Equis ISSN 2398-2977

Bone: osteochondrosis

Synonym(s): OCD, Osteochondritis dissecans

Contributor(s): Patrick Colahan, David Moll, Graham Munroe, Vetstream Ltd, Chris Whitton


  • Cause: developmental orthopedic disease   →   defective endochondral ossification + accelerated growth rate   →   damage to cartilage and subchondral bone:
    • 10-25% of horses affected.
    • Range of breeds.
  • Signs: lameness, effusion; sites affected:
    • Stifle (femoropatellar joint   Stifle: femoropatellar osteochondrosis  : lateral and medial trochlear ridges of the femur, lateral facet of patella, medial femoral condyle).
    • Hock (tarsocrural joint   Tarsus: osteochondrosis  : distal intermediate ridge of the tibia, lateral and medial trochlear ridges of talus, medial malleolus of tibia, central and third tarsal bones).
    • Fetlock (sagittal ridge of distal MC3 and MT3, medial condyle, proximal phalanx).
    • Shoulder, elbow, carpus, hip and cervical spine are less commonly affected.
  • Diagnosis: radiography, arthroscopy, scintigraphy.
  • Treatment: restricted exercise, nutritional management, intra-articular medication, arthroscopic surgery.
  • Prognosis: variable, depending on site, location, extent of lesion(s) and secondary pathology.
  • See also:
Print off the Owner factsheet on Osteochondrosis to give to your clients.



  • Unknown.
  • Multifactorial - may be a complex interaction of environmental influences and genetic susceptibility. 
  • 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, eg copper deficiency, excess phosphorous.
    • Congenital deformities - abnormal joint surface   →   excessive biomechanical loading.
  • 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.


  • When foals are fed according to requirements, there is a lower incidence of osteochondrosis.
  • Excess energy (carbohydrate and/or fat) may   →   cause abnormal development of cartilage.
  • Mineral homeostasis - excess phosphorus, excess calcium and copper deficiency are implicated.
  • Excess carbohydrate can influence endocrine factors in cartilage development, eg hyperinsulinemia   Pancreas: hyperinsulinemia  /hyperglycemia, hypothyroxemia   →   chondrocyte maturation   →   endochondral ossification.
  • High dietary phosphorus can   →    abnormal endochondral ossification.


  • 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.


  • Biomechanical factors have not be 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



  • The pathophysiology of osteochondrosis has not been resolved, although it is most commonly regarded as a developmental condition.
  • Hypothesis: a primary failure of endochondral ossification. Disorder in chondrocyte development is the primary 'essential lesion'.
  • Biomechanical and other contributory causes are involved.
  • 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).
  • Primary lesion is rarely recognized before cycles of repair, remodeling and re-injury have occurred   →   degenerative joint disease   Musculoskeletal: osteoarthritis (joint disease)  .
  • Osteochondrosis is a disorder of cartilage development   →  
    • Cartilage injury.
    • Subchondral injury.
  • It is a developmental orthopedic disease and may be a precursor for other developmental orthopedic conditions, see also:


  • 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.
  • Etiologic classification:
    • Hereditary.
    • Traumatic.
    • Toxic.
    • Nutritional.
    • Developmental.
  • Some joint conditions have been attributed to osteochondrosis, but have proved to have a traumatic or other specific etiopathogenesis - for example, in the fetlock the following conditions have been attributed to osteochondrosis: fetlock plantar osteochondral fragmentation (POFs), ununited palmar fragment of the proximal phalanx (UPEs) and plantar condylar necrosis of the cannon bone (MC/MTIII) - see Fetlock: developmental disease   MCP / MTP joint: developmental orthopedic diseases  .
  • Osteochondrosis   →   joint surface susceptible to injury during development   →   subchondral bone cysts   Stifle: femorotibial subchondral bone cyst  and degenerative joint disease   Musculoskeletal: osteoarthritis (joint disease)  .
  • Inconsistencies in hypothetical etiopathogenesis:
    • Single or multiple lesions can occur, metabolic or developmental disorders typically have a multifocal effect on relevant body system.
    • It occurs in sites where endochondral ossification has ceased.
    • Retained cartilage cores and thickened cartilage are not consistent findings.
  • Summary:
    • Unknown initiating factor   →   lesion in proliferative or hypertrophic zone of articular/epiphyseal cartilage   →   degenerative joint disease and other clinical conditions.
  • Normal endochondral ossification:
    • Capillary buds and osteophytes invade the mineralized cartilage matrix and chondrocytes disappear.
    • Osteoblasts secrete osteoid and form woven bone to later be replaced by mature bone.
  • Osteochondrosis:
    • Capillary sprouts 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.
  • Development of pathology after osteochondrosis lesion depends on anatomy, biomechanics and other factors, eg management.
  • Range of entities may result:

Typical disease pattern

  • One or two lesions, bilaterally symmetric, clinical evidence may be unilateral.
  • Lesions range from fissures, flaps, fragments, cysts and delayed ossification.
  • Stifle  Stifle: femoropatellar osteochondrosis  :
    • Lateral trochlea ridge of femur   Stifle: OCD 01 - arthroscopy    Stifle: OCD 03 - arthroscopy      Stifle: OCD 13 - bilateral    Stifle: OCD 14 - LM radiograph    Stifle: OCD 15 - CdCr radiograph      Stifle: OCD 16 - post mortem  .
    • Lateral facet of patella.
    • Medial femoral condyle.
    • Medial trochlear ridge - lesions may occur at any age.
  • Hock  Tarsus: osteochondrosis  :
    • Distal intermediate ridge of tibia   Tarsus: osteochondrosis 04 - DMPaLO radiograph  .
    • Medial malleolus of tibia.
    • Lateral and medial trochlear ridge of talus.
    • Central tarsal and third tarsal bones.
  • Fetlock  MCP / MTP joint: developmental orthopedic diseases  :
    • Palmar/plantar eminence third metatarsal or metacarpal bones.
    • Mid-saggital 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   PIP joint: osteochondrosis - LM radiograph  .
  • Elbow:
    • Rare.
    • Medial humeral condyle.
    • Proximal radius.
  • Shoulder:
    • Glenoid fossa   Shoulder: OCD 01 - LM radiograph   of scapula.
    • Humeral head.
  • Areas uncommonly affected:
    • Hip.
    • Cervical vertebra joints.

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.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Wright I M & Minshall G J (2014)Identification and treatment of osteochondritis dissecans of the distal sagittal ridge of the third metacarpal bone.Equine Vet J46(5), 585-588 PubMed.
  • Robert C (2013)Further evidence for better prevention of equine osteochondrosis.Vet Rec172(3), 66-63 PubMed.
  • Van der Heyden Let al(2013)Association of breeding conditions with prevalence of osteochondrosis in foals. Vet Rec172(3), 68 PubMed.
  • Machado T S Let al(2012)Synovial fluid chondroitin sulphate indicated abnormal joint metabolism in asymptomatic osteochondritic horses.Equine Vet J44(4), 404-411 PubMed.
  • Lykkjen S, Roed K H & Dolvik N I (2012)Osteochondrosis and osteochondral fragments in Standardbred trotters: Prevalence and relationships.Equine Vet J44(3), 332-338 PubMed.
  • Jonsson L, Dalin G, Egenvall A, Nasholm A, Roepstorff L & Philipsson J (2011)Equine hospital data as a source for study of prevalence and heritability of osteochondrosis and palmar/plantar osseous fragments of Swedish Warmblood horses.Equine Vet J43(6), 695-700 PubMed.
  • Voute L C, Henson F M D, Platt D & Jeffcott L B (2011)Osteochondrosis lesions of the lateral trochlear ridge of the distal femur in four ponies.Vet Rec168(10), 265 PubMed.
  • Bourzac C, Alexander K, Rossier Y & Laverty S (2009)Comparison of radiography and ultrasonography for the diagnosis of osteochondritis dissecans in the equine femoropatellar joint.Equine Vet J41(7), 686-692 PubMed.
  • van Grevenhof E M, Ducro B J, van Weeren P R, van Tartwijk J M F M, van den Belt A J & Bijma P (2009)Prevalence of various radiographic mainfestations of osteochondrosis and their correlations between and within joints in Dutch Warmblood horses.Equine Vet J41(1), 11-16 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 J41, (1), 34-40 PubMed.
  • 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 J40(5), 442-454 PubMed.
  • Donabedian M, van Weeren P R, Perona Get al(2008)Early changes in biomarkers of skeletal metabolism and their association to the occurrence of osteochondrosis (OC) in the horse.Equine Vet J40(3), 253-259 PubMed.
  • Robert C, Valette J-P, Paragon B-M, Denoix J-M & Blanchard G (2008)Phalangeal hyperostosis due to nutritional imbalance in three yearlings.Vet Rec162(3), 92-94 PubMed.
  • Wright I & Minshall G (2005)Diagnosis and treatment of equine osteochondrosis.In Pract27(6), 302-309 VetMedResource.
  • Knight D A, Weisbrode S Eet al(1990)The effects of copper supplementation on the prevalence of cartilage lesions in foals.Equine Vet J22, 426-432 PubMed.
  • Kold S E, Hickman J (1986)An experimental study of the healing process of equine chondral and osteochondral defects.Equine Vet J18(1), 18-24 PubMed.

Other sources of information

  • Ross M W & Dyson S J (2003) EdsDiagnosis and Management of Lameness in the Horse.Elsevier Science, USA.