ABSTRACT
BACKGROUND: Glucocorticoids play an essential role in osteoblast differentiation, but excessive glucocorticoids will inhibit the osteoblastic phenotype. Regulation of 11β-hydroxysteroid dehydrogenase (11β-HSD) contributes to optimizing the effect of glucocorticoids.OBJECTIVE: To summarize the effect of 11β-HSD in bone metabolism.METHODS: The corresponding author retrieved PubMed and CJFD databases for the articles published before 2016 using the keywords "11β-HSD, bone" in English and Chinese, respectively. Totally 115 articles were retrieved, including 98 English and 17 Chinese articles, and finally 45 eligible articles were included in accordance with the inclusion criteria.RESULTS AND CONCLUSION: Glucocorticoid action can be regulated at prereceptor level by 11β-HSD. 11β-HSD1 activity may predict individual susceptibility to glucocorticoids, which instructs the individualized application of glucocorticoids precisely. 11β-HSD1 activity is closely related to osteoblast differentiation and the presence of an intrinsic differentiation-driven molecular switch inhibits the activity of 11β-HSD1. Instead of regulating the mesenchymal progenitors directly, gucocorticoids regulate the mesenchymal progenitors to differentiate into cranial skeleton mainly through mature osteoblasts. Short-term glucocorticoid exposure directly increases 11β-HSD1 activity and continuous exposure to glucocorticiod indirectly inhibits 11β-HSD1 activity.