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Bone remodeling consists of two equal phases: resorption and formation. During resorption, osteoclasts remove old or damaged bone matrix by secreting enzymes and hydrogen protons, creating erosion cavities. In the formation phase, osteoblasts deposit new bone tissue through ossification of organic matrix called osteoid, which includes collagen fibers that contribute to bone structure and flexibility.

Osteoclasts cling tightly to the bone surface and secrete lysosomal enzymes and hydrogen protons that degrade the organic components of the bone matrix. This process dissolves the old or damaged material, creating erosion cavities. Once resorption is complete, osteoclasts undergo apoptosis, a programmed cell death that prevents further bone destruction and allows the formation phase to begin.

Parathyroid hormone (PTH) maintains blood calcium homeostasis by regulating bone resorption. When blood calcium levels drop, PTH is released and stimulates osteoblasts to produce immune molecules that promote osteoclast differentiation. This increases bone resorption, releasing calcium into the blood. Once calcium levels normalize, negative feedback prevents further PTH release, balancing the remodeling process.

After osteoblasts deposit new bone matrix during the formation phase, they can differentiate into flattened bone lining cells that cover the bone surface, or they can become buried within the bone as osteocytes. Osteocytes are mature bone cells that sense mechanical stress and signal other cells to initiate new remodeling cycles, maintaining bone architecture throughout life.

Estrogen limits osteoclast formation and promotes their destruction through apoptosis, ensuring bone formation exceeds bone resorption. After menopause, estrogen levels decline significantly, disrupting this balance. Bone resorption then outpaces formation, leading to reduced bone density and increased fracture risk, which explains why osteoporosis is more prevalent in postmenopausal women.

When mature bone cells called osteocytes sense mechanical stress, they signal other cells to the bone site to initiate remodeling. This process helps maintain bone architecture and repair damage. For example, the ends of the femur are replaced every six months through this stress-responsive mechanism, ensuring bones remain strong and functional despite continuous use.

Osteoporosis is a disease where bone resorption exceeds bone formation, resulting in reduced bone density and weakened bone structure. This imbalance can occur due to hormonal changes, such as declining estrogen levels in postmenopausal women, or other factors affecting the remodeling process. The condition increases fracture risk and is more prevalent in women than men.