10.13

Bone Remodeling and Repair

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Bone remodeling occurs for various purposes, including repairing minor damage and regulating blood calcium levels.

During bone remodeling, osteoclasts are connective tissue cells that destroy the old matrix and osteoblasts are the cells that deposit a new one.

Bone remodeling occurs in three distinct steps--bone resorption, reversal, and formation.

When a bone first forms, osteoblasts are buried in the newly formed matrix and transform into osteocytes. Osteocytes sense mechanical stress and signal osteoclasts to the bone site.

Osteoclasts are multinucleated cells that initiate the bone resorption phase. They have finger-like projections containing vesicles that secrete enzymes for the degradation of organic bone components.

The degradation creates shallow depressions called resorption bays and releases calcium into the bloodstream.

In the reversal phase, the osteoclasts self-destruct via apoptosis, and mononuclear phagocytes appear at the degradation site. These cells prepare the degradation site for bone formation.

In the formation phase, the osteoblasts move into the resorption bays and deposit new bone through the ossification of the organic matrix, leading to bone growth.

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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during bone resorption and secrete several enzymes, including acid phosphatase. The acid phosphatase mineralizes the bone by degrading organic collagen and releasing calcium and phosphorus.

Bone remodeling is a skeletal change that occurs regularly in coordination with bone formation. This balances the breakdown and formation of new bone. However, after around 40 years of age, bone resorption occurs more frequently than formation, resulting in a reduction in bone density. This results in osteoporosis, which makes the bones weaker and brittle, increasing the risk of fractures.

Several hormones and proteins regulate the process of bone resorption. The Receptor activator of nuclear-factor kappa or RANK binds to its ligand and stimulates bone resorption. Calcitonin, a hormone released by the thyroid gland, reduces circulating calcium in the blood and inhibits bone resorption, thereby promoting bone formation. Similarly, parathyroid hormone or PTH increases the calcium level in the blood. Additionally, it also increases the activity of RANKL, promoting bone resorption. Growth hormone stimulates the activity of both osteoblasts and osteoclasts, thereby enabling both bone resorption and formation simultaneously.

The hormone estrogen negatively regulates bone resorption. A deficiency in estrogen increases bone resorption and bone remodeling. Calcitonin inhibits the resorption process by binding to calcitonin receptors on osteoclasts. Thus, calcitonin plays a role in calcium homeostasis and is used to treat osteoporosis.

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