Abstract
Zinc administration prevents bone loss in rats with ovariectomy, skeletal unloading, hydrocortisone treatment, adjuvant arthritics and diabetic condition in rats. Zinc has been shown to play a role in the preservation of bone mass by stimulating osteoblastic bone formation and inhibiting osteoclastic bone resorption in rat bone tissues. The cellular mechanism of zinc action in inhibiting osteoclastic bone resorption is reviewed. Zinc inhibits bone resorption which is stimulated by various bone-resorbing factors including parathyroid hormone (PTH), 1, 25-dihydroxyvitamin D3 [1, 25(OH)2D3], and prostaglandin E2 (PGE2) in rat bone tissue culture in vitro. Also, zinc has an inhibitory effect on the bone-resorbing factors-induced osteoclast-like cell formation in mouse marrow culture in vitro. The stimulatory effect of bone-resorbing factors on osteoclastogenesis is mediated through receptor activator of NF-κB ligand (RANKL), which plays a key role in development of osteoclasts from preosteoclasts. Zinc inhibits RANKL stimulation in osteoclastogenesis. RANKL is expressed in osteoblasts. In addition, zinc may inhibit RANK expression which is mediated through Ca2+ signaling (protein kinase C) by stimulation of PTH, 1, 25(OH)2D3 or PGE2 in osteoblasts. Zinc plays an inhibitory role in the regulation of osteoclastogenesis.
