Osteoarthritis of the knee (OA) belongs to the category of rheumatic diseases and is one of the main causes of knee pain and a common cause of long-term disability in middle-aged and elderly people. 60% to 90% of people over 65 years of age have OA, and 25% to 30% of people between 45 and 65 years of age. Its main lesions are degenerative changes in the knee cartilage and secondary osteophytes. 1, etiology The exact cause of knee OA is not fully understood, may be related to the following factors: ① Age: with the growth of age, the incidence of knee OA is gradually increasing, so knee OA was considered an age-related degenerative disease. However, recent studies have found that the pathological changes of knee OA include the destruction of knee cartilage and the formation of bone fragments at the edge of the knee joint, of which the formation of bone fragments is a kind of repair performance, so it is believed that knee OA is not a degenerative lesion. The high incidence in the elderly may be due to the slow course of the disease, with early trauma, deformity and disease causing cartilage damage, and the manifestations of knee OA appearing years later as the biomechanics of the joint changes. (②Chondral matrix changes in the knee joint: the decrease of proteoglycan content in the cartilage matrix in the elderly, the increase of collagen fibers, the decrease of cartilage elasticity, and the vulnerability to injury and abnormal changes. (③) Knee synovial fluid changes: Studies have shown that the synovial fluid composition of knee OA patients has changed, and the content of hyaluronic acid has decreased, making its lubrication, cushioning and other functions weakened and resulting in the destruction of articular cartilage. Animal experiments have shown that surgical removal of most of the synovial membrane of the knee joint or long-term braking of the knee joint can cause changes in knee OA, and regular intra-articular injections of hyaluronic acid can prevent or reduce this pathological change. ④Injury: Knee cartilage injury can be caused by intra-articular fracture, meniscal injury, patellar dislocation, etc. ⑤ Infection or inflammation: Infection within the knee joint can cause cartilage destruction of the knee joint. (6) Extra-articular deformity of the knee joint: poor joint alignment due to internal or external knee deformity can cause damage to the articular cartilage. (7) Knee instability: Knee instability caused by ligaments and joint capsule laxity around the knee joint can lead to articular cartilage damage. (8) Other: excessive weight bearing and obesity can increase the load on the knee joint and accelerate the development of degenerative changes. 2, pathogenesis 2.1 traumatic factors due to injury, knee deformity or inflammation and other factors caused by changes in the gravitational line of the knee joint, so that the effective weight-bearing area of the knee joint surface is reduced, the joint surface is unevenly stressed, the impact concentration of the site that occurs in the articular cartilage damage, and cause small fractures of the trabeculae (subfracture), bone collapse, followed by the phenomenon of subchondral bone sclerosis. At the same time, as the articular cartilage matrix and synovial fluid composition of knee OA patients change, the elasticity of the cartilage and the lubrication of the surrounding synovial fluid are lost, making the cartilage vulnerable to wear and tear. The periarticular osteochondral hyperplasia is a repair phenomenon of joint injury, and the body compensates for the hyperplasia in order to increase the weight-bearing area of the joint and reduce the pressure on it. 2.2 Autoimmune reaction After the knee cartilage is damaged by mechanical and other factors, the “hidden antigens” of articular cartilage cells, mucopolysaccharide and collagen are exposed, causing autoimmune reaction and secondary damage to cartilage. Patients with knee OA often present with joint swelling, recurrent synovitis, increased monocytes, immunoglobulins and complement commonly seen in the synovial fluid, and marked congestion and monocyte infiltration in the synovial membrane, all of which suggest that knee OA may be related to autoimmune reactions. 3, Pathology Knee OA lesions include degenerative changes in cartilage, cartilage softening, erosion, exposure of bone ends, and changes in synovium, joint capsule and muscles. ① Articular cartilage: normal knee cartilage is smooth and blue-white with regular and neat edges. Early OA of the knee joint articular cartilage softening, loss of elasticity and luster, light yellow color, wear and tear occurs during activity, cartilage fragmentation, exfoliation, resulting in the exposure of subchondral bone, wear and tear of small peripheral cartilage surface proliferation and hypertrophy, through the cartilage internalized bone and the formation of bone superfluous. (ii) Subchondral bone: the central part of the subchondral bone that is worn out undergoes ivory changes, the bone density increases and hardens, the periphery bears less stress, the subchondral bone atrophies, and cystic cavity-like lesions appear. (iii) Synovial membrane: The synovial membrane shows proliferation and edema, causing fluid to accumulate in the knee joint, which contains more mucin and is more viscous. (iv) Joint capsule and muscles: the joint capsule undergoes fibrous degeneration and thickening, and the muscles around the joint develop protective spasm, which restricts the knee joint movement. 4, diagnosis 4.1 symptoms Knee OA patients often have the following symptoms: ① subpatellar pain: subpatellar pain and friction is an early symptom of knee OA, mostly occurs when too much activity, aggravated by cold, moisture, easy to go up and down stairs, there may be knee interlocking phenomenon. (ii) Repeated swelling of the joint: Mild trauma causes joint effusion, swelling and pain, which can be relieved naturally after 1 to 2 months of rest, but will recur. Knee joint dysfunction: Knee stiffness is another major symptom of knee OA, often manifested as “morning stiffness”, which usually lasts no more than 15 minutes and is relieved after activity. With the gradual development of the disease, the knee joint appears inversion or valgus deformity, periarticular bone growth, limited range of motion of the joint, pain when walking or standing, joint instability, and in severe cases, knee flexion contracture deformity. 4.2 Physical signs Patients with knee OA can see quadriceps atrophy, occasional swelling of the synovial membrane of the knee and positive floating patella test, deep patellar surface and pressure pain around the knee joint. Mild or moderate restriction of joint movement is seen, and in severe cases, inversion or valgus deformity of the knee is seen. In the early stage of knee OA, the X-ray examination may be normal, and occasionally there is osteophyte growth on the upper and lower edges of the patella, later there is narrowing of the knee joint space, sclerosis of the subchondral bone, osteophyte growth on the knee joint edge and intercondylar ridge, and small cystic changes of the subchondral bone with a layer of dense bone encapsulation on the wall of the capsule. The severity of knee OA can be classified into 5 levels according to the x-ray presentation. Joint space narrowing (50% articular cartilage wear) is I°, joint line loss is II°, mild bone wear is III°, moderate bone wear (0.5-1 cm wear) is IV°, and severe bone wear and joint subluxation is V°. 4.4 Laboratory examination Blood and urine routine and blood sedimentation are generally normal. Knee synovial fluid examination shows leukocytosis and positive mucin test. Diagnostic criteria for knee OA: knee pain and x-ray showing bony redundancy, with any one of the following three conditions, age >50 years, knee stiffness <30 minutes, and bone friction sound in the knee. 5, Treatment 5.1 Conservative treatment: ①General treatment: No special treatment for asymptomatic or mild symptoms; avoid weight-bearing on the knee if symptoms are present; physiotherapy can help relieve joint pain and reduce stiffness. ②Medication: For those with obvious symptoms, non-steroidal anti-inflammatory drugs, such as anti-inflammatory pain, fotarine and nabumetone, can be used to reduce pain. Chondroprotective agents: In recent years, the following types of chondroprotective agents are used in clinical practice: a. Hyaluronic acid: can be injected into the joint cavity, has the role of protecting cartilage, replenishing the hyaluronic acid in the joint fluid and lubricating cartilage. In foreign countries, it has been used as a regular drug for the treatment of OA. b. Peroxide dismutase: Intra-articular injection can remove peroxide and hydroxide from damaged tissues, reducing their inflammatory effects and relieving symptoms. c. Others: Glucosamine sulfate has the effect of protecting cartilage and promoting repair. 5.2 Surgical treatment For patients with OA of the knee with severe disease, persistent pain, and significant functional impairment. The main surgical methods are: ① Arthroplasty: This procedure was first advocated by Magnuson (1946) and is suitable for mild to moderate knee OA, where the patients are mostly over 40 years old, and the main symptoms are knee swelling, pain, obvious bony bulge, free body in the joint, history of knee interlocking, as well as less serious misalignment of the force line of the joint and some mobility of the joint. The surgery is performed through a medial knee incision around the inner edge of the patella, and the intra-articular bony bulge located at the edge of the cartilage colliding with the articular surface is removed, the intra-articular free body is removed, the inflammatory hyperplasia of the periosteum is removed, the unsmooth articular cartilage surface is repaired, and the meniscus should be removed or partially removed or repaired if there is rupture or loosening of the meniscus. After surgery, negative pressure drainage should be applied for 24 to 48 hours, and local pressure dressing should be applied. Continuous passive functional exercise can be performed after surgery to prevent joint adhesions. Osteotomy: Osteotomy is an early surgical method used to treat OA, through osteotomy to correct the force line, improve joint weight-bearing, promote hemodynamic changes, thereby reducing symptoms. Commonly used procedures are: a. Upper tibial high osteotomy: This procedure is suitable for lesions mainly unicondylar, and consistent with knee inversion and valgus, knee flexion and extension range of motion > 90 °, no obvious lateral instability. Unilateral tibial plateau depression does not exceed 0.5 cm, inversion deformity <12° or valgus <15°, no severe arterial ischemia or large varicose veins on the affected side, sufficient postoperative muscle strength to perform rehabilitation exercises, and age <65 years. b. Distal femoral osteotomy: For knee valgus >12° deformity, distal femoral osteotomy should be used. The indications are the same as above. Coventry calculates the size of the osteotomy using 1° for every 1 mm long correction at the base of the wedge. 4-6 weeks of postoperative plaster brace immobilization of the long leg, and 1 day of postoperative abduction to the floor to exercise the quadriceps. With the development of single-chamber arthroplasty, there is a tendency to reduce the number of osteotomies. (iii) Arthroplasty, also known as fusion: This is for young and strong people who are engaged in manual labor and have severe OA of the unilateral knee or failed knee arthroplasty. The patient loses joint movement after surgery, so it has been used less recently. ④Artificial knee replacement: In the 1950s, artificial knee prosthesis was developed successfully, but the results were not satisfactory, since the early 1970s condylar artificial knee joint began to be used in clinical practice, after 10 years of follow-up, its success rate has been nearly 90%. There are various types of knee prostheses, which are divided into single-lumen, double-lumen and triple-lumen according to the replacement site; non-constrained, semi-constrained and fully-constrained joints according to the prosthesis design; bone cement fixation, porous surface and tight pressure fit according to the fixation method. At present, the more applied is the three-lumen replacement prosthesis, semi-constrained type (commonly known as knee total condylar surface replacement prosthesis), which includes three parts: metal femoral prosthesis, ultra-high polymer polyethylene tibial prosthesis, patellar prosthesis. This surgery is suitable for patients with knee OA who are >50 years old and have been treated with conservative treatment or other surgical treatments that are ineffective or recurrent, with the aim of reducing pain, correcting deformity, and maintaining stability of knee motion. Key points of the operation: ① Pay attention to restore the normal axis of the limb during the operation. ②In cases of knee flexion contracture, attention should be paid to the removal of the bony redundancy and loosening of the surrounding soft tissues to facilitate knee balance and stability. ③Bone grafting is needed to fill in the collapsed tibial plateau with bone defect. ④Pay attention to restoring the normal range of motion of the patella. ⑤The negative pressure drainage was removed 48 hours after surgery. ⑥Start CPM on the first postoperative day and increase the range of motion of the knee joint from 30° of flexion to 90°. (7) Exercise the quadriceps contraction and extend and flex the ankle joint first, and walk on the ground after feasible straight leg raising with the help of double crutches. Common complications of this procedure include infection, prosthesis loosening, prosthesis wear, common peroneal nerve injury, patellar dislocation, fracture and unexplained pain.