Rickets induced by calcium or phosphate depletion.
We studied the effects of calciopenia and phosphopenia on longitudinal growth, skeletal mineralization, and development of rickets in young Sprague-Dawley rats. At an age of 21 days, two experimental groups were given diets containing 0.02% calcium or 0.02% phosphorus; otherwise the diets were nutritionally adequate. After 7, 14, and 21 days, five animals from each group were randomly chosen. The animals were anaesthetized and blood samples were drawn for analysis of calcium, phosphorus, and immunoreactive parathyroid hormone, whereupon the animals were killed. Length, weight, and specific weight of the left femur were measured. After 28 days on the respective diet the remaining animals were killed and one proximal tibia from each animal was processed for light microscopy and subjected to stereological analysis. Both experimental groups developed progressive growth retardation, more so the phosphate-depleted group. The calciopenic animals developed severe hypocalcaemia and secondary hyperparathyroidism, whereas the phosphate-depleted animals, in spite of marked secondary hypercalcaemia, had unaltered levels of immunoreactive parathyroid hormone. By 28 days both experimental groups displayed rachitic changes, more pronounced in the phosphate-depleted animals. This paper provides quantitative data demonstrating that calciopenia per se may cause rickets in young rats, but that the rachitic changes in this condition are less severe, and the growth pattern different from those in phosphate depletion.
Department of General Surgery, Karolinska Institute, Huddinge University, Hospital, Sweden.
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Abugassa
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Svensson
D000818:Animals; D002118:Calcium / Q000172:deficiency*; D004838:Epiphyses / Q000473:pathology; D008297:Male; D010710:Phosphates / Q000172:deficiency*; D051381:Rats; D011919:Rats, Inbred Strains; D012279:Rickets / Q000209:etiology* / Q000473:pathology; D013977:Tibia / Q000473:pathology*
D010710:Phosphates; D002118:Calcium