Abstract
Osteoporosis is a major health problem characterized by compromised bone strength predisposing patients to an increased risk of fracture. It may cause morbidity and mortality in elderly men and women. The etiologic factors that lead to senile osteoporosis still are unclear. Based on the available experimental and clinical evidence, we update our earlier proposal that zinc deficiency plays a role in the pathogenesis of senile osteoporosis. However, the mechanism of zinc deficiency in osteoporosis remains unclear. Zinc deficiency may lead to the increase of endogenous heparin probably causing degranulation of mast cells and release of endogenous heparin, and an increase in the bone-resorbing effect of prostaglandin E2. Endogenous heparin and prostaglandin E2 are probably cofactors of parathyroid hormone and may have a role in the pathogenesis of senile osteoporosis enhancing the action of parathyroid hormone. Therefore, zinc replacement by dietary zinc supplementation might be valuable to prevent or treat senile osteoporosis. Additional studies are necessary for the evaluation of the possible role of zinc in the etiology of senile osteoporosis. Level V (expert opinion). See the Guidelines for Authors for a complete description of the levels of evidence.
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