Abstract
By application of light and electron microscopy, histochemistry, tracer procedures and a collagenolytic assay procedure, it was established that the osteolytic response of grey-lethal mice to acute parathormone (PTH) therapy was decidedly more vigorous than that elicited from their normal littermates. Time and calcium dependency studies conducted on a cell-free extract obtained from PTH-treated grey-lethal mouse bone indicated that the collagenolytic factor present in the preparation was collagenase. The osteoclasts seen in osteopetrotic mouse bone eighteen hours after PTH injection were characteristically intensely basophilic and possessed secretory inclusions apparently derived from their nuclei. Karyorrhexis was of common occurrence in these cells. Histologic evidence indicated that osteocytes promote resorption of bone matrix in anticipation of becoming fused into osteoclasts. A large proportion of the epithelial cells in the thyroid glands of the PTH-treated grey-lethal mice was identified as parafollicular, light cells. Osteopetrosis may be considered a congenital endocrinopathy, the primary lesion of which is hyperplasia of the calcitonin-producing parafollicular cells of the thyroid gland.
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