Pathology of Experimental Vitamin D Deficiency in Chickens and Effects of Treatment with Vitamin D Metabolites

Abstract

Structural changes in bone, parathyroid, and ultimobranchial body were examined in three groups of chicks fed a vitamin D-deficient diet; one group was treated with vitamin D3 and another with 1,25(OH)2D3. Diets were fed from day of hatching until 5 weeks old, when deficient chicks were near death due to hypocalcemic tetany, loss of fat and muscle, and marked bone deformities. In deficient chicks, parathyroid mass increased linearly to 7.5 times normal at 5 weeks. Parathyroid cells were irregular and vacuolated, with few granules. 1,25(OH)2D3 had normal parathyroids until the fifth week, when parathyroid mass increased greatly. There were few differences in length of growth cartilage, but marked changes in length of metaphyses. Deficient chicks had metaphyses nearly five times longer than vitamin D3-treated chicks. Metaphyses in chicks given 1,25(OH)2D3 were twice as long as those of vitamin D-treated chicks at 5 weeks. Both osteoblasts and osteoclasts were more numerous in deficient chicks. These studies suggest that vitamin D3 is more effective than 1,25(OH)2D3 in preventing parathyroid and bone lesions of vitamin D deficiency.

A Review of the Aetiology and Pathology of Leg Weakness in Broilers in Relation to Welfare

“…Broadly, there are two types of rickets (EC 2000) based on pathology: hypocalcaemic rickets is characterised by an accumulation of proliferating chondrocytes (Jande & Dickson, 1980), while in hypophosphataemic (phosphorus deficient) rickets the hypertrophic chondrocytes accumulate with normal metaphyseal vessel invasion (Lacey & Huffer, 1982). Vitamin D3 deficiency produces a similar lesion to calcium deficiency (Cheville & Horst, 1981). In the case of dyschondroplasia, however, there is an accumulation of pre-hypertrophic chondrocytes, with failure of metaphyseal invasion (Hargest et al, 1985a).…”

“…The role of vitamin D3 metabolism in rickets is believed to be the absorption of calcium and phosphorus from the intestine (Jande & Dickson, 1980) and the injection of 1,25(OH)2D3 has been shown to prevent the development of rickets in birds fed on a vitamin D3 deficient diet (Spencer et al, 1976;Cheville & Horst, 1981;Taylor & Dacke, 1984;Dickson et al, 1984). In the absence of flourescent lighting and 1,25-(OH)2D3, 27.5 ug/kg cholecalciferol reduced the incidence and severity of rickets to levels equivalent to those produced by either fluorescent lighting or 1,25-(OH)2D3 alone (Elliot and Edwards 1996).…”

Medical Management of Hypovitaminosis D With Cholecalciferol and Elastic Therapeutic Taping in Red-legged Seriema (Cariama cristata) Chicks

“…9 Dietary vitamin D 3 is considered a more significant source for avian species than cholecalciferol synthesized in the skin. 18 One study reports that clinical response in vitamin D-deficient chicks is more rapid with supplemental calcitriol, 19 whereas another found dietary cholecalciferol to be equally effective to fluorescent lighting or dietary calcitriol alone in reducing the severity of hypovitaminosis D in chicks. 20 Broiler chicks have a cholecalciferol requirement of 10 lg/kg diet (12.5 nmol/L 25-hydroxycholecalciferol) with a theoretical maximal response in bone calcium content seen at 20 lg/kg diet (25 nmol/L 25-hydroxycholecalciferol).…”

Metabolic bone disease in wild collared doves (Streptopelia decaocto)

“…It would be expected that hypocalcaemia and hypophosphataemia would develop in birds with rickets (Cheville and Horst 1981). However, normal calcium levels were found in two of the doves with bone disease, possibly because parathyroid hormone activity maintained normocalcaemia at the expense of bone (Woodard 1997).…”