Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
Parathyroid hormone (PTH) maintains homeostatic control of blood calcium levels by regulating bone resorption. PTH is released from the parathyroid glands in response to low levels of calcium in the blood. It stimulates osteoblasts to produce immune molecules that promote the differentiation of precursor cells into osteoclasts. Activation of osteoclasts promotes bone resorption, causing the mineralized bone matrix to break down and release calcium into the blood. When blood calcium levels are restored, a negative-feedback loop prevents further release of PTH.
Osteoporosis is a disease in which bone resorption exceeds bone formation, resulting in reduced bone density. Osteoporosis is more prevalent in women, especially after menopause. This is due to the critical role played by the female sex hormone—estrogen—in bone remodeling. Estrogen limits the formation of osteoclasts and promotes their destruction via apoptosis. This ensures that bone formation is higher than bone resorption. However, estrogen levels decline severely in menopausal women. Therefore, bone resorption outpaces its creation, leading to a loss of bone strength and increased risk of fractures.
