Effects of Low Dose Dexamethasone on Bone Microstructure and Bone Metabolism in Growing Mice
Glucocorticoids can inhibit the differentiation and activity of osteoblasts, and increase the apoptosis of osteoblasts and osteoblasts, which leads to the continuous decline of bone formation. The effects of low dose dexamethasone on bone microstructure and bone metabolism in growing mice were observed. The expression of serum type Ⅰ procollagen N-terminal peptide (PINP) and bone type Ⅰ collagen cross-linked C-terminal peptide (β - CTX) protein, the expression of osteoprotegerin (OPG) and nuclear factor kappa B receptor activator ligand (RANKL) in metaphysis of tibia, the osteoclasts were detected by anti tartaric acid phosphatase (TRAP) staining and one tibia was analyzed by micro CT scanning. The apparent bone density and volume fraction of tibia in dex group were significantly higher than those in the control group (P. The levels of PINP and β - CTX in serum of DEX group decreased significantly (P<0.05). In dex group, the expression of OPG was significantly increased, but the expression of RANKL had no significant change. Compared with the control group, the ratio of OPG / RANKL was increased. Trap staining showed that the number of osteoclasts in the tibial metaphysis of DEX group was less than that of the control group. Intermittent administration of low dose dexamethasone may maintain bone mass in growing mice by increasing the OPG / RANKL ratio.