Tibial dyschondroplasia, a cartilage abnormality in poultry

Abstract

Tibial dyschondroplasia is characterized by a calcification defect and by the presence of an abnormal mass of unvascularized cartilage in the proximal metaphysis of chick and turykey tibio tarsus. The gross appearance of the lesion shows some similarities with rickets, but the histological figures are quite different, without any modification of the proliferating zone of the epiphyseal plate. The figures of the chemical composition of abnormal cartilage and the blood parameters related to mineral metabolism both remain normal. The abnormal cartilage plug seems to result from the proliferation of prehypertrophic cells in relation to the lack of metaphyseal vascularization. Tibial dyschondroplasia is under genetic control and can be eliminated after three generations of divergent selection. In the field, its incidence is proportional to the growth rate of the flocks and males are more sensitive than female birds. In unselected birds, tibial dyschondroplasia can be induced by feeding a purified diet containing all known nutrients; corn and soybean meal have preventing properties. The abnormality can not be prevented by any known essential nutrient, such as minerals or vitamins. Metabolic acidosis due to ammonium chloride ingestion or only to an excess of chloride, strongly increases the defect incidence, while growth simultaneously decreases. This adverse effect of chloride can be overcome by the addition of a sufficient level of sodium and potassium into the died, restoring body weight to a normal value. Although the tibial dyschondroplasia condition presents a clinical picture quite different from that of rickets, the possible intervention of a vitamin D metabolite is discussed since it is known that metabolic acidosis impairs the renal transformation of 25-(OH)CC into 1,25-(OH)2CC.