterally symmetrical.
    • Probably nutritional or toxic etiologies.
    • Atypical locations within classically affected joint.
    • A combination of typical and atypical lesions can occur in the same animal.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Nichols S & Lardé H (2014) Noninfectious joint disease in cattle. Veterinary clinics of north america: Food Animal Practice 30 (1) 205-223 PubMed.
  • Robert C (2013) Further evidence for better prevention of equine osteochondrosis. Vet Rec 172 (3), 66-63 PubMed.
  • Dávila U M, Méndez-Angulo J L, Sierra M A & Méndez A (2013) Osteochondrosis in young fighting bulls: pathology, frequency and severity in spanish farms. Journal of Comparative Pathology 148 (1), 98.
  • Laverty S & Girard C (2013) Pathogenesis of epiphyseal osteochondrosis. The Veterinary Journal 197 (1), 3-12 PubMed.
  • Relave F, Meulyzer M, Alexander K, Beauchamp G & Marcoux M (2009) Comparison of radiography and ulstrasonography to detect osteochondrosis lesions in the tarsocrural joint: a restrospective study. Equine Vet J 41 (1), 34-40.
  • Lecocq M, Girard C A, Fogarty U, Beauchamp G, Richard H & Laverty S (2008) Cartilage matrix changes in the developing epiphysis: Early events on the pathway to equine osteochondrosis? Equine Vet J 40 (5), 442-454 PubMed.
  • Tryon K A & Farrow C S (1999) Osteochondrosis in Cattle. Veterinary Clinics of North America: Food Animal Practice 15 (2), 265-274 PubMed.
  • Tryon K A & Farrow C S (1999) Osteochondrosis in Cattle. Bovine medical imaging 15 (2) 256-274.

Other sources of information

  • Mulon P Y (2009) Chapter 57 - Osteochondrosis in Cattle. In: Food animal practice. 5th edn. pp 262-263.


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