Extracorporeal shock wave therapy alleviates glucocorticoid-induced injury and dysfunction of bone microvascular endothelial cells via the PI3K/AKT/FOXO1 pathway.

Background: Glucocorticoid-induced osteonecrosis of the femoral head (ONFH) is a common orthopedic condition with a high disability rate, and its pathogenesis remains incompletely understood. Increasing evidence suggests that glucocorticoid-induced damage and dysfunction of bone microvascular endothelial cells (BMECs) play a crucial role in the development and progression of ONFH. Glucocorticoids can cause damage and apoptosis of vascular endothelial cells, triggering coagulopathy and sustained inflammation. These pathological alterations contribute to thrombosis and microcirculatory disturbances, eventually leading to ischemic ONFH. As a non-invasive treatment modality, extracorporeal shock wave therapy (ESWT) offers several advantages, including its non-invasive nature, adjustable stimulation intensity, low procedural risk, and minimal complications. ESWT has been shown to relieve pain, improve hip joint function, and delay disease progression in ONFH patients. Moreover, several studies have reported that the therapeutic efficacy of ESWT is superior to that of core decompression or core decompression combined with bone grafting. However, the underlying mechanisms of its effectiveness remain unclear. This study aimed to investigate the effects and potential mechanisms of ESWT in an Methods: An Results: Our study demonstrated that the biological effects of ESWT exhibit a dose-dependent pattern, and 0.06 mJ/mm Conclusions: Our findings indicate that ESWT mitigates glucocorticoid-induced BMECs injury and dysfunction by activating the PI3K/AKT/FOXO1 signaling pathway.