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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

Effect of GCs on the histological morphology of bone formation. Histological changes of femur specimens were observed by hematoxylin and eosin staining under a light microscope. In the GC-treated group, an empty lacunae within the necrotic bone trabeculae, bone marrow cells, including adipocytic necrosis and an accumulation of cell debris in the medullary space in most areas of the femoral head, were observed in 16/37 (43%) mice. No lesions were observed in the control group. GC, glucocorticoid.
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f2-mmr-14-02-1054: Effect of GCs on the histological morphology of bone formation. Histological changes of femur specimens were observed by hematoxylin and eosin staining under a light microscope. In the GC-treated group, an empty lacunae within the necrotic bone trabeculae, bone marrow cells, including adipocytic necrosis and an accumulation of cell debris in the medullary space in most areas of the femoral head, were observed in 16/37 (43%) mice. No lesions were observed in the control group. GC, glucocorticoid.

Mentions: All mice were sacrificed under isoflurane anesthesia after the 8 week experimental period. The left femur specimens were collected and the histological changes of femur specimens were observed under a light microscope. Osteonecrosis was observed in 16/37 mice (43%) in the GC-treated group, and no osteonecrotic lesions were observed in the control group. Fig. 2 shows the histopathological appearance of the femoral head following H&E staining. Empty lacunae within the necrotic bone trabeculae, bone marrow cells, including adipocytic necrosis, and an accumulation of cell debris in the medullary space in most areas of the femoral head were observed after 8 weeks in the GC-treated group (Fig. 2).


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)

Effect of GCs on the histological morphology of bone formation. Histological changes of femur specimens were observed by hematoxylin and eosin staining under a light microscope. In the GC-treated group, an empty lacunae within the necrotic bone trabeculae, bone marrow cells, including adipocytic necrosis and an accumulation of cell debris in the medullary space in most areas of the femoral head, were observed in 16/37 (43%) mice. No lesions were observed in the control group. GC, glucocorticoid.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f2-mmr-14-02-1054: Effect of GCs on the histological morphology of bone formation. Histological changes of femur specimens were observed by hematoxylin and eosin staining under a light microscope. In the GC-treated group, an empty lacunae within the necrotic bone trabeculae, bone marrow cells, including adipocytic necrosis and an accumulation of cell debris in the medullary space in most areas of the femoral head, were observed in 16/37 (43%) mice. No lesions were observed in the control group. GC, glucocorticoid.
Mentions: All mice were sacrificed under isoflurane anesthesia after the 8 week experimental period. The left femur specimens were collected and the histological changes of femur specimens were observed under a light microscope. Osteonecrosis was observed in 16/37 mice (43%) in the GC-treated group, and no osteonecrotic lesions were observed in the control group. Fig. 2 shows the histopathological appearance of the femoral head following H&E staining. Empty lacunae within the necrotic bone trabeculae, bone marrow cells, including adipocytic necrosis, and an accumulation of cell debris in the medullary space in most areas of the femoral head were observed after 8 weeks in the GC-treated group (Fig. 2).

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