Pathological Mechanism of Glucocorticoid-induced Osteoporosis

Hyun-Ju Kim

doi:10.3803/jkes.2009.24.4.231

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Kim: Pathological Mechanism of Glucocorticoid-induced Osteoporosis

Original Article

J Korean Endocr Soc 2009;24(4):231-236.

Published online: 10 January 2009

DOI: https://doi.org/10.3803/jkes.2009.24.4.231

Pathological Mechanism of Glucocorticoid-induced Osteoporosis

Hyun-Ju Kim

Skeletal Diseases-Genome Research Center, Department of Medicine, Kyungpook National University School of Medicine

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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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 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 is its cytoskeletal organization, namely polarization. Once polarized, the osteoclasts resorb the mineralized component of bone.

Fig. 2.

Capn6 promotes cytoskeletal organization, microtubule stability, and the expression of β3 integrin protein in osteoclasts and its inhibition may be a means by which glucocorticoids suppress bone remodeling.

Fig. 3.

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 phase: the osteoblasts deposit 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 (GIO). Newly formed bone is in gray.

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