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Role of zinc in bone formation and bone resorption

Zinc is essential for the growth of the human and other animals. Bone growth retardation is a common finding in various conditions associated with zinc deficiency, suggesting a physiological role of zinc in the growth and mineralization of bone tissue. Bone zinc content is decreased by development w...

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Bibliographic Details
Published in:The journal of trace elements in experimental medicine 1998, Vol.11 (2-3), p.119-135
Main Author: Yamaguchi, Masayoshi
Format: Article
Language:English
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Summary:Zinc is essential for the growth of the human and other animals. Bone growth retardation is a common finding in various conditions associated with zinc deficiency, suggesting a physiological role of zinc in the growth and mineralization of bone tissue. Bone zinc content is decreased by development with aging, skeletal unloading, and postmenopausal conditions. Zinc deficiency may play a pathophysiological role in the deterioration of bone metabolism. Zinc has been demonstrated to have a stimulatory effect on bone formation and mineralization; the metal directly activates aminoacyl‐tRNA synthetase in osteoblastic cells, and it stimulates cellular protein synthesis. Moreover, zinc inhibits osteoclastic bone resorption by inhibiting osteoclast‐like cell formation from marrow cells. Zinc may act on the process of bone‐resorbing factors‐induced protein kinase C activation, which is involved in Ca2+ signaling in osteoclastic cells. Zinc plays a role in the preservation of bone mass. AHZ is a zinc compound, in which zinc is chelated to β‐alanyl‐L‐histidine. The stimulatory effect of AHZ on bone formation was more intensive than that of zinc sulfate. It is confirmed that bone‐forming effect of AHZ is a greater than that of various bone‐regulating hormones and other factors. The oral administration of AHZ has a fine restorative effect on osteopenia with various pathophysiological conditions. Zinc compound may be a new drug in the therapy of osteoporosis. J. Trace Elem. Exp. Med. 11:119–135, 1998. © 1998 Wiley‐Liss, Inc.
ISSN:0896-548X
1520-670X
DOI:10.1002/(SICI)1520-670X(1998)11:2/3<119::AID-JTRA5>3.0.CO;2-3