PTH is a systemic hormone that regulates calcium levels in the blood in part by triggering calcium release from the bone. Chief cells within the parathyroid gland produce PTH when serum calcium levels are low . The increase in circulating PTH triggers bone remodeling, and subsequently, osteoclasts release calcium from the bone into the blood to maintain homeostasis . This ability to stimulate remodeling has led to the development of synthetic PTH for osteoporosis treatment. However, PTH is another signaling factor with a dual role in osteoclastogenesis. Circulating PTH stimulates osteoclast activity by increasing the RANKL to OPG ratio but inhibits osteoclast formation by decreasing sclerostin and DKK1 . Exogenous PTH alters bone remodeling differently depending on the administration schedule. Continuous administration decreases overall levels of bone density, whereas intermittent administration increases bone density levels . This has led many researchers to develop mathematical models to understand the mechanisms of PTH regulation.