Pathogenic mechanisms of glucocorticoid-induced osteoporosis

Glucocorticoid (GC) is one of the most prescribed medicines to treat various inflammatory and autoimmune diseases. However, high doses and long-term use of GCs lead to multiple adverse effects, particularly glucocorticoid-induced osteoporosis (GIO). Excessive GCs exert detrimental effects on bone cells, including osteoblasts, osteoclasts, and osteocytes, leading to impaired bone formation and resorption. The actions of exogenous GCs are considered to be strongly cell-type and dose dependent. GC excess inhibits the proliferation and differentiation of osteoblasts and enhances the apoptosis of osteoblasts and osteocytes, eventually contributing to reduced bone formation. Effects of GC excess on osteoclasts mainly include enhanced osteoclastogenesis, increased lifespan and number of mature osteoclasts, and diminished osteoclast apoptosis, which result in increased bone resorption. Furthermore, GCs have an impact on the secretion of bone cells, subsequently disturbing the process of osteoblastogenesis and osteoclastogenesis. This review provides timely update and summary of recent discoveries in the field of GIO, with a particular focus on the effects of exogenous GCs on bone cells and the crosstalk among them under GC excess.

Automated summary

Glucocorticoid (GC) is commonly used to treat inflammatory and autoimmune diseases, but its high doses and long-term usage can lead to adverse effects, especially glucocorticoid-induced osteoporosis (GIO). Excessive GCs have harmful effects on bone cells, inhibiting osteoblast proliferation and differentiation, enhancing osteoblast and osteocyte apoptosis, and promoting osteoclastogenesis and bone resorption. GCs also disrupt the secretion of bone cells, affecting the process of osteoblastogenesis and osteoclastogenesis.