AI Article Synopsis
- Glucocorticoid-associated osteonecrosis of the femoral head (GA-ONFH) leads to bone damage and hip dysfunction, with sclerostin playing a key role in bone health and breakdown.
- The study used various cell models and animal models to examine how sclerostin affects bone cells under glucocorticoid treatment.
- Results showed that high levels of sclerostin contribute to the progression of GA-ONFH by hindering bone growth and blood vessel formation, highlighting its potential as a target for treatment.
Article Abstract
Background: Glucocorticoid-associated osteonecrosis of the femoral head (GA-ONFH) is a progressive bone disorder which frequently results in femoral head collapse and hip joint dysfunction. Sclerostin (SOST) is principally secreted by osteocytes in bone and plays an important role in bone homeostasis and homeostasis of skeletal integrity. Our previous study reported that short-term use of glucocorticoid increased serum sclerostin levels. Here this study is aimed to identify whether sclerostin played an essential role in the occurrence and development of GA-ONFH.
Methods: Glucocorticoid-induced osteonecrosis of femoral head (ARCO stage II) samples were collected and sclerostin staining was conducted. Osteocyte cell line Ocy454, MC3T3-E1 and endothelial cells was used. MC3T3-E1 or endothelial cells were co-cultured with Ocy454 or SOST-silencing Ocy454 in presence of dexamethasone to mimic the crosstalk of various cells in the bone niche. GA-ONFH rat model and SOST knockout model was built to better understand the phenomenon in vivo.
Results: Sclerostin was highly concentrated in osteonecrosis patient sample in the necrotic area. Co-culture with osteocytes aggravated the inhibition of dexamethasone on MC3T3-E1 and endothelial cells. Sclerostin derived from osteocytes impaired osteogenesis and angiogenesis via inhibiting the Wnt pathway. In GA-ONFH rat model, SOST knockout ameliorated the incidence of osteonecrosis and improved bone metabolism compared with the wild type group through histological, immunohistochemical and bone metabolic analyses.
Conclusion: Sclerostin contribute to pathologic process of GA-ONFH by impairing osteogenesis and angiogenesis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439244 | PMC |
| http://dx.doi.org/10.1186/s10020-024-00933-5 | DOI Listing |
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