1. Bone maintenance, repair, and physiology. A. Bone remodeling
Bone maintenance, repair, and physiology. A. Bone remodeling. This highly schematic figure represents a Volkmann's canal and adjacent tissue in compact bone to summarize osteoclast formation and activity. (1) Osteoblasts can express the signaling protein RANK-ligand (RANKL) on their surface and secrete macrophage colony-stimulating factor (M-CSF). (2) These two signals stimulate the formation of osteoclasts from monocytes, which express the RANK receptor for RANKL. Alternatively, osteoblasts can secrete osteoprotegerin (OPG) to cover RANKL and reduce the rate of monocyte fusion. (3) Individual osteoclasts will resorb limited amounts of bone, whereas groups of osteoclasts will tunnel into bone, eventually remodeling a volume into a new osteon. (4) The tunnel is lined by osteoprogenitor cells and osteoblasts that fill in the space created with new bone tissue. A blood vessel and associated loose connective tissue also enter as the basis of a Haversian canal to supply the new osteon that forms behind the osteoclasts. B. Bone fracture repair. A fracture in compact bone interrupts the blood supply to the central areas, resulting in the formation of a blood clot, the death of osteocytes, and the loss of some additional bone tissue. Signals generated by the clot and cell death stimulate the proliferation of cells in the periosteum and endosteum, which penetrate the clot and produce a soft callus of connective tissue and hyaline cartilage. This is then converted to a hard callus of primary bone via intramembranous and endochondral ossification and eventually remodeled into secondary bone. C. Bone regulation of body Ca2+. Bone contains a large reservoir of Ca2+ and phosphate. Exchange between bone salts containing Ca2+ and phosphate and their soluble ionic forms in extracellular fluid help maintain constant levels of these ions in blood. Parathyroid hormone (PTH) stimulates the release of Ca2+ from bone matrix by an indirect mechanism. PTH binds to osteoblasts, causing them to express RANKL and secrete M-CSF, stimulating the production of osteoclasts, which then degrade bone. Calcitonin binds directly to osteoclasts, inhibiting their activity, and thus decreasing the release of Ca2+ from bone into the blood.
Source: BONE, The Big Picture: Histology
Citation: Ash R, Morton DA, Scott SA. The Big Picture: Histology; 2017 Available at: Accessed: September 25, 2017
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