Femoral head necrosis is a common orthopedic disease, patients are often 20 to 50 years old, the cause of the disease is caused by alcohol, hormones, trauma and other conditions, so that the blood vessels are damaged or blocked, affecting the blood flow to the femoral head, and eventually lead to ischemic necrosis of the femoral head. Clinical manifestations: The main clinical manifestations of femoral head necrosis are hip joint pain and claudication. Signs: pressure pain slightly below the midpoint of the groin or the stopping point of the adductor muscle, atrophy of the muscles around the affected hip and thigh muscles, “4” sign (+) may appear; when the necrotic femoral head is severely collapsed and both lower limbs are unequal, Allice (+) may appear; when the hip joint is subluxated and the gluteus medius muscle is weak, Trendelenber (+) may appear. sign (+). In the early stage, patients may have mild limitation of abduction and internal rotation activities. As the disease progresses, the range of motion of the hip joint in all directions is gradually reduced until it is severely restricted. The diagnosis is confirmed by combining clinical symptoms and signs. Commonly used imaging examinations are X-ray and MRI. The diagnosis of femoral head necrosis is based on Ficat’s typing, combined with functional examination, and divided into four stages and six types: Stage I. It is characterized by no abnormal radiological signs. There is only transient joint stiffness and pain, usually accompanied by some limitation of joint movement. The symptoms are relieved after rest and no positive findings are seen on X-ray, occasionally uniform or speckled areas of osteoporosis may be seen. The lack of hemodynamic, isotopic, and histopathological studies often prevents the diagnosis from being made. Stage II This stage is characterized by the appearance of signs of bone reconstruction on x-ray without any change in the shape of the femoral head or joint space. Weight holding and hip pain occurs with prolonged standing. This stage is subdivided into two types A and B: ⅡA: Mild restriction of hip movement, diffuse bone sparing, with obvious overlapping images, which may involve the acetabulum. The entire center of the femoral head shows a homogeneous and consistent osteosclerotic zone with relatively obvious demarcation, with punctate and lamellar hypodense areas and isolated cystic changes visible around it. IIB: It is characterized by the presence of a mixture of bony hyperdensity and hypodense areas, usually with fan-shaped or subchondral fractures, and occasionally the crescent sign (a sign of separation or collapse of subchondral trabeculae from cartilage). The presence of the crescent sign is a prodromal sign of trabecular necrosis. Stage III This stage is characterized by a break in the continuity of the subchondral trabeculae, with marked capsular changes, often surrounded by a sclerotic rim, and a flattening of the femoral head due to subchondral fracture, mainly in the weight-bearing zone. The joint space is normal or slightly narrowed because the overlying cartilage remains normal. Hip pain is mild but more persistent, with insignificant relief at rest. Stage IV It is characterized by progressive enlargement of subchondral osteonecrosis, manifested by narrowing of the joint space and typical osteoarthritic changes. This type is also divided into two stages: ⅣA: further flattening and compression of the femoral head, collapse of both the inner and outer sides of the head, narrowing of the joint space, and small bony and cystic changes visible below the subchondral bone of the head and in the weight-bearing part of the acetabulum, which are signs of osteoarthritis of the hip joint. IVB: Further compression and destruction of the femoral head part and acetabulum with degenerative joint changes, so that necrosis and arthritis can no longer be clearly distinguished. To accommodate the flattened deformity of the femoral head, the acetabular roof also undergoes deformation, changing from a spheroid joint to a cylindrical joint. In some cases, the femoral head is fragmented and a fracture of the femoral head is also seen. Although a greater range of flexion is preserved, it leads to a total loss of abduction and rotation functions, i.e., signs of subluxation. We can roughly consider stages I and II as early-stage femoral head necrosis and stages III and IV as advanced femoral head necrosis. In terms of treatment, for early stage femoral head necrosis, we can treat it with medication, combined with minimally invasive surgery such as percutaneous perforation drilling for medullary core decompression, necrotic lesion removal + bone grafting, and tantalum rod internal fixation, which can effectively alleviate the progress of femoral head necrosis or even reverse the course of the disease to cure it. Advanced femoral head necrosis is mainly treated with joint replacement surgery, which can enable patients to regain normal joint activities, allowing them to resume their normal lives and effectively relieve their pain.