Abstract
Research in the 1920's established that rickets, a bone disease in which newly synthesized osteoid matrix does not calcify, was caused by a dietary deficiency in the fat-soluble vitamin D. These investigators concluded that vitamin D was necessary for the normal mineralization of bone. After 50 years of study the exact role of vitamin D in the mineralization process is still obscure. | A major problem in determining the mode of action of vitamin D on the mineralization of bone is that the cellular and molecular mechanisms of bone mineralization are unknown. | Historically, bone mineralization was considered to be a physicochemical process which depended on an adequate supply of Ca+2 and HP04-2 ions in extracellular fluid for the spontaneous precipitation of bone mineral. The impaired mineralization that was observed in a vitamin D-deficiency was probably a result of the lower Ca+2 and/or HPO4-2 concentrations in blood which were also mirrored in the fluids bathing the bone. Vitamin D was considered to be indirectly involved in bone mineralization through the regulation of blood Ca+2 and/or HPO4-2 levels.