J Korean Orthop Assoc.  2009 Apr;44(2):151-158.

Glucocorticoid-induced Osteoporosis; Update

• Kim SY
• Kim HJ

Abstract

No abstract available.

Figure

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  Fig. 1 Regulation of osteoclast formation and function. Osteoclasts are derived from hematopoietic mononuclear precursors of the monocyte/macrophage lineage. The proliferation and survival of osteoclast precursors is dependent on the M-CSF. Activation of RANK by RANKL (RANK-Ligand) commits the cell to the osteoclast fate. The initial event in development of the resorptive capacity of the mature osteoclast (OC) is its cytoskeletal organization, namely polarization. Once polarized, the osteoclasts resorb the mineralized component of bone.

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  Fig. 2 Comparison of a normal cycle of bone remodeling (A) with an abnormal one caused by glucocorticoid excess (B). Resorptive phase: activated osteoclasts resorb a discrete area of mineralized bone matrix. Reversal phase: subsequently osteoblasts migrate into resorption lacuna, possibly by factors produced by the osteoclast. Formative pahse: the osteoblasts deposite new bone matrix, possibly by factors produced by the osteoclast or released from the bone matrix. Resting phase: once embedded, the osteoblasts mature into terminally differentiated osteocytes. Note the impaired recruitment and decreased number of osteoblast as well as the incomplete repair of bone in glucocoticoid-induced osteoporosis. Newly formed bone is in gray.

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  Fig. 3 The effects of Glucocorticoids on bone cells (A) GCs directly inhibit osteoblast proliferation, differentiation, survival and function, with consequent suppression of bone formation. (B) GCs directly inhibit osteoclast function by suppressing its cytoskeletal organization, which, in the context of remodeling, in turn leads to the failure to effectively recruit and activate osteoblasts, thus suppressing bone formation.

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