Osteoarthrosis (OA) is the most common disease and a major cause of disability in middle-aged and elderly people, seriously affecting patients’ quality of life and social productivity. With the process of population aging, numerous countries have entered the aging society. The number of people over 60 years old in China now exceeds 130 million, and it is expected that by 2015 the total number of people over 60 years old will exceed 200 million. According to WHO estimates, 10% of the world’s population over 60 years of age suffer from OA, 80% of OA patients have mobility problems, and 25% are unable to engage in daily activities. The prevalence of OA in the age group of 20 years is reported to be only 20%, while the age group of 70 years is 85%. Statistics show that about 40 million adults in the United States suffer from arthritis, of which OA accounts for 43%, and 90% of women and 80% of men over the age of 65 suffer from the disease. With the increasing aging of the world’s population, the incidence of OA is showing a rising trend year by year globally, and degenerative joint diseases in the elderly have become one of the most important topics in medical research today. Strengthening research on age-related osteoarthritic diseases is conducive to improving the quality of life of the elderly, promoting social and economic development, and improving the health of the nation. Section I. Etiology of osteoarthritis Osteoarthritis (abbreviated as OA) was first proposed by Garrod in 1890, when such diseases were defined as functional changes in bone and joint due to the inflammatory process in bone and joint. Osteoarthritis is a chronic degenerative osteoarthritic disease of the elderly, characterized by degenerative changes in the articular cartilage with meniscal and synovial lesions as the main pathologic feature.The exact etiology of OA remains unclear. It is currently thought to be related to age, mechanical wear and tear, and impingement factors, and it has been found to be related to immune response, free radicals, increased intraosseous pressure, and cytokines, which are still under further investigation. The age factor is an important factor in OA because degeneration of articular cartilage will be inevitable as age increases, water content decreases, viscoelasticity decreases, and resistance to impingement and abrasion decreases. Most scholars now believe that although articular cartilage has strong wear resistance, its ability to resist impact is poor. Physiologic degeneration of articular cartilage is only a potential causative factor for the occurrence of OA, not a decisive factor. Articular cartilage damage is directly proportional to age and amount of exercise; the older the age and the more accumulated damage, the more severe the degree of articular cartilage degeneration. After cartilage damage, the resistance to mechanical, cumulative and repeated small impacts decreases, which can aggravate the degeneration of articular cartilage, leading to cartilage surface or deep layer damage, thus forming a vicious circle to further aggravate the damage. It has been suggested that OA is associated with increased intraosseous pressure. Some studies have shown that the subchondral bone internal pressure is increased in OA patients, and the bone tissue can be necrotic under the action of excessive internal pressure, and the necrotic bone trabeculae can be absorbed and reconstructed, so that the sclerosis gradient of subchondral bone is increased, and the ability of absorbing the oscillation is decreased, which makes the cartilage suffer from unequal force, and the local pressure is large, resulting in or aggravating the damage to the cartilage. Immune response is a new doctrine proposed in recent years. In the study of OA, it was found that when the mechanical factors were removed, the progression of OA did not stop, and the clinical symptoms of OA patients appeared repeatedly, which was difficult to be explained by the pure mechanical trauma cause. The recurrent joint swelling and synovitis in the patients were obvious, and it was hypothesized that the development of OA might be related to the immune response. Donohue’s theory of “hidden antigen” suggests that damaged cartilage exposes components that are normally isolated from the body’s autoimmune surveillance system, which act as antigenic stimuli and lead to autoimmune reactions.Cooke et al. detected immunoglobulin against type I collagen and complement C3 in the diseased cartilage of patients with OA, which made the “immune etiology” theory more difficult to explain. Cooke et al. detected immunoglobulin against type I collagen and complement C3 in the cartilage of OA patients, thus making the “immune etiology theory” more convincing. Free radicals are molecules, atoms, groups of atoms, and ions with unpaired electrons, and Pelletier et al. demonstrated that fragments of damaged articular cartilage stimulate phagocytosis in the synovial membrane to produce large amounts of oxygen free radicals. Oxygen free radicals can attack the chondrocyte membrane, causing chondrocyte morphology to change, function to be impaired, and synthesis and secretion of proteoglycans and collagen to be impeded, resulting in physiological function of the cartilage matrix to be altered. The relationship between cytokines and OA is currently a hotspot in the study of OA etiology. It has been reported that the levels of cytokines such as IL-1 (Interleukin 1) and TNF (Tumor Necrosis Factor) are significantly elevated in the synovial fluid of patients with OA, and in 1983 Wood et al. reported that high levels of IL-1 were detected in the synovial fluid of patients with osteoarthritis and rheumatoid arthritis, which was mainly secreted by the cells of synovial tissues lining the synovial lining layer and by chondrocytes. It was found by immunohistochemical methods that, under normal conditions, only a few chondrocytes located in the superficial layer of cartilage showed a positive reaction for IL-1 secretion, while the middle and upper cells and stroma of OA cartilage tissues showed a strong positive reaction for IL-1. In addition, IL-l mRNA expression was found in osteoblasts associated with intramembranous osteogenesis in OA osteochondral tissues, suggesting that IL-l may be directly involved in the pathological process of osteoarthritis. The ultrastructural changes of OA articular cartilage were more complex, both solidification, fragmentation and necrosis of chondrocytes could be seen, and the metabolic activity of some chondrocytes was enhanced, which was manifested by the appearance of intracellular rough endoplasmic reticulum, Golgi apparatus and a large number of microfilaments, and the disorganized arrangement of collagen fibers in the cartilage matrix with the deposition of crystalline calcium salt particles.Degradation of OA articular cartilage, in addition to causing the changes of its own biological properties and mechanical properties It also inevitably affects the subchondral bone. Microfracture occurs when the subchondral bone tissue is subjected to high compressive stress conduction, followed by trabecular necrosis and the formation of bone cystic degeneration. In the process of bone tissue repair and remodeling, the subchondral bone will form osteoid when repairing its own destruction and cartilage defects. The destruction of cartilage and bone can form tiny free bodies in the joint, which can stimulate the synovial membrane and cause inflammation. Section 2: Clinical Diagnosis of Osteoarthritis The clinical diagnosis of osteoarthritis involves comprehensive history taking, physical examination, and a thorough evaluation of the condition. The first question should be about the duration and severity of the lesion. Painful symptoms usually begin insidiously and tend to persist for months before the patient sees a physician. Patients are often uncomfortable with prolonged standing, walking or running, and symptoms usually resolve with rest. As the extent of the lesion increases, daily activities and sleep can be affected. In addition to pain, there is a grinding sensation and popping in the joint. Cartilage or meniscus damage or free bodies can cause “strangulation” symptoms, often affecting flexion and squatting. The internal, external and anterior compartments of the knee are further clarified by physical examination. Poor knee valgus alignment is more common than knee valgus, and changes in the line of force of the lower extremity in the standing position and flexion deformity are often indicative of severe involvement of the knee joint. Joint line interval tenderness and McMurray’s test generally elicit discomfort in the involved compartment. The ligaments are stable in most patients, but it is important to rule out underlying ligamentous instability. Pain in the patellofemoral and tibiofemoral joints under weight-bearing is predominant, especially when walking, walking up and down stairs, squatting and standing up, and may be sudden and painful when walking, hitting a weak leg or falling. Cartilage peeling, exposed subchondral bone, is stimulated by pressure leading to reflexive, spasmodic tension of the quadriceps muscle, due to meniscus wear and cartilage damage, strangulation symptoms can occur. Due to the wear of the cartilage of the patella, the subchondral bone is exposed, which reflexively causes the spasm of the quadriceps muscle, so the patella pushes the activity to be limited, and the patella grinding test is positive. Due to the synovial membrane hyperplasia and hypertrophy, congestion and edema, the synovial tissue is embedded in the joint space, and swelling, pain and functional limitation of the joint cavity can occur. Obese people are often accompanied by knee joint internal and external deformity and patella subluxation, standing X-ray stress side joint space narrowing, subchondral bone sclerosis or hyperplasia. Physical examination reveals knee valgus deformity or valgus deformity, standing flexion deformity, knee flexion and extension activities can be touched with friction sensation or hear twisting or tearing friction sound, joint space and patellar edge pressure pain, patellar migration activities are limited, patellar milling test is positive, and knee floating patella test is positive. In patients with long-term physical therapy, the color of the skin around the knee joint was altered and patchy, and the skin was leopard skin-like changes. Squatting and rising is very difficult and requires two hands to support the ground. Imaging of the knee joint helps in clinical diagnosis and understanding to determine the extent of articular cartilage lesions. In the early stage of chondropathy, X-ray examination includes weight-bearing anteroposterior (PA) orthopantomograms of the knee, and X-ray films of the knee in weight-bearing flexion at 20°-30°. The PA flexion image, compared with the knee in weight-bearing extension, can clearly show the narrowing of the joint space, unequal widening of the two sides, sharpness of the tibial spine, flattening of the joint margins, sclerosis or cystic changes of the subchondral bone, inversion or valgus deformity, and cartilage changes in the knee joint. The radiographic features include subchondral bone sclerosis, sharpening of the tibial spine, osteophyte formation and narrowing of the intercondylar fossa of the femur, lip hyperplasia of the tibiofemoral joint margins, subluxation of the patellofemoral joint, and osteophyte formation on the superior and inferior poles of the patella. Tibial and femoral lines of force were assessed by X-ray of the knee in the weight-bearing position, but full-length X-rays of the lower extremity were required to assess the mechanical axis. Magnetic resonance imaging (MRI) is noninvasive, and MRI clearly shows cartilage changes when the radiographs do not show joint space narrowing changes before, i.e., in the early stages of articular cartilage pathology, proton density fat-saturated fast-spinning echo (PDFSE), and three-dimensional gradient echo (3D SPGR) scans. Section 3, Selective Limited Arthroscopic Clearance for Osteoarthritis Treatment of osteoarthritis The treatment of osteoarthritis is divided into conservative and surgical therapies. Conservative treatment is based on systemic medication and intra-articular local medication. In early OA patients, oral anti-inflammatory and analgesic drugs or drugs that activate blood circulation and remove blood stasis can be given symptomatically to improve symptoms and quality of life. Intra-articular injection of hyaluronic acid, an articular cartilage protector, has some effect. For OA patients with obvious joint pain and swelling, walking dysfunction, MRI showing cartilage destruction, free bodies in the joints, bone redundancy hyperplasia or with meniscus injury, surgery should be resorted to. Surgical treatments for OA include arthroscopic cleanup, drilling and decompression microfracture in the area of total cartilage damage, high tibial osteotomy with corrective force line, and prosthetic arthroplasty. The application of chondrocyte transplantation, growth factors and gel carriers are in the research and trial stage. Arthroscopic cleanup can be performed with epidural or local anesthesia. Local anesthesia should be applied with 20ml of 2% lidocaine + 40mm of saline + 0.1% epinephrine solution 0.1ml as a mixture, which is injected into the surgical entrance and the joint cavity respectively for local infiltration anesthesia, and the operation can be carried out after 10 minutes. To maintain a clear intraoperative field of vision, saline 3000 ml + 0.1% epinephrine injection 1 ml was used as the perfusion solution, which could eliminate the need for surgery under tourniquet control. Arthroscopic examination was performed in sequence to fully understand the intra-articular lesions, and arthroscopic surgery was performed. Arthroscopically, the joint was seen to be suspended particles, the synovial tissue of the patellofemoral joint was hyperplastic and hypertrophied, the cartilage was fragmented and curled, the suprapatellar capsule was white with slender fibrous villi, some synovial blood vessels were tortuous and congested, and the edematous synovial tissue was fusiform, grapelike, and other synovial anomalous alterations. The intercondylar fossa of the femur is narrowed, the cartilage is peeled off, the subchondral bone is exposed and uneven, and the meniscus is worn out in the corresponding part of the cartilage injury. Meniscus injury in turn can exacerbate cartilage wear, and the degree of meniscus injury is directly proportional to the degree of cartilage injury. Cartilage and meniscus injuries are causative of each other and affect each other. Meniscus abrasion, thinning, fibrous hyperplasia, free edge of the canine-like mutilation, can stimulate the synovial membrane hyperplasia, causing knee pain or strangulation symptoms. Intercondylar fossa or suprapatellar bursa with different forms of free body is a common cause to induce strangulation symptoms. There are more arthroscopic cleaning methods, and radiofrequency pneumatization or planing and grinding are generally used to deal with the free edge of meniscus injury and trim its stump. The anterior horn of the meniscus has relatively good blood flow and has the possibility of healing, so in principle, it is preserved as much as possible and resection is avoided as much as possible. In some cases, the anterior horn is shutter-like or bundle fiber-like injury, but the body and posterior horn of the meniscus are normal, radiofrequency crumpling can be used to flatten the injury wound, while the torn anterior horn of the meniscus is sutured using the inside-out method, and the meniscus is braked for 4-6 weeks after the operation. Preservation of the meniscus plays an important role in preventing cartilage damage. Degeneration of articular cartilage is more prevalent in the weight-bearing areas of the patella, femoral condyles, and tibial plateau, and is characterized by wrinkled swelling and elevation, cracking of cartilage, patchy exfoliation, and exposure of subchondral bone. The uneven trajectory of the femoral and tibial articular surfaces is often secondary to or exacerbates meniscal wear. Resection or trimming of the ruptured meniscus, grinding of the bony obstruction that affects joint movement, and release of the joint strangulation factors and dysfunction are of great value in interrupting the vicious cycle of the inflammatory process and improving the clinical symptoms. The range of total cartilage damage is less than 2cm, the method of subchondral bone drilling can be applied, and fibrocartilage can be formed. If extensive cartilage degeneration, there is no good strategy to save, only the unstable free edge can be cleaned and smoothed, not a wide range of extensive scraping or cleaning, otherwise the clinical symptoms are bound to aggravate, and it is difficult to return to normal. Intercondylar fossa of femur narrowing and tibial intercondylar spine hyperplasia of bone impingement, can affect the knee joint extension function. Clinical manifestations of knee flexion deformity, standing position of the knee can not be completely straightened, the knee is arch bridge-like, accompanied by knee inversion or eversion deformity. The posterior horn of meniscus and cartilage wear of femoral condyle were aggravated due to the negative weight and stress backward movement of knee joint. Arthroscopic dynamic examination revealed that the tibial tuberosity impinged on the intercondylar fossa, and the ACL degenerated by the embedded pressure and abrasion of the tuberosity of the intercondylar fossa, losing its luster, becoming deformed and thinning, and spreading out in a bundle. The intercondylar fossa of the femur was enlarged by biting off or grinding the growths, and the space of the intercondylar fossa was enlarged until the impingement disappeared and the knee extension function improved, and the ACL was not abraded, and the wound was hemostatized by radiofrequency vaporization, and the ACL fibers that had been scattered in bundles were crumpled and restored to their tension by radiofrequency. We found that after enlargement and molding of the intercondylar fossa of the femur and resection of the tibial tuberosity, the knee inversion or valgus deformity was improved accordingly, which may be related to the shift of the point of impingement formed by the proliferation of the intercondylar fossa and the tibial tuberosity, which led to a change in the line of force and aggravated or induced the knee inversion or valgus deformity. It has been suggested that in osteoarthritis of the knee, the lateral patellar support band is strained, which restricts the normal movement of the patella in the patellofemoral joint kinematic trajectory, further increasing the pressure on the patellofemoral joint, leading to wear and tear of the patellofemoral joint cartilage and aggravation of the clinical symptoms.Merchant(1974),firstly reported on the lateral patellar support band release, and Breitenfelder(1987) carried out a long term Fulkson et al. (1986) suggested that the selection of lateral patellar support band release is mainly based on the knee symptoms, the presence of patellar tilt on X-ray, and the formation of lateral patellar tuberosity, etc. Henry et al. (1986) believed that a detailed preoperative history and physical examination is an important basis for the selection of indications for the operation.Kolowich et al. conducted a long-term follow-up on 202 lateral patellar support band release patients, and the comparative effectiveness of the procedure was shown. Kolowich et al. conducted a long-term follow-up of 202 patients to compare the preoperative physical examination of the effective group and the failed group, and he found that the patellar tilt test was the most important sign affecting the final treatment outcome, followed by the patellar internal displacement test, and the results of the X-ray examination did not have much influence on the treatment outcome. The author believes that for patients who are younger and whose articular cartilage wear is not very severe, early release of the lateral patellar support band is an effective way to relieve pain due to increased lateral patellar pressure and to reduce articular cartilage wear. However, if the patient is of advanced age, has fairly severe cartilage wear, and has developed a distinct motion track, lateral patellar support band release, which may aggravate the clinical symptoms and is not conducive to functional recovery, should not be performed as a rule and should be performed on a case-by-case basis. Friedman et al. reported on the efficacy of arthroscopic debridement in the treatment of osteoarthritis, with functional improvement obtained in 60% of cases. They found that the age of the patient had a direct impact on the efficacy of the procedure, with 86% of those under 40 years of age improving, while only 53% of those over 40 years of age improved, and Bert reported that arthroscopic cleanup had an excellent rate of 50% to 76%. OA is a geriatric, degenerative change, and no single method can stop aging. The so-called arthrocentesis is only relative, and it is impossible to reverse the degeneration of the joint that has already developed. Cleaning and repairing the unstable cartilage trauma, unblocking and impinging on the trajectory of movement, and removing the pain-causing factors, cartilage degradation particles, macromolecule components, debris and microcrystallization of the articular cartilage after wear and tear, inflammatory factors, and pain-causing substances from the joint are conducive to the restoration of function. Poor postoperative efficacy of the factors in addition to the advanced age of articular cartilage degeneration, knee internal and external deformity of the lower limb force line changes, and the size of the surgical trauma is directly related to the larger the surgical trauma the worse the efficacy of the trauma is small in favor of functional recovery. Therefore, we advocate local anesthesia arthroscopic selective, limited minimally invasive cleanup, do not interfere too much with the intra-articular tissue. In order to facilitate microscopic observation, the synovial tissue that obscures the field of view of hyperplasia and hypertrophy can be shaved, without extensive removal. Excise the intercondylar fossa of femur and intercondylar tibia de osteophyte proliferation, release the intercondylar fossa stenosis; repair the worn meniscus and cartilage defect area, remove the peeling separation and unstable cartilage fragments in the joint, take out the free body, grind the unevenness affecting the joint activities of the bony obstruction, remove the intra-articular pain-causing substances, and wash with large amounts of physiological saline. If there is an abnormal change in the line of force of the lower limb, the stress on the joint surface can be reduced by osteotomy to free the damaged joint surface, such as high tibial osteotomy. Postoperative ice pack cold compress on the affected knee for 24~48 hours can achieve the purpose of stopping bleeding and pain. For those with obvious postoperative swelling, blood and fluid accumulation in the joint cavity should be withdrawn, and sodium hyaluronate should be injected into the joint cavity after 7-10 days. Functional exercises of quadriceps muscle of knee joint after operation are favorable for functional recovery.