The pathogenesis of osteonecrosis is not very clear, and the possible factors are: (1) osteoclastic factors: the theory of cumulative cellular dysfunction suggests that the pathology of ischemic necrosis of the femoral head has three factors: anatomical site, systemic metabolic disorders and glucocorticoid application: local anatomical factors determine that bone ischemic necrosis occurs in the femoral head and humeral head; systemic metabolic disorders, chronic renal failure, alcohol consumption, hormones related to metabolism, and Systemic metabolic disorders, chronic renal failure, alcohol consumption, hormones related to metabolism, systemic lupus erythematosus, hemoglobinopathies, etc., can cause dysfunction of bone cells and gradually aggravate them, manifesting as changes in calcium and phosphorus metabolism and bone histological changes (bone softening and osteoporosis); and the application of hormones is the final destructive blow to bone cells, causing irreversible changes in bone cells that were originally in a pathological state, and finally bone cell necrosis. In addition, alcohol also has cytotoxic effects on bone cells. (2) Arterial factors: According to Jones (1994), fat emboli embolizing small blood vessels in bone release free fatty acids under the action of lipase, the latter directly causing an increase in prostaglandins, while oleic acid, the main component of neutral fat, can cause capillary lining exfoliation, passive edema and congestion, resulting in local platelet aggregation, fibrin deposition and thrombosis, leading to bone ischemic necrosis. In addition, increased intra-articular pressure also causes a decrease in blood flow to the femoral head; the frog position fixation in patients with congenital hip dislocation also decreases blood flow to the femoral head. (3) Venous factors: Arlot et al. believe that hormones and alcohol first stagnate the intramedullary veins and cause intramedullary hypertension, resulting in reduced intramedullary microcirculation, tissue hypoxia, edema, blood exudation, which aggravates microcirculatory disorders, and eventually ischemic necrosis of bone cells. Hormones increase platelets, leading to a hypercoagulable state of blood and causing venous thrombosis. Decompressive bone ischemic necrosis is caused by nitrogen precipitation, obstruction of blood vessels and compression of blood vessels. In addition, nitrogen has a toxic effect on adipocyte membranes, which can cause swelling of adipocytes and a sudden decrease in the amount of blood in venous sinuses. The presence of Gaucher cells with a diameter of 20 to 200 μm in Gaucher disease directly causes microvascular embolism. In hemoglobinopathy, sickle cells accumulate in blood sinuses and small veins, resulting in local thrombosis, which directly causes microvascular embolism leading to ischemic necrosis of the femoral head. (4) Extravascular factors in bone: Small arteries, capillaries and small veins in bone may be affected by extravascular factors and neurovascular reflexes to develop microcirculatory disorders. (5) Neurovascular factors: Ficat et al. suggested that extensive stagnation of venous blood due to motor paralysis of the intraosseous plexus or contraction of the precapillary sphincter due to neurological reflexes allows arterial blood to short-circuit directly into the vein without going through microcirculation, resulting in tissue ischemia. All of the above causes are due to the gradual decrease of blood flow to the femoral head causing bone marrow tissue hypoxia, followed by tissue edema, which further increases the intraosseous pressure, leading to the occurrence of bone ischemic necrosis, i.e., the progressive ischemia theory.