Alcohol and corticosteroid abuse can cause osteonecrosis: Osteonecrosis often affects young and middle-aged people and is a disabling disease. According to the latest information, there are 300,000 to 600,000 osteonecrosis patients in the United States. Our population is five times that of the United States, and alcohol and corticosteroid abuse is serious, so it is presumed that our patients are between 3 million and 5 million. Studies on the natural course of osteonecrosis of the femoral head have found that without effective treatment, about 80% of the femoral head will collapse within 1 to 3 years. Once the femoral head collapses, the hip joint will inevitably develop into osteoarthritis and seriously affect the function of the hip joint, necessitating artificial joint replacement. At the present level, the long-term outcome of artificial hip replacement for young and active patients is still not satisfactory, and some patients may have to undergo two to three replacement surgeries for this reason. This will bring a huge economic burden and pain to the society and patients and families. Therefore, it is necessary to seek practical and effective prevention, intervention and preservation of femoral head treatment for such patients. Ninety percent of the osteonecrosis seen clinically is associated with hormone use and alcohol abuse. However, some of the same people who use hormones and alcohol do not develop osteonecrosis. In the population we investigated, some people used nearly 30,000 mg of methylprednisolone without osteonecrosis, while others used only 175 mg and experienced multiple joint necrosis. Some people with lifelong alcohol abuse did not develop osteonecrosis; conversely, a few people who consumed only small amounts of alcohol developed osteonecrosis. The pathogenesis of non-traumatic osteonecrosis is still not very clear, and in recent years, more research at home and abroad is the theory of intravascular coagulation. 1974, American scholars such as Jones in the study of osteonecrosis hypothesized that the intravascular coagulation activated by various underlying diseases may be the common pathway that eventually causes thrombosis and osteonecrosis in bone. 1992, Jones formally proposed that non-traumatic osteonecrosis is a common pathway that causes the formation of thrombosis and osteonecrosis in bone. Jones formally proposed the theory of intravascular coagulation in nontraumatic osteonecrosis, and continued to refine it in subsequent studies. He concluded that intravascular coagulation, an intermediate mechanism, is the most likely final common pathway for the development of osteonecrosis. Intravascular coagulation allows intraosseous fibrin thrombosis and intraparenchymal hemorrhage, which causes nontraumatic osteonecrosis. Abnormal coagulation and fibrinolysis may play an important role in the development of osteonecrosis. This hypercoagulable and hypofibrinolytic state is not the direct cause of osteonecrosis and these factors can be reversible or irreversible, additive or compound, congenital or acquired, but can occur through an intermediate mechanism that initiates intravascular coagulation. Osteonecrosis occurs as a complex physiopathological process based on a multifactorial combination of high lipid, high coagulation and low fibrin. Thrombosis and fibrinolysis is a complex process and a problem at any one link in the whole waterfall chain reaction may stimulate the final thrombosis. Patients who develop osteonecrosis often have abnormal indicators and genetic variants of hypercoagulable and hypofibrinolytic tendencies, while others who use a lot of hormones or alcohol but do not have osteonecrosis often have normal indicators of these. Therefore, by testing for these indicators and genes in people who require hormone use or alcohol abuse, the development of osteonecrosis can be predicted. Detection of multiple factors and genes can prevent osteonecrosis: Our research through a large number of cases has shown that the occurrence of osteonecrosis in the national population is associated with a number of hypercoagulable and hypofibrillar factors in the blood such as protein C (PC), activated protein C resistance (APC-R), fibrinogen activator inhibitor (PAI), and genes associated with them. The incidence of testing abnormalities in the osteonecrosis population is over 85%, so testing for these factors and genes can predict the national population at high risk for osteonecrosis. In clinical practice, screening for these factors and genes in people who must use corticosteroids during the treatment of diseases such as nephritis, organ transplantation and systemic lupus erythematosus, as well as alcohol abuse, and screening for high-risk groups, and applying pharmacological interventions to high-risk groups while using hormones, will reduce the occurrence of osteonecrosis. In addition, once osteonecrosis has occurred, these tests will clarify the cause and the use of anticoagulant and pro-fibrinolytic drugs will correct the patient’s blood status before irreversible collapse occurs in the early stages of osteonecrosis, thus interrupting or even reversing the course of the disease and avoiding surgical treatment and disability.