JPC SYSTEMIC PATHOLOGY
MUSCULOSKELETAL SYSTEM
April 2022
M-M21

Signalment (JPC #3106281): 6-week-old female mixed breed horse

 

HISTORY:  This horse had a five day history of lameness of the right rear leg.  Radiographic findings were interpreted as septic arthritis of the right coxofemoral joint.

 

HISTOPATHOLOGIC DESCRIPTION:  Articular epiphyseal cartilage complex:  A focally extensive 10mm long area of the epiphyseal cartilage is markedly thickened up to 2mm deep, twice the thickness of adjacent unaffected cartilage, extending into the underlying epiphyseal cancellous bone.  At the deep margin, large segments of the affected cartilage are pale (loss of matrix proteoglycans) or are necrotic characterized by eosinophilic matrix with loss of cellular detail and lacunae that are empty or contain necrotic chondrocytes.  Multifocally, cartilage canals within the affected cartilage are necrotic with absence of normal vascular channels, and with loss of endothelial lining and replacement with scant loose fibrous connective tissue and debris which extends outward from vascular channels and replaces chondrous matrix.  At the deep edge of the thickened articular epiphyseal cartilage complex, bony trabeculae contain retained cartilage cores; within this area there are several fragmented, displaced bony trabeculae (microfractures) that focally coalesce (infraction) surrounded by abundant polymerized fibrin and hemorrhage. Focally extensively in the subchondral bone, normal hematopoietic elements are replaced by increased numbers of fibroblasts and fibrous connective tissue admixed with few lymphocytes and plasma cells. 

 

MORPHOLOGIC DIAGNOSIS:  Articular epiphyseal cartilage complex:  Chondronecrosis, multifocal, moderate, chronic, with loss of cartilage proteoglycans, subchondral microfractures and infraction, and failure of endochondral ossification (osteochondrosis manifesta), mixed breed, equine.

 

CONDITION:  Osteochondrosis

 

SYNONYMS:  Dyschondroplasia, osteochondrosis dissecans, osteochondritis dissecans

 

GENERAL DISCUSSION:

• Osteochondrosis affects growing animals; primary lesion of osteochondrosis is a focal failure of endochondral ossification due to failure of blood supply to growing cartilage
  • May involve both the physeal growth cartilage (i.e. the growth plate) as well as the articular-epiphyseal cartilage complex (AECC) (more commonly described in AECC); the lesions differ in appearance in the two locations and may have a different pathogenesis
• Pathogenesis is considered multifactorial; heredity and anatomic factors are most important, and growth rate, nutrition, trauma, infection/bacteremia, and other environmental conditions play only a secondary role in disease progression
• Three stages of the disease are recognized:
  • Osteochondrosis latens: Focal area of chondronecrosis that is confined to growth cartilage and involves neither the overlying articular cartilage nor underlying subchondral bone
  • Osteochondrosis manifesta: Presence of a focal failure of endochondral ossification which is visible macroscopically as a thickening of the zone of hypertrophy
  • Osteochondrosis dissecans: A fissure which forms in the area of necrotic cartilage and dissects through the articular cartilage forming a flap or loose body
• OC in the horse: Young horses of several breeds affected, especially in lateral trochlear ridge, medial condyle of the femur, patella, dorsal edge of sagittal ridge of distal tibia, and various sites in the tarsal and fetlock joints
  • Osteochondrosis manifesta lesions are also known as subchondral bone cysts (also pseudocysts, which lack an epithelial lining) which occur commonly at the medial femoral condyle, but not all subchondral cysts are associated with osteochondrosis (Olstad, Vet Pathol. 2015)
  • Possibly linked to copper deficiency, zinc excess, sepsis
  • Osteochondrosis was recently found as one of the most common lesions in horses with cervical stenotic myelopathy in cervical vertebrae C2-C7 (Janes, Vet Pathol. 2015)

 

PATHOGENESIS:

• Heritable trait or predisposing anatomic feature(s) favoring premature necrosis and chondrification of cartilage canal blood vessels > focal ischemic necrosis of growth cartilage > failure of mineralization and vascular penetration of cartilage > failure of endochondral ossification
  • Growth plate à accumulation of preserved, hypertrophic chondrocytes
  • AECC à necrosis of epiphyseal cartilage
• Predisposition to occur at areas that have vessels which make a parallel loop that crosses the ossification front twice (most common at the caudomedial, cranial, and craniolateral abaxial aspects of the distal femur in the horse)
• Experimental studies have shown that bacteremia can occlude vasculature and may account for a subset of cases

                                                                   

TYPICAL CLINICAL FINDINGS:

• Osteochondrosis latens: Many lesions resolve spontaneously without clinical signs
• Osteochondrosis manifesta: Usually asymptomatic, however weakened growth cartilage and underlying subchondral bone may be predisposed to progression to osteochondrosis dissecans due to trauma or normal biomechanical forces
• Osteochondrosis dissecans: Severe lameness with secondary degenerative joint disease

 

TYPICAL GROSS FINDINGS:

• Lesion maybe bilaterally symmetrical
• Osteochondrosis latens: None
• Osteochondrosis manifesta: Focal areas of thickened growth cartilage in the articular epiphyseal cartilage complex or in the physeal plate
• Osteochondrosis dissecans: Fissure in articular cartilage with formation of a flap or cleft of cartilage or formation of free joint body; the secondary lesions of degenerative joint disease often overshadow the primary lesion of osteochondrosis
  • Detached cartilage may be free floating and grow within the joint space or integrate with the synovial membrane

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Osteochondrosis latens: Focal area of necrosis confined to the growth cartilage with multifocal necrosis of cartilage canals; NO involvement of subchondral bone or overlying articular cartilage
  • Necrotic vessels surrounded by areas of coagulative necrosis
• Osteochondrosis manifesta: Thickened, irregular tongues of growth cartilage extending into the primary spongiosa, the tongues of cartilage are not mineralized or invaded by epiphyseal blood vessels; prominent necrosis of large areas of affected growth cartilage with necrosis of cartilage canals; osteosclerosis of underlying subchondral bone +/- infraction, inflammation, osteonecrosis
• Osteochondrosis dissecans: Fissure which extends through articular cartilage into the deep layers of necrotic cartilage; focal collapse of subchondral bone; formation of loose body (joint mouse); may see subchondral bone cysts
• In physeal plate: Cone-shaped focus of retained cartilage extending into the metaphysis consisting of viable hypertrophic chondrocytes; irregular eosinophilic streaks between disorganized columns of physeal chondrocytes

 

DIFFERENTIAL DIAGNOSIS:

• Physeal lesions closely resemble those of rickets; rickets lacks the prominent eosinophilic streaks and cavitations (chondronecrosis) within the disorganized physis of osteochondrosis
• Similar lesions occur in middle-aged to older large breed dogs, not preceeded by osteochondrosis.

 

COMPARATIVE PATHOLOGY:

Osteochondrosis in other species:

• Swine: Seen in up to 100% of rapidly growing pigs 2-7 months old
  • Articular osteochondrosis (OC) in swine arises due to vascular failure and ischemic chondronecrosis (Olstad, Vet Pathol. 2019)
  • Joint surface: medial humeral and femoral condyles, humeral head, dorsal acetabulum
  • Physis: distal ulna, distal femur, costochondral junction, femoral head, humeral head, ischial tuberosity
  • Early lesions at the articular surface appear as thickened, white foci of cartilage or depressed and wrinkled
  • Prevalence of osteochondrosis lesions in wild boars is low compared to domestic pigs (Etterlin, Vet Pathol. 2017)
• Dog: Young fast growing males of large and giant breeds in caudal aspect of humeral head, medial aspect of humeral condyle, lateral and medial condyle of the femur, and medial trochlear ridge of tibial tarsal bone; there is controversy over whether elbow dysplasia (ununited anconeal process, fragmented coronoid process) is associated with osteochondrosis, with conflicting reports in the literature
• Ox: May be more common than currently recognized, typically affects the stifle joint; recently reported in bulls raised on concrete floors with a unilateral to bilateral distribution and in lame and non-lame bulls and possibly complicated by sepsis (Levi, Vet Pathol. 2017)
• Deer: Farmed red deer and wapiti x red deer hybrids in New Zealand, up to 30% affected, usually involves the femoral head
• Sheep: Rare cause of lameness in rapidly growing young Suffolk rams in the distal radial physis; may be a cause for angular limb deformities in sheep when it involves the growth plate
• Chickens: Severe osteochondrosis in the free-thoracic vertebra of young chickens is a crucial component to the pathogenesis of Enterococcus cecorum (Borst, Vet Pathol. 2017)

 

REFERENCES:

1. Borst LB, Suyemoto MM, Sarsour AH, et. al. Pathogenesis of enterococcal spondylitis caused by enterococcus cecorum in broiler chickens. Vet Pathol. 2017;54(1):61-73.
2. Craig LE, Dittmer K, Thompson KG. Bones and joints. In: Maxie MG, ed. Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals. Vol 1. 6th ed. St. Louis, MO; Elsevier: 2016; 132-135.
3. Craig LE, Reed A. Age-associated cartilage degeneration of the canine humeral head.  Vet Pathol. 2013;50(2): 264-268.
4. Etterlin PE, Ekman S, Strand R, Olstad K, Ley CJ. Osteochondrosis, synovial fossae, and articular indentations in the talus and distal tibia of growing domestic pigs and wild boars. Vet Pathol. 2017;54(3):445-456.
5. Janes JG, Garrett KS, McQuerry KJ, et. al. Cervical Vertebral Lesions in Equine Stenotic Myelopathy. Vet Pathol. 2015;52(5):919-927.
6. Levi M, Dittmer KE, Gentile A, et. al. Growth Plate lesions of fattening bulls. Vet Pathol. 2017;54(3):437-444.
7. McInnes EF, McKeag S. A brief review of infrequent spontaneous findings, peculiar anatomic microscopic features, and potential artifacts in Göttengen minipigs. Toxicol Pathol. 2016;44(3)385-45.
8. Olson EJ, Carlson CS. Bones, joints, tendons, and ligaments. In: McGavin MD, Zachary JF, eds. Pathologic Basis of Veterinary Disease. 7th ed. St. Louis, MO: Elsevier; 2022:1060-1063.
9. Olstad K, Ekman S, Carlson CS. An update on the pathogenesis of osteochondrosis. Vet Pathol. 2015; 52(5):782-802.
10. Olstad K, Østevik L, Carlson CS, Ekman, S. Osteochondrosis can lead to the formation of pseudocysts and true cysts in the subchondral bone of horses. Vet Pathol. 2015; 52(5):862-72.
11. Olstad K, Wormstrand B, Kongsro J, Grindflek E. Osteochondrosis in the Distal Femoral Physis of Pigs Starts With Vascular Failure. Vet Pathol. 2019;56(5):732-742.
12. Stidworthy, MF, Denk D. Sphenisciformes, Gaviiformes, Podocopediformes, procellariiformes, and Pelecaniformes, In: Terio K, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals, San Diego, CA: Elsevier 2018:660.
13. Wormstrand B, Østevik L, Ekman S, Olstad K. Septic arthritis/osteomyelitis may lead to osteochondrosis-like lesions in foals. Vet Pathol. 2018;55(5):693-702.

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