ZINC, COPPER AND MANGANESE DEFICIENCIES AND THE RUMINANT SKELETON: A REVIEW

Abstract

This review deals with changes in the morphology and composition of the skeleton of ruminants caused by trace element deficiencies, specifically with respect to zinc, copper and manganese. When ruminants are fed a zinc-deficient diet, bone abnormalities occur. Zinc is also reported to be of value in the prevention or cure of footrot in cattle and sheep. Depletion of zinc reserves appears to lead to alterations in bone mineralization and reduction of bone zinc concentration. The bones of copper-deficient ruminants are fragile and easily broken. The most prominent symptom of this deficiency is a very marked stiffness of the legs. Copper-deficient animals show symptoms of rickets with beading of the ribs and enlargement of the ends of the long bones. Histologically, the affected bones show widening of the growth plate and the overall appearance of the lesion is that of osteoporosis. Crosslinking between collagen precursors is impaired in copper deficiency, which affects the structural integrity of collagen. There is no evidence of any correlation between the concentration of copper in bone and the severity of malformation. A relationship between low manganese intake by gestating ruminants and increased incidence of deformed calves or lambs has been demonstrated. The deformities observed included enlarged joints and twisted forelimbs. Histological examinations of the affected bones revealed retarded growth. Since manganese plays an active role in bone matrix formation, synthesis of mucopolysaccharide is reduced in the deficient bones. The synthesis of chondroitin sulfate, which is involved in maintaining the rigidity of connective tissue, is also affected during manganese deficiency, resulting in skeletal abnormalities.