Having observed previously that the reduction of levels of biological markers of nutrition in postmenopausal osteoporosis may be related to zinc deficiency, we measured plasma and urinary zinc concentrations in 30 women with postmenopausal osteoporosis and in 30 healthy postmenopausal women who served as controls. Plasma zinc levels did not differ between groups, but urinary zinc excretion was significantly higher in the women with postmenopausal osteoporosis (p = 0.002). The relation between total body bone mineral content corrected for body weight (TBBMC/W) and markers of nutrition was significant (multiple regression analysis: p < 0.0001) in the women with postmenopausal osteoporosis but not in the healthy postmenopausal controls. Likewise, the relation between TBBMC/W and plasma and urinary zinc levels also was significant in the women with postmenopausal osteoporosis but not in the controls (multiple regression analysis: p = 0.0022). Neither group showed any correlation between plasma or urinary zinc concentrations and levels of biological markers of nutrition. Urinary zinc concentration correlated significantly with serum tartrate-resistant acid phosphatase level (simple linear regression analysis: r = 0.583, p < 0.001) in the women with postmenopausal osteoporosis but not in controls. TBBMC correlated with urinary zinc concentration significantly in the women with postmenopausal osteoporosis (simple linear regression: r = 0.567, p = 0.0015), but the correlation was nonsignificant in healthy postmenopausal controls. These findings indicate that the elevation of urinary zinc elimination in osteoporosis is dependent on bone resorption.

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The effect of exposure to lead on the longitudinal development of bone and on bone mass was studied in rats. A group of 35, 50-day-old female Wistar rats was divided into a control group of 15 rats and an experimental group of 20 rats fed a diet supplemented with 17 mg of lead acetate per kg feed for 50 days. Total body bone densitometry (TBBMC) was performed the day before ending the 50-day experiment. On day 50, all rats were killed and their right femur and 5th lumbar vertebra were dissected. The bones were cleaned of soft tissue and femoral length and vertebral length were measured with a caliper and all bones were weighed on a precision scale. Final body weight (P < 0.05), TBBMC (P < 0.005), and femur weight (P < 0.005) were significantly lower in the control group. Femur length did not differ between groups, but the length of the 5th lumbar vertebra was greater in the control group (P < 0.05). Histomorphometry of the femur showed that Cn-BV/TV, Tb-N, Tb-Th were lower (P < 0.05 in all) and Tb-Sp was higher (P < 0.05) in the group given the lead-supplemented diet. These findings suggested lead-induced inhibition of axial bone development and a histomorphometric decrease in bone mass, produced mainly by enhanced resorption, and a densitometric increase in bone mass, produced by lead accumulation in bone.