Abstract
Osteoclasts differentiate from hematopoietic cells and resorb the bone in response to various signals, some of which are received directly from noncellular elements of the bone. In vitro, adherence to the bone triggers the reduction of cell–cell fusion events between osteoclasts and the activation of osteoclasts to form unusual dynamic cytoskeletal and membrane structures that are required for degrading the bone. Integrins on the surface of osteoclasts are known to receive regulatory signals from the bone matrix. Regulation of the availability of these signals is accomplished by enzymatic alterations of the bone matrix by protease activity and phosphorylation/dephosphorylation events. Other membrane receptors are present in osteoclasts and may interact with as yet unidentified signals in the bone. Bone mineral has been shown to have regulatory effects on osteoclasts, and osteoclast activity is also directly modulated by mechanical stress. As understanding of how osteoclasts and other bone cells interact with the bone has emerged, increasingly sophisticated efforts have been made to create bone biomimetics that reproduce both the structural properties of the bone and the bone’s ability to regulate osteoclasts and other bone cells. A more complete understanding of the interactions between osteoclasts and the bone may lead to new strategies for the treatment of bone diseases and the production of bone biomimetics to repair defects.
Highlights
Bones are a stable foundation of the vertebrate body [1,2]
Much of the regulation of osteoclasts is indirect through osteocytes [19,20,21], osteoblasts [19,22,23], lining cells [19] and even immune cells [15], in this review article, we will focus on what is known about the direct interaction of osteoclasts with the bone, and outstanding questions in the area
Synaptotagmin VII localizes to vesicles in the cytosol of osteoclasts, and as the osteoclasts activates, it is concentrated in the ruffled border exactly like V-ATPase and is there
Summary
Bones are a stable foundation of the vertebrate body [1,2]. Barring injury or pathologies, each bone maintains shape and structural properties throughout adulthood, despite being constantly remodeled. The RANKL/RANK/osteoprotegerin signaling network is central to bone remodeling, the activity of bone cells is controlled by their physical environment [1] This includes signals that are present in the organic elements of the bone, in the mineral component of the matrix, and in response to mechanical forces exerted on them in their bone microenvironment [1]. Together, these signals act in concert with various intercellular signals and hormones to trigger necessary bone resorption and to produce coupling factors that stimulate bone formation to replace the bone that is removed by osteoclastic resorption [18]. Much of the regulation of osteoclasts is indirect through osteocytes [19,20,21], osteoblasts [19,22,23], lining cells [19] and even immune cells [15], in this review article, we will focus on what is known about the direct interaction of osteoclasts with the bone, and outstanding questions in the area
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