The occurrence of osteoarthritis is thought to be caused by the mechanical environment specific to the joint in a systemic situation, and the causative factors can be divided into mechanical and systemic types. According to the etiological classification, there are two types of osteoarthritis, primary and secondary. 1. Weight: A study by Werb et al. found, using the Framingham method, that weight change in women had an effect on the occurrence of osteoarthritis of the knee. In a later study that used the Framingham method for the basic evaluation of people without arthritis, it was further confirmed that the risk of osteoarthritis is high in those with a high body mass index (BMI) and that weight change is directly related to the risk of osteoarthritis. It has also been reported in foreign literature that the incidence of osteoarthritis in obese patients ranges from 12% to 43%, while osteoarthritis patients with obesity account for 12% to 45%. Some people have collected material from patients with osteoarthritis for more than 30 years prior to the onset of the disease and found that the risk of osteoarthritis was 1.5 times higher in men who were over 20% of their standard weight at the age of 37 than in those of standard weight, and 2.1 times higher in women. The main mechanism for the occurrence of osteoarthritis is that increased body weight leads to increased weight bearing on the joints, resulting in increased mechanical damage to the joints during activity. For example, increased body weight increases the compressive stress on the medial cartilage of the knee joint, and the medial side of the joint is a good site for osteoarthritis, suggesting that obesity may be an important risk factor for severe knee disease. Changes in posture, gait and exercise habits due to increased body weight may also be a cause of osteoarthritis. The hip joint is also a weight-bearing joint, but the incidence of hip osteoarthritis is lower in obese people; the distal interphalangeal joint of the hand is not a weight-bearing joint, but finger osteoarthritis also increases with the increase in body weight. Therefore, it is presumed that these may be related to obesity coexisting lipid, purine and sugar metabolism abnormalities. 2, age: age is one of the most important pathogenic risk factors for osteoarthritis. The prevalence of the disease increases with age, and a longitudinal study of the Chingford population by Hart showed an increased risk of knee osteoarthritis in the three highest age groups. The specific mechanisms may include two aspects: first, after middle age (40-50 years), a person’s muscle function gradually decreases, the peripheral nervous system becomes less functional, reflexes weaken, and nerve conduction times lengthen, resulting in uncoordinated nerve and muscle movements that can easily cause muscle damage. Secondly, as people grow older, the inorganic content of bone increases progressively (e.g., 50% in young people, but 66% and 80% in middle-aged and elderly people, respectively), and the increased inorganic content makes the bones less elastic and tough. At the same time, reduced blood flow to the joints can lead to changes in the function and cartilage properties of the chondrocytes in the articular cartilage, as well as different responses to cytokines and growth factors. The weight-bearing capacity of the joint decreases and once the mechanical forces exceed the capacity of the articular cartilage, damage to the collagen matrix occurs and chondrocytes are damaged, releasing degradative enzymes and leading to cartilage loss. In addition, with aging, joint protective nerve and mechanical damage, increasing the chances of joint damage. 3, over application and injury: Most knee injuries, including cruciate ligament and meniscal tears are common causes of knee osteoarthritis. Osteoarthritic changes occur in up to 89% of people who have had their meniscus removed. Osteoarthritis is associated with a variety of sports, including marathon sports (hip osteoarthritis) and soccer (knee and medullary wide arthritis). Unpreparedness for even seemingly minor loads, such as a footfall on the side of the road or a stair step, can cause joint damage and become a major cause of “primary” osteoarthritis. This is because the time from impact loading to the neuromuscular apparatus radiological response takes about 1/1000s, and the unexpected loading does not give the nerves and muscles enough time to activate protective reflexes, in which case the load may be transmitted to the joint and cause injury. In addition, people with damage to the supporting structures of the weight-bearing joints such as ligaments, tendons or menisci, or those who develop muscle atrophy with age, are susceptible to osteoarthritis due to reduced or lost joint protection even if they do not engage in stressful sports that increase joint loading. Poor stability of the knee joint can lead to osteoarthritis of the knee. 4. Hormone levels: Women after the age of 50 have a higher chance of developing osteoarthritis than men of similar age. Epidemiological studies have shown that women who take estrogen have less radiographic osteoarthritis than those who do not. The final study also found that estrogen receptors in articular cartilage in humans and several animal species, and that estrogen may affect levels of pro-inflammatory cytokines and growth factors that regulate cartilage breakdown and anabolism. The above findings suggest that estrogen may play a role in the development of osteoarthritis. However, some studies have come to the opposite conclusion, such as: estrogen can worsen osteoarthritis in rabbit models with meniscectomy; estrogen has no effect on symptomatic knee or medullary osteoarthritis or even worsens the symptoms. 5, genetic: genetic factors on osteoarthritis may include congenital structural abnormalities and defects (such as congenital hip dislocation, acetabular dysplasia and dislocation of the femoral epiphysis), abnormalities in cartilage or bone metabolism, obesity and osteoporosis. It was recognized as early as the 1940s that women with osteoarthritis with Heberden’s nodes had mothers and sisters with osteoarthritis two and three times more often than the general population, respectively. The most common hereditary osteoarthritis is associated with HLA-A1B8 and HLA-A1B8 haplotypes and α1-antitrypsin isoforms. It has also been suggested that osteoarthritis may be heterozygous, including mutations in genes encoding trace amounts of collagen such as IV, X, and D, and genes encoding extracellular matrix and proteins such as chondroitin sulfate proteoglycans, connexins, and hyaluronic acid are involved in the development of osteoarthritis. Studies on the relationship between cartilage components-collagen and genetic factors also support a genetic association with the development of osteoarthritis.Palotie et al. used restriction endonucleases and restriction fragment length polymorphism studies to find that certain familial osteoarthritis is associated with abnormalities in COL2AL, a gene encoding type II collagen on the long arm of chromosome 12, which encodes an alpha chain A base at position 519 is mutated and the codon for arginine is replaced by a codon for cysteine. 6. Other factors (1) Altered cartilage matrix: Patients with hemochromatosis, brownish yellow disease, Wilson’s disease, gouty arthritis and dihydroxypyrophosphate crystal deposition disease, respectively, damage chondrocytes directly or indirectly by increasing matrix stiffness due to the deposition of iron-containing heme, mare’s uric acid polymers, copper, urate crystals and dihydroxypyrophosphate crystals in the cartilage matrix. However, it is not known whether foreign body deposition is preceded by biochemical or physicochemical changes in the matrix. (2) Elevated intraosseous pressure: Under normal conditions, a dynamic equilibrium is maintained between the intraosseous and soft tissue blood circulation systems. When intraosseous venous return is obstructed for various reasons, when there is excessive arterial blood inflow, or when intra-articular pressure rises significantly, this can cause an increase in intraosseous pressure, which in turn affects the blood supply to the bone tissue and leads to degenerative lesions of the articular cartilage. In conclusion, osteoarthritis disease has not yet been elucidated, and its pathogenesis is not due to a single factor, but may be the result of multifactorial effects.