Osteonecrosis of the femoral head (ONFH) can be divided into two categories: non-traumatic and traumatic. In China, the main cause of non-traumatic ONFH is the application of glucocorticoids (also known as corticosteroid, hereinafter referred to as hormone) and long-term heavy alcohol consumption, other rare causes such as sickle cell anemia, decompression sickness, Gaucher’s disease, etc. The main cause of traumatic ONFH is displaced femoral neck fracture, followed by acetabular fracture, hip dislocation, etc. Sometimes there is no obvious fracture and dislocation of the hip, but there is a serious hip sprain and contusion can also occur femoral head necrosis, presumably due to the impaired blood circulation in the femoral head caused by the hematoma in the hip joint. Our country is a big country of osteonecrosis. According to a reliable basis, it is presumed that the annual incidence of ONFH in China is between 150,000 and 300,000, and the cumulative number of cases requiring treatment can reach 5-7 million, and this number still has the trend of increasing year by year. Research on the natural course of ONFH shows that without effective treatment, about 70%-75% of ONFH will progress to femoral head collapse in 1~5 years from the onset of the disease. Once the femoral head has collapsed, about 87% of the collapsed femoral head will progress to the point where an artificial joint replacement is necessary within 1-3 years. Since ONFH, especially non-traumatic ONFH, mostly involves middle-aged and young adults (Mont reported a mean age of 38 years in the United States and Li Zirong reported 38.6±11.5 years in China). Studies have shown that the mid- to long-term (≥20 years) outcome of prosthetic hip replacement in young and middle-aged people remains unpredictable. Therefore, it is imperative to find effective methods of treatment for preserving the patient’s own joints (joint-preserving procedures). At present, there are many joint-preserving treatment methods, including non-surgical treatment (Chinese and Western medicine, protective weight-bearing, electromagnetic field, hyperbaric oxygen, etc.); minimally invasive treatment (extracorporeal shock wave, fine needle medullary decompression, etc.); lesion removal plus various types of bone grafting (compression bone grafting, with or without vascularized fibula, iliac bone graft, myofascial graft, porous tantalum rod support, etc.); osteotomy (rotational osteotomy via the femoral rotor, internal and external osteotomy, etc.) (internal and external osteotomy, etc.). All kinds of treatment, such as the appropriate selection of indications, have certain efficacy. However, it has been found that the common reason for the failure of various types of bone grafting is that the subchondral bone plate of femoral head necrosis cannot be completely and effectively repaired, which eventually leads to the collapse of the articular cartilage surface and impairment of joint function. In recent years, research on bone marrow stem cell transplantation and tissue engineering has been on the rise. The application to the treatment of osteonecrosis is also beginning to emerge. Relevant basic research and clinical applications have shown initial efficacy, but there are many problems that require further research to deepen and improve. Related basic research: The relationship between non-traumatic ONFH and bone marrow mesenchymal stem cells (MSCs) has been studied in depth and found to be closely related to each other. Therefore, some scholars refer to non-traumatic osteonecrosis as bone marrow MSCs disease. In this regard, the use of cell therapy ONFH in clinical trials. The relationship between red bone marrow and osteonecrosis: clinical observation found that both hormone- or alcohol-induced non-traumatic osteonecrosis occurred at bones containing yellow bone marrow, while bones rich in red bone marrow, such as the iliac bone, sternum and vertebral bones, rarely occurred osteonecrosis. It was also found that hormone-induced osteonecrosis was rare in children under 10 years of age (Legg-Perthes disease is not essentially osteonecrosis, but epiphyseal chondritis, which has the ability to repair itself completely). Thus, it is hypothesized that red bone marrow has a role against osteonecrosis and also provides clues for red bone marrow treatment of osteonecrosis.1. The number of bone marrow MSC in the proximal femur and femoral head is reduced in patients with nontraumatic ONFH. This phenomenon has been reported by many investigators. hernigou found a hormone-induced decrease in the number of cells in the pool of proximal femoral MSCs in ONFH. weinstein et al. found that hormones caused apoptosis of osteoblasts and osteocytes and inhibited osteogenesis. A study by Bai-Liang Wang at the Osteonecrosis Center of China-Japan Friendship Hospital also found that compared with patients with femoral neck fractures, hormonal ONFH had significantly reduced value-added activity of MSCs in the proximal femur, a significantly delayed plateau phase of the cell growth curve, a significantly higher ratio of Go/G1 cells, and a lower ratio of S+G2/M phase cells, suggesting a decreased ability of cells to proliferate and divide.Hofbauer et al. found that hormones Hofbauer et al. found that hormones inhibited the transcription and expression of OPG (osteoprotegerin) in osteoblasts and promoted the expression of ODF/OPGL (osteoclast differentiation and receptor activation) thereby activating osteoclasts, leading to a decrease in the number of osteoblasts.2. Increased lipogenesis and decreased osteogenesis of MSCs in the proximal femur of patients with non-traumatic ONFH. Wang Guozhao et al. in the United States confirmed as early as the 1990s that the osteogenic differentiation ability of MSCs treated by hormones was significantly decreased, while the lipogenic differentiation ability was increased. Subsequently, Cui Quanxing et al. also confirmed that clonal bone marrow cell populations exposed to alcohol had reduced osteogenic gene expression and increased lipogenesis. Yin et al. demonstrated that hormone-induced increase in lipogenesis and decrease in osteogenesis in MSCs was caused by increased expression of lipogenic gene 422 (ap2), increased triglyceride synthesis, and decreased expression of bone marker genes and cells.3 Many animal experiments have confirmed that the application of concentrated bone marrow mononuclear cells (BM-MNCs) transplantation has a significant repair effect on necrotic femoral head, and the repair effect is achieved by increased osteogenesis The repair effect was achieved through increased osteogenesis and angiogenesis. Zhang Changqing et al. applied rabbits as a model of osteonecrosis and compared two groups: simple decompression and autologous BM-MNCs implantation, and found that neovascularization and bone repair were significantly higher in the necrotic bone of the cell-injected animals than in the control group.4. In vitro experiments with bone marrow MSCs, when given osteogenic conditions (dexamethasone and Vit C) in culture, they can differentiate into osteoblasts and subsequently become osteogenic, but it remains questionable whether in vivo conditions can be osteogenic. Hernigou observed the retention of MSCs implanted in the femoral head by tracer-labeling bone marrow stromal stem cells, and showed that 80% of the transplanted cells were retained in the femoral head necrosis foci, which proved the feasibility of MSCs transplantation, but he did not further investigate the proliferation and differentiation of MSCs. The Osteonecrosis Center of China-Japan Friendship Hospital used a dog as a model, and made a defect inside the femoral head of the dog, and used carbolic acid to cauterize the area around the bone defect, resulting in the death of bone cells, to make a model of bone defect similar to the human femoral head after the removal of the necrotic lesion. Autologous bone marrow MSCs were cultured in vitro and labeled with Brdu (5-bromodeoxyuridine nucleoside) and SPIO (superparamagnetic iron oxide), respectively, and then implanted into the femoral head defect area, and the results showed that the transplanted MSCs were viable and the labeled MSCs could stay in the osteonecrosis and bone defect area and differentiate and proliferate. The transplanted labeled MSCs could differentiate into a variety of cells, including osteoblasts, osteocytes and chondrocytes. In addition to osteogenesis, they are also involved in neovascularization. It has also been demonstrated that MSCs can increase the transformation ability of artificial bone when transplanted in composite with artificial bone.