5 male and 1 female 22 day old Ross 308 broiler chickens, Gallus galls domesticsSix chickens were received for necropsy from a flock of 14000 individuals. The chickens showed signs of poor growth during the first 2 weeks, and on day 11 a new batch of feed was introduced. In the 3rd week the chickens weighed 40-50 grams less than normal. The feed intake was slightly increased. From day 18 signs of leg problems were observed in the flock, and tibiotarsal fractures were detected. On day 20, 40 chickens had fractures and 235 had been euthanized. From day 22, another new batch of feed was introduced. On day 27, an improvement in flock health had occurred and the remaining flock was slaughtered at normal time.

Gross Description:  

The 6 chickens had been euthanized and they weighed 482-654 grams. Four chickens had a unilateral fracture in the distal tibiotarsus, one chicken had a unilateral fracture in a femur, and in one chicken no fractures were detected. Surrounding the fractures there were moderate to large hemorrhages. Mineralization of bones was severely reduced in all 6 chickens. The hypertrophic zone of the growth plate in the proximal tibiotarsus was moderate to severely widened towards the metaphysis in all 6 chickens. Enlarged parathyroid gland was not detected macroscopically.

Histopathologic Description:

In the proximal tibiotarsus there is severe widening of the hypertrophic zone of the growth plate. The hypertrophic zone is dominated by wide cartilage columns consisting of large hypertrophic chondrocytes in an orderly fashion. These cartilage columns are either naked or lined by a very narrow zone of osteoid. Multifocally the lining of the columns are ragged and scalloped, and in some areas with clusters of osteoclasts.

The thickness of the proliferating zone of the growth plate was considered normal. In the metaphysis, the cortical bone is severally thinned, and there is mild multifocal proliferation of fibroblasts subperiosteally. In some sections bacterial emboli are seen in medullary vessels.

Morphologic Diagnosis:  

Proximal tibiotarsus



Contributor Comment:  

Rickets in chickens is characterized by severe fragility of long bones and bending of long bones due to poor mineralization, and it may be caused by an imbalance between calcium and phosphorus or vitamin D deficiency.(3) The histopathology of rickets differs depending on the cause of the disease.(3,9) A hypocalcemic form is characterized by accumulation of proliferating chondrocytes,(2) and chickens fed a diet low in calcium showed, by 2 weeks of age, a variably lengthened and disorganized proliferating zone and shortened cartilage columns of the hypertrophied zone.(7) A hypophosphatemic form is characterized by accumulation of hypertrophic chondrocytes in the metaphyseal zone (4). Chickens fed a diet low in phosphorus showed, by 2 weeks of age, lengthening of the hypertrophic zone,(6) and a diet with excess calcium caused similar lesions (6). These two forms differ in histopathology from the rickets of vitamin D deficiency.(3) In vitamin D deficiency, the enlargement of the epiphyseal plate initially is due to widening of the proliferating and hypertrophic zones; as the deficiency progresses, it may be primarily the former.(3) The extensive lengthening of the hypertrophic zone found in these chickens may indicate a hypophosphatemic rickets; however, preliminary analyses of the feed used for this flock showed decreased levels of vitamin D3, while calcium and phosphorus were within normal range.

JPC Diagnosis:  

1. Proximal tibiotarsus: Physeal chondrodystrophy with marked elongation of the zone of hypertrophy, delayed endochondral ossification, and cortical osteopenia.
2. Proximal tibiotarsus: Fibrous osteodystrophy.

Conference Comment:  

Although the lesions may be most similar to hypophosphatemic rickets, the history and dietary analysis are convincing for hypovitaminosis D. Conference participants discussed the importance of relying on dietary analysis to determine the type of deficiency rather than fine variations in bone lesions.

Some slides have areas of poor tissue preservation or autolysis with colonies of coccoid bacteria and homogeneous, eosinophilic, acellular material filling medullary spaces. PTAH and Massons trichrome histochemical stains were performed to determine if the acellular material is widespread fibrin exudation; however, PTAH did not stain fibrin, and conference participants considered serous atrophy of fat affecting the metaphysis and epiphysis as the more likely cause for the acellular material. The Massons trichrome revealed perivascular fibrosis of vessels penetrating the growth plate, mild peritrabecular fibrosis in the metaphysis, endocortical fibrosis, fibrosis in the vascular spaces of the cortex, and minimal fibrosis in the epiphysis interpreted as fibrous osteodystrophy secondary to hypovitaminosis D, similar to case 1(3).

Also similar to case 1 are the findings of cortical osteopenia with woven bone in the cortex and increased cortical porosity due either to delayed osteonization or increased cortical lysis. Rickets in avian species differs from that in mammals in that there is delayed onset of osteoid deposition, atrophy of osteoblasts on cartilage cores, and retention and minimal disorganization of hypertrophied chondrocytes in wide regular columns which often extend deep into the metaphysis. As mentioned by the contributor, the multifocal marked osteoclast hyperplasia of metaphyseal trabeculae and endocortical surfaces at the diaphysis was interpreted by conference participants as normal endocortical osteoclasis, or modeling of the endocortical surface of a rapidly growing bird(1,3).

The primary differential diagnosis in this case is tibial dyschondroplasia (TD), a spontaneous lesion of rapidly growing birds which is characterized by a large mass of avascular cartilage in the tibiotarsal metaphysis with necrosis of the prehypertrophic zone of chondrocytes, and is similar to osteochondrosis in mammals. The lesions in TD are very similar to those of rickets, and are the result of failure of chondrocytes to fully differentiate and allow vascularization, mineralization, and resorption of cartilage matrix(3,5,8).


1. Hedstrom OR, Cheville NF, Horst RL. Pathology of vitamin D deficiency in growing turkeys. Vet Pathol. 1986 Jul; 23(4):485-98.

2. Jande SS, Dickson IR: Comparative histological study of the effects of high calcium diet and vitamin D supplements on epiphyseal plates of vitamin-D-deficient chicks. Acta Anat (Basel) 108:463-468, 1980

3. Klasing KC: Nutritional diseases. In: Saif YM, ed. Diseases of Poultry. 12th ed. Oxford, England: Blackwell Publishing; 2008:1121-1148.

4. Lacey DL, Huffer WE: Studies on the pathogenesis of avian rickets. I. Changes in epiphyseal and metaphyseal vessels in hypocalcemic and hypophosphatemic rickets. Am J Pathol 109:288-301, 1982

5. Leach RM jr, Gay CV. Role of epiphyseal cartilage in endochondral bone formation. J Nutr. 1987 Apr;117(4):784-90.

6. Long PH, Lee SR, Rowland GN, Britton WM: Experimental rickets in broilers: gross, microscopic, and radiographic lesions. I. Phosphorus deficiency and calcium excess. Avian Dis 28:460-474, 1984

7. Long PH, Lee SR, Rowland GN, Britton WM: Experimental rickets in broilers: gross, microscopic, and radiographic lesions. II. Calcium deficiency. Avian Dis 28:921-932, 1984

8. Orth MW, Cook ME. Avian tibial dyschondroplasia: a morphological and biochemical review of the growth plate lesion and its causes. Vet Pathol. 1994 Jul;31(4):403-4.

9. Randall CJ: Nutritional deficiencies and metabolic disorders. In: A colour atlas of diseases and disorders of the domestic fowl and turkey, ed. Randall CJ, 2nd ed., pp. 109-124. Wolfe Publishing Ltd, London, 1991

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