The etiology of osteoarthritis is unclear and may be related to the following factors: i. Age As we age, cartilage becomes hypertrophic and thickens, nutrient supply is inadequate, cartilage degeneration, chondrocytes decrease, cartilage tears, and strong type I collagen replaces type II collagen. Hyaline cartilage becomes fibrocartilage, and the elasticity and viscosity of articular cartilage decreases. Secondly, muscle and peripheral nerve function decreases, resulting in uncoordinated nerve and muscle function, which can easily cause joint injury. In addition, inorganic material in bones gradually increases, and the elasticity and toughness of bones decrease. As age increases, the blood flow supplying the joints decreases, the cartilage becomes thinner due to the decrease of nutrition, and the cartilage organism decreases and fibrosis occurs. On the basis of the above unfavorable factors, easy to cause damage to cartilage cells, resulting in future degenerative joint cartilage and bone lesions. The incidence of osteoarthritis in Heberden’s node and bouchard’s node is 2-3 times higher than that of the general population. Osteoarthritis of the hip and carpometacarpal joints is more common in Caucasians. Genetic analysis of biploidy in osteoarthritis has identified mutations in the gene in the region 23-35 on the short arm of chromosome 2 that are associated with osteoarthritis. Osteoarthritis may also be associated with the type II procollagen gene (COL2A1), which is responsible for encoding type II collagen in cartilage. Third, joint injury and overuse Any cause of abnormal joint shape can alter the transmission of joint loads and increase the local load and wear on the cartilage surfaces of the joints, all of which can cause osteoarthritis. For example, strenuous exercise, congenital dislocation of the hip, inversion or valgus deformity of the knee and poor fracture repositioning, and post-articular dislocation cruciate ligament resection can cause excessive pressure to form throughout the joint or localized in the joint, destroying the cartilage reticular structure, which in turn causes metamorphosis of cartilage cells and reduced matrix synthesis, resulting in osteoarthritis. In addition, osteoarthritis is also related to joint wear and repeated long-term use of certain joints, such as textile workers more hand osteoarthritis, and track and field athletes more knee osteoarthritis. Obesity increases the load on the weight-bearing joints, and the incidence of knee osteoarthritis is directly proportional to the increase in weight. Foreign literature reports ‘obese people osteoarthritis incidence rate stomach 12-43%, significantly higher than the non-obese population. In addition, the risk of osteoarthritis in obese people is 1.5 times higher than normal weight, and the risk of osteoarthritis in obese women is 2.1 times higher than normal weight. Obese patients with osteoarthritis in China account for 53.7. Weight loss in obese people can reduce the severity of the disease. Five, bone density Osteoporosis patients with subchondral trabeculae thinning and hardening, the ability to withstand pressure is reduced. Easy to injury, such as subchondral trabecular fracture, indirectly affect the ability of joint cartilage to withstand pressure, resulting in bone destruction, therefore, osteoporosis patients have a higher chance of osteoarthritis.