In 1959, Curtiss and Kincaid described a clinical syndrome characterized by patients presenting with hip pain during pregnancy and reduced bone density on X-ray1. With the development of MRI, there are several terms associated with the finding of bone marrow edema, such as "transient osteoporosis", "transient demineralisation" and "regional wandering osteoporosis". In 2004, Hoffman et al. introduced the generic term "bone marrow edema syndrome " (BMES)2. The cause of BMES is not yet known. Still, known risk factors include vitamin D deficiency, anemia, late pregnancy, bone metabolism disorders, cirrhosis, lipid metabolism disorders, chemotherapy and radiotherapy3,4,5, etc. The pathophysiology of BMES remains controversial, and previous studies have shown that minimal trauma is a major risk factor for bone marrow edema. However, some studies have shown that bone marrow edema is related to intramedullary pressure, which may be a secondary cause of venous circulation obstruction3. MRI often diagnoses BMES within 48 hours of symptom onset (a decrease in signal intensity on T1-weighted images and an increase in signal intensity on T2-weighted images )6,7. At the same time, increased radionuclide uptake was detected in nuclear medical imaging8, and other laboratory results were generally normal. At present, BMES patients are rare and often misdiagnosed and mistreated. As a self-limited disease, the symptoms can be relieved without treatment, so the treatment of BMES is still controversial, and there is no unified treatment. We reviewed the previous literature, there are various treatment regimens for BMES, which are roughly divided into symptomatic treatment, extracorporeal shock waves, pulsed electromagnetic fields, hyperbaric oxygen, vitamin D, iloprost, bisphosphonates, denosumab, and surgery, etc. This review summarizes these therapeutic regimens to provide a reference for the treatment of BMES.