The role of zinc as a stimulatory factor on bone formation was reviewed. Bone growth retardation is a common finding in various conditions associated with zinc deficiency. The mechanism of zinc action on bone metabolism, however, has not been clarified so far. The oral administration of zinc sulfate (0.5-10 mg Zn/100 g body weight) to weanling rats can produce an increase in dry weight, alkaline phosphatase activity, calcium, collagen and deoxyribonucleic acid (DNA) contents in the femoral diaphysis, indicating that zinc has a stimulatory effect on bone formation and calcification. In tissue culture by using the calvaria from weanling rats, it has been demonstrated that zinc (10-6-10-4M) can stimulate bone protein synthesis, and that the zinc effect is based on activation of aminoacyl-transfer ribonucleic acid (tRNA) synthetase. The depletion of endogenous zinc in bone cells by treatment with dipicolinate, a chelator of zinc, can retard the synthesis of bone protein. Zinc is an essential factor in the systhesis of bone protein. Increasing age induces the deterioration of bone metabolism, and it decreases bone cellular zinc and protein systhesis. These decreases, however, can be restored by supplement of zinc. Thus, it has been introduced that zinc, an essential trace element, plays an important role in the stimulation of bone formation.
