Pathological changes: At the beginning of the lesion, the synovial membrane is congested, edematous, and thickened, and the intra-articular exudate increases due to increased vascular permeability. The synovial membrane gradually thickens, forming vascular opacities on the surface that erode and grow into the cartilage and bone surface, blocking the cartilage from obtaining nutrients from the synovial fluid and causing erosions and ulcers to form on the cartilage surface. In addition, inflammatory cells such as proliferating synovial cells, macrophages and neutrophils release proteoglycanases and collagenases that degrade proteoglycan and collagen in the cartilage matrix, thereby aggravating cartilage destruction. Synovial inflammation can lead to fibrinous exudative resorption mechanization, resulting in fibrous ankylosis of the relative articular surfaces. Fibrosis of the joint capsule, ligamentous tendon relaxation, muscle spasm and atrophy can lead to joint contracture and subluxation, resulting in joint deformity. Due to joint deformity and restricted movement, adjacent osteoporosis and muscle atrophy occur. Clinical manifestations: The disease is usually seen in young adults, with a female predominance. The onset of the disease is usually insidious, with prodromal symptoms such as weakness, poor circulation, low fever, and numbness of the hands and feet, followed by single or multiple joint swelling and pain, most often in small joints. Almost all rheumatoid patients have hand and wrist joints. Early clinical symptoms of rheumatoid arthritis involving the hip are often not obvious, and the joint swelling and thickened synovial membrane are often not easily detected due to the depth of the joint. Pain in both hips, abnormal gait and limited joint movement are common manifestations of hip involvement. In the late stage, the joint becomes stiff and deformed until it loses its function, and there is atrophy of the bone and epiphysis. Laboratory tests: accelerated blood sedimentation, positive rheumatoid factor, elevated CRP or ESR. Imaging techniques: X-rays are an important diagnostic tool, and most diagnoses can be confirmed by combining X-rays of other parts of the body with clinical manifestations; CT is better than plain films in showing the details of the lesion; MRI can clearly show articular cartilage, vascular opacities, and small foci of bone erosion, and is valuable in early diagnosis and observation of lesion activity. When the inflammatory response becomes moderate or mild, the patient should be encouraged to do functional exercises within the pain-free range and actively use the affected limb. Intra-articular injection of hydrocortisone acetate or prednisolone may provide symptomatic relief. Various physical therapies can accelerate the regression of inflammation and reduce pain. For patients with severe pain, limited to a few steps, and significantly limited joint function, arthroplasty or total joint replacement can be used. In recent years, for most patients, even non-elderly patients, the latter surgery can be used to obtain more satisfactory results. If you want to know more: (1) Joint space narrowing and disappearance: This is a manifestation of joint cartilage destruction. In the early stages of rheumatoid arthritis, there is inflammatory proliferation of the synovial membrane and cytokinin enters the joint cavity from the blood circulation (cytokinin is a very strong chondrolysin, which destroys the superficial layer of the cartilage matrix). Chondrocyte destruction then occurs, releasing proteolytic enzymes, including histoproteinases, which accelerate cartilage destruction through self-digestion. Depending on the extent and degree of synovial inflammation, destruction of articular cartilage may be confined to the center of the joint or to the entire joint, and osteoporosis may occur along with changes in the joint space due to congestive calcium deficiency. (2) Acetabular protrusion: This condition occurs after the loss of the central joint space of the acetabulum, and the continuous microfracture and repair of the central wall of the acetabulum makes the central wall of the acetabulum into a bony thin plate. The femoral head is compressed statically and dynamically, and the acetabulum is gradually protruding into the pelvis in an arch shape. (3) Femoral head atrophy: In the maximum weight-bearing area of the hip joint, i.e. between the upper part of the femoral head and the top of the acetabulum, the articular cartilage is destroyed and local degenerative changes occur, which can lead to atrophy of the femoral head and the femoral head gradually becomes mushroom-shaped or shattered and deformed, resulting in upward and outward subluxation of the hip joint or central hip dislocation. In severe rheumatoid arthritis of the hip joint, the head and neck of the femur may completely collapse, the acetabulum becomes large, and even a fracture of the neck of the femur occurs. (4) Joint ankylosis: In rheumatoid arthritis, the joint surface is marginal hyperplasia, sclerosis, bone spur formation, complete loss of joint space, and joint fusion and ankylosis.