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Multinucleated osteoclasts resorb bone to form resorption pits known as Howship’s lacunae. (Schematic figure is adapted from Clarke B et al. Clin. J. Am. Soc. Nephrol. 2008 Nov;3 Suppl 3:S131-9) 

Multinucleated osteoclasts resorb bone to form resorption pits known as Howship’s lacunae. (Schematic figure is adapted from Clarke B et al. Clin. J. Am. Soc. Nephrol. 2008 Nov;3 Suppl 3:S131-9) 

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Context 1
... are the only cells that are known to be capable of resorbing bone ( Figure 2). Activated multinucleated osteoclasts are derived from mononuclear precursor cells of the monocyte-macrophage lineage 5 . Mononuclear monocyte- macrophage precursor cells have been identified in various tissues, but bone marrow monocyte-macrophage precursor cells are thought to give rise to most osteoclasts. Osteoclast formation, activation, and resorption are regulated by the ratio of receptor activator of NF- κ B ligand (RANKL) to osteoprotegerin (OPG; Figure 1), IL-1 and IL- 6, macrophage colony stimulating factor (M-CSF), parathyroid hormone, 1,25- dihydroxyvitamin D, and calcitonin 5,6 . Resorbing osteoclasts secrete hydrogen ions via H + -ATPase proton pumps and chloride channels in their cell membranes into the resorbing compartment to lower the pH within the bone-resorbing compartment to as low as 4.5, which helps mobilize bone mineral 7 . Resorbing osteoclasts secrete tartrate-resistant acid phosphatase, cathepsin K, matrix metalloproteinase 9, and gelatinase from cytoplasmic lysosomes 8 to digest the organic matrix, resulting in formation of saucer-shaped Howship’s lacunae on the surface of trabecular bone (Figure 2) and Haversian canals in cortical bone. The resorption phase is completed by mononuclear cells after the multinucleated osteoclasts undergo apoptosis 9,10 . RANKL and macrophage CSF (M- CSF) are two cytokines that are critical for osteoclast formation. Both RANKL and M-CSF are produced mainly by marrow stromal cells and osteoblasts in membrane- bound and soluble forms, and osteoclastogenesis requires the presence of ...
Context 2
... are the only cells that are known to be capable of resorbing bone ( Figure 2). Activated multinucleated osteoclasts are derived from mononuclear precursor cells of the monocyte-macrophage lineage 5 . Mononuclear monocyte- macrophage precursor cells have been identified in various tissues, but bone marrow monocyte-macrophage precursor cells are thought to give rise to most osteoclasts. Osteoclast formation, activation, and resorption are regulated by the ratio of receptor activator of NF- κ B ligand (RANKL) to osteoprotegerin (OPG; Figure 1), IL-1 and IL- 6, macrophage colony stimulating factor (M-CSF), parathyroid hormone, 1,25- dihydroxyvitamin D, and calcitonin 5,6 . Resorbing osteoclasts secrete hydrogen ions via H + -ATPase proton pumps and chloride channels in their cell membranes into the resorbing compartment to lower the pH within the bone-resorbing compartment to as low as 4.5, which helps mobilize bone mineral 7 . Resorbing osteoclasts secrete tartrate-resistant acid phosphatase, cathepsin K, matrix metalloproteinase 9, and gelatinase from cytoplasmic lysosomes 8 to digest the organic matrix, resulting in formation of saucer-shaped Howship’s lacunae on the surface of trabecular bone (Figure 2) and Haversian canals in cortical bone. The resorption phase is completed by mononuclear cells after the multinucleated osteoclasts undergo apoptosis 9,10 . RANKL and macrophage CSF (M- CSF) are two cytokines that are critical for osteoclast formation. Both RANKL and M-CSF are produced mainly by marrow stromal cells and osteoblasts in membrane- bound and soluble forms, and osteoclastogenesis requires the presence of ...