الفهرس 
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Abstract
Cadmium (Cd) is a toxic, bio-accumulating, non-essential and highlypersistent heavy metal. It is unique among metals because of the combination of its toxicity in low dosage, predominant storage in soft tissues, long biological half life (10-30 years) and low rate of excretion.
On the other hand, lead is one of the oldest known and most widely studied occupational and environmental poisons. Bone stores of Pb, built up from environmental exposure, are found in most people, and have recently been linked to the development of bone damage. In adults, about 95% of the total body burden of Pb is stored in the skeleton.
The most severe form of chronic Cd poisoning and Cd induced skeletal damage is “Itai-Itai disease”, in addition to osteomalacia and calciuria, osteoporosis and decreased BMD, increased incidence of fractures and decreased bone formation and increased resorption with increased susceptibility to Cd-induced bone injury especially in females.
Cd may directly affect bone by: (1) direct interference with collagen production in bones; (2) direct stimulation of bone resorption by prostaglandin production; (3) direct interference with incorporation of Ca into bone cells; and (4) impairment of bone formation by impending alkaline phosphatase activity. Furthermore, the following mechanisms are proposed for indirect influence of Cd on bonematter: (1) reduction of gastrointestinal calcium absorption; (2) increased urinary calcium excretion; (3) impairment of vitamin D activity in the kidney; (4) decreased Parathyroid (PTH) stimulation of adenylcyclase; and (5) the direct action of Cdon bone mineralization with derangement of collagen metabolism.
The detrimental effects of lead on bones included inhibition of matrix production, decreased bone density and bone calcium content, decreased trabecular bone volume, increased bone resorption, disruption of mineralization and chondrocyte organization and inhibition of axial bone development.
The effects of lead on the skeleton may be produced through two general processes. First, effects may be indirect and secondary to lead effects on the endocrine organs, which synthesize or produce hormones regulating bone function and bone mineral metabolism. Second, lead may directly perturb bone cell function by a) producing overt toxicity and cell death in bone cells, b) interfering with essential cell process including cell division, motility, and enzyme function, and c) by altering stimulus-response coupling, and/or osteoblast-osteoclast coupling through effects on the calcium messenger system