Pathology of experimental vitamin D deficiency rickets in growing chickens. I. Bone

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Abstract
Experiments were done to determine the characteristics and to study the development of avian rachitic lesions caused by vitamin D deficiency, and to investigate the cause of rickets which occurred in growing broiler chickens from 1974 to 1975 in Japan. Two kinds of vitamin D3 deficient diets, and feed of the same formula as that in use during outbreaks of rickets, were fed to day‐old commercial broiler chicks until they were 7 weeks of age. Bones from the birds were examined for pathological changes at weekly intervals. Pathological changes caused by the three experimental diets were identical in character though somewhat variable in degree. The main gross lesions were marked retardation of body growth, enlargement of the ends of the long bones, hypertrophy of the bones, widening of the epiphyseal plate, thickening of the cortical bone, softening of the bone, and enlargement of the parathyroid gland. Histologically, changes at the epiphyseal plate started with widening of both proliferating and hypertrophic zones. After that, the latter became paramount, but this was soon replaced by osteoid trabeculae resulting from accelerated endochondral ossification. Finally, the epiphyseal plate consisted mostly of a conspicuously widened proliferating zone. In the metaphysis and diaphysis, abnormal endosteal and periosteal osteogenesis appeared in the fairly early stages. The porosity of the cortical bone with osteogenous tissue was due to dilatation of the canal systems and demineralisation on the walls of Haversian canals. In brief, it was observed that lesions of vitamin D deficient rickets in growing chickens varied with time and that the entire bone including the cortical bone as well as the epiphyseal plate and metaphysis was involved. From the experimental results, it appeared that the rickets which occurred in Japanese commercial flocks was due to a vitamin D deficiency. The possibility that enlargement of the parathyroid gland, hyperparathyroidism, might play an important role in the development of this disease is discussed.