Fine structure of the parathyroid glands in baboons, <i>Papio hamadryas</i> in response to experimental hypercorticoidism

Abstract

Female baboons maintained under laboratory conditions were subjected to a series of 10 weekly injections (4 mg/kg body weight) of the synthetic glucocorticoid, triamcinolone hexacetonide. In response to the treatment, serum immunoreactive parathyroid hormone (PTH) levels were raised, though blood calcium levels remained within normal physiological limits. Light and electron-microscopic studies were made on the parathyroid glands at the end of the experimental period. The baboon parathyroid glands were composed of ‘light’ and ‘dark’ forms of the chief cells in varying ratios from gland to gland even within a single animal. Glucocorticoid-induced parathyroid hyperactivity as measured by circulating PTH levels was not accompanied by cellular hypertrophy, though there was an increase in the relative number of ‘light’ cells. At the ultrastructural level, after treatment, many of the ‘light’ cells were found to contain more free ribosomes, larger profiles of granular endoplasmic reticulum and had better developed mitochondria. Interdigitations between adjacent chief cells were more complex in treated glands. Apart from these features, chief cells of treated glands were basically similar to those of untreated controls. Our study showed that functional parathyroid hyperactivity in baboons is not necessarily accompanied by significant ultrastructural changes in chief cells.

Elevated concentrations of synthetic fluorinated glucocorticoid analogs transiently increase the intracellular exchangeable calcium in cultured bone cells

“…However, the mechanism of their action on bone is rather complex as these hormones appear to act simultaneously on a number of different target cells. Hence their overall effect may result from a direct action on bone growth centers as well as their effects on calcium transport in the intestinal mucosa and/or their stimulatory effects on the parathyroid gland [6][7][8]. Thus in vivo studies do not distinguish between the primary and secondary effects of glucocorticoids on skeletal elements such as bone cells.…”