Chapter 36: Drugs Affecting Calcium and Bone Formation

Bone strength is derived from the mineralization of hydroxyapatite on the bone matrix, a process characterized by a continuous cycle of remodeling where osteoclasts break down bone and osteoblasts build it back up. This equilibrium is primarily managed by three key hormones: vitamin D, which enhances intestinal calcium absorption; parathyroid hormone (PTH), which raises blood calcium levels by stimulating bone resorption and renal recovery; and calcitonin, which acts to lower plasma calcium by inhibiting osteoclast activity. The text provides an in-depth look at common skeletal disorders, including osteoporosis—a condition of reduced bone mass prevalent in postmenopausal women—as well as Paget disease and osteomalacia. To treat these conditions, the pharmacological toolkit includes antiresorptive agents like bisphosphonates, which bind to bone minerals to stop bone loss, and denosumab, a monoclonal antibody that disrupts the RANKL pathway essential for osteoclast survival. For patients requiring bone growth, anabolic therapies such as teriparatide mimic PTH signaling to actively stimulate new bone formation. Additionally, the chapter covers the clinical use of selective estrogen receptor modulators (SERMs) like raloxifene, the management of hypercalcemia through saline diuresis and calcimimetics like cinacalcet, and the foundational necessity of lifelong calcium and vitamin D supplementation to prevent fractures and maintain metabolic balance.