Formation of the callus at the site of a femoral fracture in rats without vitamin D deficiency is accompanied by an increase in the specific mass and mineralization of the unaffected pair bone, which indicates general intensification of the processes of mineralization occurring in the skeleton during fractures. Vitamin D deficiency leads to hypocalcemia, retardation of callus mineralization, and drastic demineralization of the intact thighbone thus pointing to pathological enhancement of skeleton resorption as the main source of calcium required for covering bodily requirements. Like vitamin D2 in a dose of 0.300 microgram, administration of 1 alpha-hydroxyvitamin D3 (1 alpha-HCD3) in a dose of 0.025 microgram daily to rats with femoral fractures kept on the vitamin D-deficient diet provides for effective calcium homeostasis maintenance and mineralization of the callus and unaffected bones. This demonstrates high biological activity of 1 alpha-HCD3 and its efficacy in promoting the processes of mineralization during fractures. The increase in the phosphorus content in the diet until the calcium/phosphorus ratio reaches 1:2 (instead of the optimal 1:1), aggravates hypocalcemia and sharply enhances demineralization of the intact bone in vitamin d-deficient rats with femoral fractures and reduces mineralization of the callus in rats given 1 alpha-HCD3. The data obtained indicate the necessity of reliable correction of potential vitamin D deficiency and optimization of the calcium-phosphorus ratio in the diet and preparations, as well as a possibility of applying 1 alpha-HCD3 in the combined treatment of fractures.