Major pathological changes in the joint: Bleeding or exudation within the joint, forming fibrous fascicles within the joint cavity, which form extensive fibrous adhesions within the joint; these fibrous fascicles are very tough and are the major pathological change in knee stiffness. The tough fascia, which prevents further flexion of the knee joint. The primary site of hemophilic arthritis is in the synovium and extends into the joint cavity. Initially, the synovial irritants from synovial fluid and hematoma are absorbed by the synovial membrane. Repeated bleeding will cause hypertrophy of the synovial membrane, loss of normal absorption, resorption of cartilage at the joint edges, and later, cartilage collapse and complete destruction, resulting in loss of joint function. Before bleeding becomes apparent in the joint, the patient has a painful discomfort in the joint. Once the blood accumulates, the joint capsule swells rapidly, and the joint becomes warm, painful, and painful to the touch, often with a purplish color due to subcutaneous stasis. Due to muscle spasm, joint dysfunction is often caused. Due to the increased tension of the joint capsule, the bleeding foci may be suspended due to pressure, but if the intra-articular capsule pressure decreases, the bleeding is often re-induced. Repeated episodes of hemorrhage will lead to severe osteoarthritic changes. Long-term involvement of the joint may result in varying degrees of contracture and dysfunction, enlargement of the epiphysis, and disuse atrophy of the muscles. Most commonly, the knee joint is flexed and movement is limited. The more specific x-ray changes of the disease are enlarged intercondylar fossa of the femur, flattening of the inferior border of the patella, and enlargement of the radial head. Related knowledge: Hemophilic arthritis is a group of bleeding disorders caused by hereditary deficiency of coagulation factors. It is classified into type A (factor VIII deficiency), type B (factor IX deficiency) and type C (factor XI deficiency) according to the deficient factors. Types A and B are X-chromosome recessive, with only males and females as carriers, and have a pronounced tendency to bone and joint hemorrhage. Type C is autosomal dominant and can occur in both sexes. It is rare, with mild bleeding and rare bone and joint involvement. Bleeding in hemophilia often involves the knee, manic, elbow, and medullary joints, which are more active and subject to gravity, with the knee being the most common. Causes of pathologic changes: The pathologic changes in hemophilic arthropathy are mainly caused by recurrent bleeding in the bones and joints. Early intra-articular bleeding causes widening of joint soft tissues and joint spaces. Iron-containing hemoglobin deposits may be present in those with recurrent bleeding. In the middle stage, synovial fibrosis and hyaline cartilage breakdown due to enzymatic action cause chronic synovitis, cartilage degeneration and joint surface erosion. Synovial proliferation causes cartilage margins and subchondral bone erosion. The degeneration and destruction of cartilage leads to narrowing of the joint space. Restricted joint motion may cause disuse osteoporosis. Subchondral sclerosis and cystic degeneration and periarticular soft tissue atrophy occur in late stages. (1) During growth and development, the disease causes bone marrow congestion, intraosseous hemorrhage, and recurrent intra-articular hemorrhage, resulting in deformation of the bone marrow, enlargement and squareness of the bone tendons or stem marrow ends, and widening and deepening of the intertrochanteric fossa of the femur. (2) Intraosseous hemorrhage (subchondral hemorrhage) causes osteolysis or cystic changes and cystic lesions in the pars interarticularis. (3) Subperiosteal hemorrhage occurs less frequently and can cause periosteal reaction, cortical thickening, and pressure erosion of the bone cortex when the hematoma is large. (4) Hemophilic pseudotumor is a rare and serious complication of hemophilia with an incidence of about 1-2%, and its formation is closely related to hemorrhage. Osteolytic destruction may be seen, and the lesion may also show distensible changes, often combined with soft tissue masses and periosteal reactions, and the hyperplastic periosteum may be destroyed again. Pathological fractures are likely to occur and do not heal easily. The disease is divided into three stages according to the pathological process: (1) early stage (simple joint hemorrhage) in which the joint is filled with blood, causing synovial thickening and joint capsule swelling; (2) middle stage (total arthritis) in which repeated bleeding in the joint causes synovial thickening, followed by cartilage erosion, resorption, and blood interference with cartilage nutrition, which can cause joint space narrowing. Bone and subperiosteal bleeding can cause subchondral cysts and hemophilia pseudotumors; (3) late stage (repair stage) intra-articular blood absorption, inflammation gradually subsides, the lighter the joint function slowly restored, the heavier the secondary osteoarthrosis or legacy of joint flexion contracture deformity. This disease is generally not advocated for surgical treatment, Mathew et al. achieved good results with isotope radiation therapy.