FIGURE 1. From: Cellular and Molecular Mechanisms of Bone Remodeling.

Schematic representation of a BMU and the associated bone-remodeling process. Prior to activation, the resting bone surface is covered with bone-lining cells, including preosteoblasts intercalated with osteomacs. B-cells are present in the bone marrow and secrete OPG, which suppresses osteoclastogenesis. Activation, the endocrine bone-remodeling signal PTH binds to the PTH receptor on preosteoblasts. Damage to the mineralized bone matrix results in localized osteocyte apoptosis, reducing the local TGF-β concentration and its inhibition of osteoclastogenesis. Resorption, in response to PTH signaling, MCP-1 is released from osteoblasts and recruits preosteoclasts to the bone surface. Additionally, osteoblast expression of OPG is decreased, and production of CSF-1 and RANKL is increased to promote proliferation of osteoclast precursors and differentiation of mature osteoclasts. Mature osteoclasts anchor to RGD-binding sites, creating a localized microenvironment (sealed zone) that facilitates degradation of the mineralized bone matrix. Reversal, reversal cells engulf and remove demineralized undigested collagen from the bone surface. Transition signals are generated that halt bone resorption and stimulate the bone formation process. Formation, formation signals and molecules arise from the degraded bone matrix, mature osteoclasts, and potentially reversal cells. PTH and mechanical activation of osteocytes reduce sclerostin expression, allowing for Wnt-directed bone formation to occur. Termination, sclerostin expression likely returns, and bone formation ceases. The newly deposited osteoid is mineralized, the bone surfaces return to a resting state with bone-lining cells intercalated with osteomacs, and the remodeling cycle concludes.

Liza J. Raggatt, et al. J Biol Chem. 2010 August 13;285(33):25103-25108.

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