JPC SYSTEMIC PATHOLOGY
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 by a dense mass of avascular physeal cartilage characterized by a thickened zone of proliferation that fails to form fully mature hypertrophied chondrocytes, and does not undergo mineralization. The mass of cartilage protrudes deep into the proximal metaphysis and primary spongiosa are thickened and irregular and have many retained chondrocytes within the cartilage matrix. Metaphyseal capillary loops are markedly widened and end abruptly at the cartilaginous junction. 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 there is a moderate amount of retained, unmineralized cartilage matrix, much of which has retained chondrocytes, within bony diaphyseal trabeculae.
MORPHOLOGIC DIAGNOSIS: Tibia, physis: Failure of endochondral ossification, focally extensive, marked, with proliferation of prehypertrophic chondrocytes, decreased 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
- 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 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 ofmeat-type domestic fowl (broiler chickens, ducks and turkeys)
- Usually appears between 3 and 8 weeks of age
- Fusarium spp: Common fungal feed contaminants with toxic principle fusarochromanone (TDP-1); induced 100% incidence of TD when fed to broilers
- Poorly understood, genetic influence is indicated
- Primarily an inability of prehypertrophic chrondrocytes to undergo terminal differentiation; previously thought to be a associated with defects in metaphyseal vasculature
- Diets containing rapeseed meal, sorghum and some soybeans associated with increased incidence
- Cysteine, homocysteine, high levels of vitamin A, copper-deficiency, dithiocarbamate fungicides, and Fusarium its product fusarochromanone all are associated with increased incidence
- Rapid growth also associated
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:
- Proximal tibial physis is thickened by an irregular mass of cartilage that is usually cone shaped (triangular) and extends beyond the growth plate
- White, opaque, unmineralized, and unvascularized mass of cartilage
- In clinical cases, the cartilage fills the entire metaphysis
- In subclinical cases, abnormal cartilage is found mainly in the posterior and medial aspects of the proximal tibia
TYPICAL LIGHT MICROSCOPIC FINDINGS:
- Thickened by an avascular core of transitional/hypertrophied cartilage
- Persistence and accumulation of pre-hypertrophic chondrocytes that do not fully hypertrophy (defect in maturation)
- Increased unmineralized cartilaginous matrix, small lacunae
- Empty lacunae, pyknotic nuclei (premature chondrocyte necrosis)
- Fewer chondroclasts
- Few vessels penetrate the abnormal cartilage from the metaphysis
- Subepiphyseal-metaphyseal vessels: Blunted, fused, and tortuous
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
- 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
- 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
- Huang S, et al. Role of angiopoietin-like 4 on bone vascularization in chickens exposed to high-altitude hypoxia. J Comp Path. 2018;161:25-33.
- 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.
- Shivaprasad HL. Miscellaneous diseases. In: Boulianne M, ed. Avian Disease Manual. 7th ed. Athens, GA: American Association of Avian Pathologists; 2013:211, 216.