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Effect of glucocorticoids on osteoclast function in a mouse model of bone necrosis.

He M, Wang J, Wang G, Tian Y, Jiang L, Ren Z, Qiu C, Fu Q - Mol Med Rep (2016)

Bottom Line: The results demonstrated that the GC-treated group had a lower mean weight compared with the control group.In addition, tartarate‑resistant acid-phosphatase staining demonstrated significantly decreased osteoclasts in the areas of bone destruction in the GCs-treated group.The results of the present study suggested that GCs influence bone remolding resulting in decreased osteoclasts formation/differentiation.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

ABSTRACT
Osteonecrosis, also termed aseptic necrosis, is the cellular death of bone components due to interruption of the blood supply. Glucocorticoid (GC) therapy is a common non-traumatic cause of osteonecrosis. However, the mechanism by which GCs induce osteonecrosis remains to be elucidated. The aim of the present study was to investigate the effects of GCs on osteoclast and osteoblast differentiation and function in a GC‑induced osteonecrosis mouse model. BALB/c male mice (n=40; 4‑weeks‑old) were treated with dexamethasone and asparaginase for 8 weeks. The control group (n=20) was administered normal saline. The results demonstrated that the GC-treated group had a lower mean weight compared with the control group. Morphologically, 16/37 (43%) mice demonstrated significant osteonecrotic lesions in the GC‑treated group. However, osteonecrotic lesions were not observed in the mice of the control group. Furthermore, immunohistochemistry demonstrated that the GC‑treated group had a higher level of osteoprotegerin compared with the control group, without any change in the expression of receptor activator of nuclear factor‑κB ligand. In addition, tartarate‑resistant acid-phosphatase staining demonstrated significantly decreased osteoclasts in the areas of bone destruction in the GCs-treated group. Furthermore, the present study demonstrated that GCs increased expression levels of osterix and osteocalcin, and decreased expression of matrix metallopeptidase‑9 to regulate the differentiation and function of osteoblasts and osteoclasts. The results of the present study suggested that GCs influence bone remolding resulting in decreased osteoclasts formation/differentiation. Therefore, regulating the differentiation and activity of the osteoclasts may be beneficial to the control and treatment of osteonecrosis.

No MeSH data available.


Related in: MedlinePlus

Effects of GCs on mice weight. The mice were sacrificed and weighed on the eighth week. The mean mice weight in the GC-treated group (19.8±1.9 g) was significantly lower compared with the control group (25.6±1.5 g) following 8 weeks of treatment. The data are presented as the mean ± standard deviation (*P<0.05, vs. the control group). GC, glucocorticoid.
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f1-mmr-14-02-1054: Effects of GCs on mice weight. The mice were sacrificed and weighed on the eighth week. The mean mice weight in the GC-treated group (19.8±1.9 g) was significantly lower compared with the control group (25.6±1.5 g) following 8 weeks of treatment. The data are presented as the mean ± standard deviation (*P<0.05, vs. the control group). GC, glucocorticoid.

Mentions: The survival rate of the GC-treated group (92.5%; 37/40 mice), prior to mice sacrifice, indicated no significant difference compared with the control group (95%; 19/20 mice; P>0.05). Furthermore, as demonstrated in Fig. 1, the mean weight of mice for the same time period in the GC-treated group (19.8±1.9 g) was significantly lower compared with those of mice in the control group (25.6±1.5 g) after 8 weeks of treatment (P<0.05).


Effect of glucocorticoids on osteoclast function in a mouse model of bone necrosis.

He M, Wang J, Wang G, Tian Y, Jiang L, Ren Z, Qiu C, Fu Q - Mol Med Rep (2016)

Effects of GCs on mice weight. The mice were sacrificed and weighed on the eighth week. The mean mice weight in the GC-treated group (19.8±1.9 g) was significantly lower compared with the control group (25.6±1.5 g) following 8 weeks of treatment. The data are presented as the mean ± standard deviation (*P<0.05, vs. the control group). GC, glucocorticoid.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940104&req=5

f1-mmr-14-02-1054: Effects of GCs on mice weight. The mice were sacrificed and weighed on the eighth week. The mean mice weight in the GC-treated group (19.8±1.9 g) was significantly lower compared with the control group (25.6±1.5 g) following 8 weeks of treatment. The data are presented as the mean ± standard deviation (*P<0.05, vs. the control group). GC, glucocorticoid.
Mentions: The survival rate of the GC-treated group (92.5%; 37/40 mice), prior to mice sacrifice, indicated no significant difference compared with the control group (95%; 19/20 mice; P>0.05). Furthermore, as demonstrated in Fig. 1, the mean weight of mice for the same time period in the GC-treated group (19.8±1.9 g) was significantly lower compared with those of mice in the control group (25.6±1.5 g) after 8 weeks of treatment (P<0.05).

Bottom Line: The results demonstrated that the GC-treated group had a lower mean weight compared with the control group.In addition, tartarate‑resistant acid-phosphatase staining demonstrated significantly decreased osteoclasts in the areas of bone destruction in the GCs-treated group.The results of the present study suggested that GCs influence bone remolding resulting in decreased osteoclasts formation/differentiation.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedics, Shengjing Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China.

ABSTRACT
Osteonecrosis, also termed aseptic necrosis, is the cellular death of bone components due to interruption of the blood supply. Glucocorticoid (GC) therapy is a common non-traumatic cause of osteonecrosis. However, the mechanism by which GCs induce osteonecrosis remains to be elucidated. The aim of the present study was to investigate the effects of GCs on osteoclast and osteoblast differentiation and function in a GC‑induced osteonecrosis mouse model. BALB/c male mice (n=40; 4‑weeks‑old) were treated with dexamethasone and asparaginase for 8 weeks. The control group (n=20) was administered normal saline. The results demonstrated that the GC-treated group had a lower mean weight compared with the control group. Morphologically, 16/37 (43%) mice demonstrated significant osteonecrotic lesions in the GC‑treated group. However, osteonecrotic lesions were not observed in the mice of the control group. Furthermore, immunohistochemistry demonstrated that the GC‑treated group had a higher level of osteoprotegerin compared with the control group, without any change in the expression of receptor activator of nuclear factor‑κB ligand. In addition, tartarate‑resistant acid-phosphatase staining demonstrated significantly decreased osteoclasts in the areas of bone destruction in the GCs-treated group. Furthermore, the present study demonstrated that GCs increased expression levels of osterix and osteocalcin, and decreased expression of matrix metallopeptidase‑9 to regulate the differentiation and function of osteoblasts and osteoclasts. The results of the present study suggested that GCs influence bone remolding resulting in decreased osteoclasts formation/differentiation. Therefore, regulating the differentiation and activity of the osteoclasts may be beneficial to the control and treatment of osteonecrosis.

No MeSH data available.


Related in: MedlinePlus