Hakeda Yoshiyuki
Meikai University School of Dentistry, Division of Oral Anatomy.
Clin Calcium. 2006 Nov;16(11):1817-22.
During the early phase of glucocorticoid (GC)-induced osteoporosis (GIO), GC increases the expression of receptor activator of NF-kappaB ligand (RANKL) in bone-forming cells and suppresses the production of interferon-beta in osteoclast progenitors, resulting in stimulation of bone resorption. On the other hand, GC represses the proliferation, differentiation and functional activities of bone forming cells, and finally induces their apoptosis throughout GIO, consequently causing the decrease in bone formation. In addition, as the number of bone-forming cells decrease, the osteoblast-dependent osteoclast formation also declines.
在糖皮质激素（GC）诱导的骨质疏松症（GIO）早期，GC增加成骨细胞中核因子κB受体活化因子配体（RANKL）的表达，并抑制破骨细胞前体细胞中β干扰素的产生，从而刺激骨吸收。另一方面，在整个GIO过程中，GC抑制成骨细胞的增殖、分化和功能活性，最终诱导其凋亡，进而导致骨形成减少。此外，随着成骨细胞数量减少，成骨细胞依赖性破骨细胞形成也会下降。
