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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Developmental disorder of bone and cartilage of unspecified etiology resulting in failure of endochondral ossification
  • The term osteochondritis dissecans or OCD is generally reserved for a detachment or “flap” of abnormal cartilage, or cartilage and bone, from the surrounding tissue. Some SBCs are also considered to be of OCD origin

Pathophysiology!!navigator!!

  • Failure of normal endochondral ossification results in thickening and retention of the hypertrophic zone of the growth cartilage. When this affects articular–epiphyseal cartilage, the disorder manifests as a flap or fragment(s) of cartilage or cartilage and bone (OCD), or defective cartilage infolding and formation of periarticular SBCs
  • These lesions may be precipitated by abnormal chondrocyte structure or function, abnormal extracellular matrix production, or a vascular disorder
  • What determines whether osteochondrosis results in the development of OCD or SBC is not fully understood. High-motion areas may subject the articular surface to shear forces predisposing to OCD, whereas SBCs tend to be located in areas of maximal compressive loads (i.e. maximal weight-bearing)
  • Trauma leading to subchondral bone microfracture and necrosis, followed by cystic resorption and collapse of overlying articular cartilage, may also be part of the pathogenesis of SBCs
  • Full-thickness articular cartilage defects at the points of maximal weight-bearing can lead to SBC development

Systems Affected!!navigator!!

Musculoskeletal—epiphyseal cartilage and bone.

Genetics!!navigator!!

  • Certain genetic lines have high heritability
  • Specific genetic defect responsible for endochondral ossification alteration not identified
  • In Scandinavian Standardbreds, tarsocrural osteochondrosis heritability ranges from 0.24 to 0.52

Incidence/Prevalence!!navigator!!

Unknown

Geographic Distribution!!navigator!!

Worldwide

Signalment!!navigator!!

Breed Predilections

Any breed, common in Standardbreds, Thoroughbreds, and Warmbloods.

Mean Age and Range

Yearlings or weanlings (range neonates to 3 years of age) most common, although it can occur at any time during bone development.

Predominant Sex

None

Signs!!navigator!!

General Comments

  • Depends on location, variable clinical signs, and physical examination findings
  • Frequently bilateral with reported incidences between 45% and 60%
  • Type and location of osteochondrosis:
    • Tarsus (tarsocrural joint)—cranial distal intermediate ridge of tibia, lateral trochlear ridge of talus, medial malleolus of tibia, lateral malleolus of tibia, medial trochlear ridge of the talus
    • Stifle—lateral trochlear ridge of femur, medial distal femoral condyle (SBC)
    • Fetlock—distal dorsal sagittal ridge of MCIII/MTIII, proximal palmar/plantar eminence of P1, proximal dorsal P1, distal MCIII/MTIII (SBC)
    • Shoulder—humeral head (OCD or SBC), distal scapula (SBC)
    • Other locations include proximal and distal P1, proximal and distal P2, proximal and distal radius, distal humerus, and distal tibia. These are infrequent and usually SBCs
    • OCD also affects the cervical vertebral articular facets, recognized cause of cervical vertebral instability or stenosis (“wobbler syndrome”)

Historical Findings

Variable findings depending on location; classically joint effusion without lameness.

Physical Examination Findings

  • Variable findings depending on location
  • Joint effusion without lameness
  • SBCs more likely to cause lameness

Causes!!navigator!!

Complex, multifactorial etiology that is incompletely understood. Several factors have a direct effect on its development.

Growth Rate

Rapid growth rate.

Dietary Factors

  • High carbohydrate load
  • Extremely low copper or excessive zinc levels
  • ±Overfeeding phosphorus and calcium

Genetics

  • Specific genetic defect responsible for alteration of endochondral ossification has not yet been identified, although highly suspected in certain breeding lines
  • Heritability of a predisposition for fast growth and larger skeletal size might be the most important factor

Trauma

  • Trauma in susceptible cartilage
  • Time-dependent window of vulnerability to trauma for growth cartilages in specific locations

Risk Factors!!navigator!!

See Causes.

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Nonseptic synovitis—rule out with radiography
  • Septic synovitis—rule out with radiography, synovial fluid analysis
  • Osteomyelitis—rule out with serial radiography, culture
  • Traumatic fracture—rule out with radiography, histology

Imaging!!navigator!!

Radiography

  • Best modality for diagnosis
  • Subchondral radiolucency along articular margin(s)
  • Osseous fragment(s) separated from subchondral bone by a radiolucent area
  • SBC—round subchondral radiolucency, often articular
  • Important to image contralateral joint

Nuclear Scintigraphy

SBC—increased radiopharmaceutical uptake; OCD flaps—often normal.

CT/MRI

Occult SBC identification.

Ultrasonography

Loss of normal cartilaginous contour, ± at sites difficult to radiograph (cervical articular facet joint).

Other Diagnostic Procedures!!navigator!!

Synovial fluid analysis and culture—differentiate from septic arthritis.

Pathologic Findings!!navigator!!

Histology—chondrocytes in mid-to-late hypertrophic zone, with failure of vascular invasion and subsequent osteogenesis resulting in retained cartilage cores.

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Reduce or eliminate joint effusion
  • Avoid the development of or reduce or eliminate lameness
  • Eliminate lesion as part of presale

Appropriate Health Care!!navigator!!

  • No treatment if an incidental finding or without active clinical signs
  • In young animals (foals, weanlings), conservative management via exercise restriction, anti-inflammatory(s), IM polysulfated glycosaminoglycans and diet modification for 6–10 months can be useful

Nursing Care!!navigator!!

Postoperative care—surgical incisions are kept clean and bandaged until suture removal 10–14 days after surgery. Bandages replaced daily and incisions inspected every 2–3 days or more often if wet, soiled, or dislodged. In areas where bandaging is not possible, the incisions are maintained covered with adhesive iodinated dressings.

Activity!!navigator!!

Restricted activity for conservative treatment and/or after surgery—stall confinement and controlled exercise program. Duration depends on severity and/or location of the lesion. In general, 2 weeks of strict stall rest followed by 4–8 weeks of stall rest with daily walking. Then, limited turnout in a small paddock for 4–6 weeks followed by another 4–6 weeks of regular paddock turnout. SBCs may require 6–12 months of restricted activity before resuming training.

Diet!!navigator!!

  • Do not overfeed foals and yearlings; prevent excessive energy (carbohydrate/protein) in dominant individuals
  • In young horses (weanlings to 2 years of age) that are at risk of developing osteochondrosis, decrease or eliminate high-energy hay (alfalfa) and high-energy concentrate
  • Mild to moderate caloric reduction of intake while stall confined or resting

Client Education!!navigator!!

  • Avoid high-energy feeds
  • Monitor sires and mares suspected of yielding offspring with osteochondrosis
  • Any young horse with persistent joint effusion should be evaluated, including radiography. Early identification and treatment of OCD and SBC can be successful in maintaining the horse's athletic ability. If left unrecognized, secondary osteoarthritis and lameness may develop

Surgical Considerations!!navigator!!

  • OCD(s)—arthroscopic removal, debridement
  • SBC(s)—arthroscopic debridement, mosaicplasty, intralesional corticosteroids, osteostixis (forage), intralesional/intra-articular therapy (stem cells, platelet-rich plasma, bone marrow aspirate concentrate, bone graft), transcortical screw

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • NSAIDs—phenylbutazone (2.2–4.4 mg/kg PO or IV every 12–24 h) or flunixin meglumine (1.1 mg/kg PO or IV every 12–24 h) for medical management or after surgery
  • For SBCs, intralesional corticosteroids—methylprednisolone acetate (40–80 mg) or triamcinolone (6–12 mg)

Contraindications!!navigator!!

In immature horses, fluoroquinolones contraindicated.

Precautions!!navigator!!

Monitor NSAID toxicity with long-term or young patient use.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

Radiographic Evaluation

Objective assessment and progression; 6–8 weeks for conservative therapy, 2 and 6 months after surgery.

Lameness Examination

  • For conservative treatment, monthly evaluation
  • For surgery, prior to controlled exercise then 3–12 months

Prevention/Avoidance!!navigator!!

  • Diet restriction in young horses at risk
  • Caution when selecting for certain breeding lines

Possible Complications!!navigator!!

  • Lameness
  • Osteoarthritis
  • ±Negatively affect sale

Expected Course and Prognosis!!navigator!!

  • Clinical signs noted in 1–3-year–olds
  • In general, arthroscopic removal of OCD(s) is favorable
  • SBCs are less favorable prognosis and more likely to develop arthritis with or without treatment
  • Joint effusion improves but may not resolve postoperatively
  • Prognosis depends on lesion location and type:
    • Tarsus—favorable, large lateral trochlear ridge OCD has less favorable racing prognosis
    • Stifle—lateral trochlear ridge OCD—fair to good, less favorable with extensive and/or bilateral disease. Medial femur SBC—fair to good prognosis with surgery, guarded for older horses, fair to guarded for conservative treatment (± intra-articular corticosteroids)
    • Fetlock—fair to good for racehorses, very good to excellent in nonracehorses. Palmar/plantar eminence P1 (good), sagittal ridge (fair to good), SBCs (guarded to fair)
    • Shoulder—guarded for athletic use ± surgical management

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Osteoarthritis
  • Cervical vertebral malformation

Age-Related Factors!!navigator!!

Clinical signs apparent in a young animal.

Pregnancy/Fertility/Breeding!!navigator!!

None

Synonyms!!navigator!!

  • Osteochondritis
  • Osteochondritis dissecans

Abbreviations!!navigator!!

  • CT = computed tomography
  • MCIII = third metacarpal bone
  • MRI = magnetic resonance imaging
  • MTIII = third metatarsal bone
  • OCD = osteochondrosis dissecans
  • P = phalanx
  • SBC = subchondral bone cyst

Suggested Reading ⬆ ⬇

Douglas J. Pathogenesis of osteochondrosis. In: Ross MW, Dyson SJ, eds. Diagnosis and Management of Lameness in the Horse, 2e. St. Louis, MO: Elsevier Saunders, 2011:617–624.

van Weeren PR. Osteochondrosis. In: Auer JA, Stick JA, eds. Equine Surgery, 4e. St. Louis, MO: WB Saunders, 2012:1239–1254.

van Weeren PR. Osteochondritis dissecans. In: McIlwraith CW, Frisbie DD, Kawcak CP, van Weeren PR, eds. Joint Disease in the Horse, 2e. St. Louis, MO: Elsevier, 2016:57–84.

Von Rechenberg B, Auer JA. Subchondral cystic lesions. In: Auer JA, Stick JA, eds. Equine Surgery, 4e. St. Louis, MO: WB Saunders, 2012:1255–1263.

Author(s) ⬆

Author: José M. García-López

Consulting Editor: Elizabeth J. Davidson