The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
Oxyphil cells, whose functions remain elusive, emerge during late puberty, adding a layer of complexity to the parathyroid gland's intricacies. In contrast, principal parathyroid cells undertake a vital role by producing the parathyroid hormone (PTH), also known as the parathormone. These cells actively monitor circulating calcium concentrations, exhibiting a dynamic response when levels decline.
Upon detecting decreased calcium levels, principal parathyroid cells release PTH, instigating a cascade of events to mobilize calcium. PTH regulates osteoblast and osteoclast activity in the bones. It initiates the secretion of the receptor activator of a growth factor called the nuclear factor-kappa-B ligament (RANKL) by osteoblasts. RANKL, in turn, amplifies osteoclast number and activity, intensifying mineral turnover and calcium release through bone matrix erosion.
Simultaneously, the heightened blood calcium levels trigger increased kidney reuptake and stimulate calcitriol secretion, reinforcing PTH activity. This feedback loop ensures a finely tuned regulation of calcium levels within the body, exemplifying the parathyroid glands' indispensable role in maintaining systemic mineral homeostasis.
