Mineral metabolism and immobilization osteopenia in ponies treated with 25-hydroxycholecalciferol.

The left thoracic limb was immobilized in a plaster cast in 6 grade weanling ponies for 6 weeks. Two ponies were injected intramuscularly each day with 2.4 micrograms of 25-hydroxycholecalciferol [25(OH)D3] per kg bodyweight, two with 1.2 micrograms and two received no injections. Immobilization of 25(OH)D3 treatment had no significant effect on mineral metabolism. Immobilization resulted in significantly decreased weight and specific gravity of metacarpus III (MCIII). Histologic examination and triple fluorochrome incorporation showed that the osteopenia was caused by atrophy of osteoblasts with failure of bone apposition. Immobilization caused retardation or cessation of proliferation of cartilage in the epiphyseal plate with thinning or premature closure. Treatment with 25(OH)D3 further reduced apposition and enhanced significantly the osteopenia as shown by quantitative morphometry of microradiographs of the MCIII metaphyses. There was parathyroid gland atrophy and fibrosis in proportion to the level of 25(OH)D3 treatment, which, in absence of hypercalcemia in all ponies, was interpreted to be a direct result of vitamin D treatment. It was concluded that immobilization osteopenia under the present design and duration is caused by failure of bone apposition and that treatment with 25(OH)D3 at dose levels applied is contraindicated.