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Effect of ascorbic acid and 1,25(OH)2D3 on bone cell metabolism in relation to the development of tibial dyschondroplasia.

Published online by Cambridge University Press:  24 November 2017

C. Farquharso ,
J.S. Rennie ,
N. Loveridge  and
C.C. Whitehead
C. Farquharso
Affiliation:
AFRC, Institute of Animal Physiology and Genetics Research, Roslin, Scotland.
J.S. Rennie
Affiliation:
AFRC, Institute of Animal Physiology and Genetics Research, Roslin, Scotland.
N. Loveridge
Affiliation:
Rowett Research Institute, Aberdeen, Scotland.
C.C. Whitehead
Affiliation:
AFRC, Institute of Animal Physiology and Genetics Research, Roslin, Scotland.
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Extract

Tibial dyschondroplasia (TD) results from a defect in endochondral ossification and is characterised by an accumulation of avascular cartilage extending distally from the growth plate. The lesion develops in young fast growing birds (broilers and turkeys) and is thought to be a result of incomplete chondrocyte differentiation. This condition can result in deformed bones and lameness and has therefore many economic and welfare implications.

Since its description 25 years ago, TD has been studied extensively. The majority of the research has focused on determining the role of nutrition in the aetiology of the disease but it has only recently been shown that this disorder can be completely prevented by supplementing the diet with 1,25(OH)2 D3 (Rennie et al., 1993).This may be related to the hormones ability to increase the rate of chondrocyte differentiation (Farquharson et al., 1993). Since ascorbic acid (AA) has been shown previously to stimulate the endogenous synthesis of 1,25(OH)2 D3 (Weiser et al. 1988), its effect on the development of TD in young fast growing broilers was investigated

Type
Metabolic Disorders
Information
Proceedings of the British Society of Animal Production (1972) , Volume 1993: Winter meeting , March 1993 , pp. 230
Copyright
Copyright © The British Society of Animal Production 1993

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References

Farquharson, C,Whitehead, CC,. Rennie, J.S. and Loveridge, N. (1993) In vivo effects of 1,25 dihydroxycholecalciferol on the proliferation and differentiation of avian chondrocytes. J. Bone Min. Res. (Submitted for publication)Google Scholar
Rennie, J.S., Whitehead, C.C. and Thorp, B.H. (1993) The effect of dietary 1,25 dihydroxycholecalciferol in preventing tibial dyschondroplasia in broilers fed diets imbalanced in calcium and phosphorus. Br. J. Nutr. (In press).Google Scholar
Weiser, H., Schlachter, M. and Bachmann, H. (1988) The importance of vitamin C for hydroxylation of vitamin D 3 to 1a25(OH)2D3 and of 24R,25(OH)2D3 to a more active metabolite. In Vitamin D, Molecular, Cellular and Clinical Endocrinology, Walter de Gruyter & Co., Berlin.Google Scholar