Zinc, a nutritional trace element, is essential for the growth of human and animals.1 Zinc is required for the growth, development, and maintenance of healthy bones. Bone growth retardation is a common finding in various conditions associated with zinc deficiency.2 In Iranian schoolboys at year 1961, zinc supplementation was first found to restore both skeletal growth and maturation.3 Zinc deficiency is associated with many kinds of skeletal abnormalities in fetal and postnatal development. Zinc may play a physiologically important role in bone homeostasis. Skeleton contains a large proportion of the total body burden of zinc.4 Bone zinc has been shown to be concentrated in the layer of osteoid prior to calcification.5
Osteoporotic patients have been shown to have lower levels of skeletal zinc than healthy individuals.6 The reduction levels of biological markers of nutrition in postmenopausal osteoporosis may be related to zinc deficiency. In postmenopausal women, urinary zinc has been used as a marker of bone resorption. Plasma and urinary zinc concentrations in 30 women with postmenopausal osteoporosis and in 30 healthy postmenopausal women who served as controls have been measured.7 Plasma zinc levels did not differ between groups, but urinary zinc excretion has been found to be significantly higher in the women with postmenopausal osteoporosis.7 The elevation of urinary zinc elimination in osteoporosis may be dependent on bone resorption8 because zinc is located richly in bone tissues. To examine the independent association between dietary zinc and plasma zinc and the association of each with bone mineral density (BMD) and 4-year bone loss in community-dwelling older men. Of the original Rancho Bernardo Study subjects, 396 men (age: 45–92 years) were used. The mean dietary zinc intake was 11.2 mg. Dietary zinc intake and plasma zinc each have a positive association with BMD in men.8
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