JPC SYSTEMIC PATHOLOGY
MUSCULOSKELETAL SYSTEM
April 2022
M-T06

SIGNALMENT (JPC #1948317):  4-week-old broiler chicken

 

HISTORY:  This chicken had been fed a ration containing Fusarium roseum since one day of age. There was marked accumulation of avascular physeal cartilage in the growth plates of long bones, especially the proximal tibiotarsus, and the diaphyses were well mineralized.

 

HISTOPATHOLOGIC DESCRIPTION:  Tibia: The proximal physis is markedly expanded up to 1cm thick by a dense mass of avascular physeal cartilage that protrudes deep into the metaphysis and is characterized by a thickened zone of chondrocytes that fail to fully hypertrophy (pre-hypertrophic chondrocytes) and do not undergo mineralization. Metaphyseal capillary loops are markedly widened and end abruptly at the cartilaginous junction, with only few extending into the thickened zone of pre-hypertrophic chondrocytes. The primary spongiosa are thickened and irregular and have many chondrocytes within retained cartilage cores. Within the metaphysis and diaphysis, there are reduced numbers of osteoclasts, and bony trabeculae are thickened (osteosclerosis) and lined by dense bands of osteoblasts. Multifocally within bony diaphyseal trabeculae there is a moderate amount of retained, unmineralized cartilage matrix, much of which contains retained chondrocytes

 

MORPHOLOGIC DIAGNOSIS:  Tibia, physis: Failure of endochondral ossification, diffuse, marked, with proliferation of prehypertrophic chondrocytes, decreased cartilage mineralization, and blunted physeal vessels, chicken, avian.

 

ETIOLOGIC DIAGNOSIS:  Toxic tibial chondrodysplasia

 

CAUSE:  Fusarochromanone toxin elaborated by Fusarium sp.

 

CONDITION:  Tibial dyschondroplasia

 

SYNONYM:  Tibial chondrodysplasia

 

GENERAL DISCUSSION:

• Tibial dyschondroplasia (TD) in poultry is a consequence of an inability of the immature pre-hypertrophic chondrocytes to undergo terminal differentiation, hypertrophy, and apoptosis, resulting in inabilty of cartilage matrix to mineralize and inability of metaphyseal vessels to penetrate, resulting in an abnormal mass of avascular, unmineralized cartilage with retained chondrocytes most commonly in the proximal metaphysis of the tibiotarsus, and occasionally in proximal and distal femur, distal tibia, proximal tarsometastarsus, and proximal humerus
• Most commonly affects proximal tibial physis of meat-type domestic fowl (broiler chickens, ducks, and turkeys)
• Usually appears between 3 and 8 weeks of age
• Fusarium are common fungal feed contaminants with toxic principle fusarochromanone (TDP-1); induced 100% incidence of TD when fed to broilers

 

PATHOGENESIS:

• Poorly understood; genetic, nutritional, and environmental factors:
  • Rapid growth and electrolyte imbalance leading to metabolic acidosis are considered primary contributing factors
  • Diets containing excessive chloride and phosphorous, or deficient in vitamin D, with respect to calcium levels are associated with increased incidence
  • Dithiocarbamate fungicides (thiram) and Fusarium mycotoxins are associated with increased incidence
• Primarily an inability of prehypertrophic chrondrocytes to undergo terminal differentiation; previously thought to be a associated with defects in metaphyseal vasculature
• Angiogenic factor ANGPTL4 (angiopoietin-like 4) may be a therapeutic target for ameliorating TD (Huang, J Comp Pathol. 2018)

 

TYPICAL CLINICAL FINDINGS:

• Often subclinical or with varying degrees of lameness
• Physeal lesions may result in valgus/varus deformities or fractures
• May resolve as growth rate slows and cartilage is resorbed and replaced by trabecular bone

 

TYPICAL GROSS FINDINGS:

• Bilateral, proximal tibial physis is thickened by an irregular mass of cartilage that is usually cone shaped (triangular) and extends beyond the growth plate
• Occurs most often in the proximal tibiotarsus, but can occur at other sites
• White, opaque, unmineralized, and unvascularized mass of cartilage
• In severe cases, the cartilage fills the entire metaphysis

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:

• Physis:
• Thickened by an avascular core of transitional (i.e. pre-hypertrophic) cartilage
• Persistence and accumulation of pre-hypertrophic chondrocytes that do not fully hypertrophy (defect in maturation)
• Increased unmineralized cartilaginous matrix, small lacunae
• Empty lacunae, chondrocytes with pyknotic nuclei (premature chondrocyte necrosis)
• Fewer chondroclasts
• Few vessels penetrate the abnormal cartilage from the metaphysis

 

DIFFERENTIAL DIAGNOSIS: 

For thickened growth plates or bone:

• Osteochondrosis: Cervical and thoracic vertebrae of broiler chickens; femoral head, antitrochanter of turkeys and broilers; physis disorganized and thickened by eosinophilic streaks, vascular thrombosis, and epiphyseal/growth plate necrosis; may cause dyschondroplasia
• Rickets: Failure of endochondral ossification, thickened metaphysis because of lack of osteoid resorption, thin irregular cortices; secondary to vitamin D, calcium, or phosphorus deficiency
• Normal variations: Neonatal chickens and turkeys have a cartilage core in long bones that extends from the growth plate into the metaphysis that regresses at one week of age
• Vitamin A toxicity: Thickened growth plates in chickens
• Osteopetrosis: Thickening of the physis and diaphysis of long bones secondary to infection with avian type C retrovirus (M-V03)

 

COMPARATIVE PATHOLOGY:

• Osteochondrosis: Similar disease seen in many rapidly growing domestic and laboratory animals
• Copper deficiency induced osteochondrosis: Swine, dogs, calves, horses, humans
• Zinc toxicity and chronic dexamethasone induced osteochondrosis: Foals, swine

 

REFERENCES:

1. 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.
2. Huang S, et al. Role of angiopoietin-like 4 on bone vascularization in chickens exposed to high-altitude hypoxia. J Comp Pathol. 2018;161:25-33.
3. Shivaprasad HL. Miscellaneous diseases. In: Boulianne M, ed. Avian Disease Manual. 8th ed. Athens, GA: American Association of Avian Pathologists; 2019:172-173.
4. Shivaprasad HL, Crespo R. Developmental, metabolic, and other noninfectious disoders In: Swayne DE, Glisson JR, McDougald LR, Nolan LK Suarez DL, Nair V, eds. Diseases of Poultry. 13th ed. Ames, IA: John Wiley & Sons, Inc.; 2013:1238-1240.

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