Chemically-Induced Injury of the Parathyroid Gland: Pathophysiology and Mechanistic C onsiderations
Parathyroid glands are composed of a single cell type concerned with the biosyn thesis of one hormone (Fig. 1). Chief cells have a normal secretory cycle, with the majority being in the inactive stage under steady-state conditions. In response to a low calcium ion signal, chief cells enter the active phase with syn thesis and packaging of a “batch” of hormone. After secretion of parathyroid hor mone (PTH), the chief cell involutes back to the resting (inactive) phase. In response to long-term stimulation, chief cells undergo a sequence of morphologic changes culminating in the formation of water-clear cells. Conversely, long-term suppression by elevated blood calcium ion results in parathyroids with predom inantly inactive and atrophic chief cells. Mitochondrion-rich oxyphil cells form in parathyroids of humans and certain animal species with advancing age. Syn thetic and secretory organelles are largely crowded out by the proliferation of mitochondria in the cytoplasm, suggesting that oxyphil cells are not actively involved in the biosynthesis of PTH.