Treatment of OA includes physical therapy, pharmacotherapy and surgery, of which pharmacotherapy is the most used. Treatment of OA drugs can be divided into two categories, namely, to improve the symptoms of fast-acting drugs, improve the structure of slow-acting drugs. 1, fast-acting drugs to improve symptoms, also known as non-specific drugs, including non-steroidal anti-inflammatory drugs (nsaids), glucocorticoids, etc.. They can provide rapid pain relief and have anti-inflammatory effects. nsaids are the most widely used class of drugs at present. Symptom-improving drugs can effectively relieve pain and other symptoms and temporarily improve joint function, but they cannot stop the progression of OA. Because the elderly are prone to adverse reactions to nsaids, and synovial inflammation in OA is not a major factor especially in the early stages, general analgesics such as acetaminophen can be used first. Acetaminophen has a good antipyretic and analgesic effect, the efficacy of the drug for OA is similar to nsaids, and safer for the gastrointestinal mucosa, liver and kidneys. nsaids are also commonly used in the symptomatic treatment of OA, especially in the inflammatory phase of OA. During anti-inflammatory therapy for OA, chondrocytes are exposed to relatively high concentrations of nsaids, which may cause or aggravate joint damage with long-term application. Some nsaids, such as aspirin, salicylic acid, pautazone, indomethacin and naproxen, have an inhibitory effect on the synthesis of articular cartilage matrix proteoglycans and should not be used for a long time; other drugs, such as diclofenac and meloxicam, have no adverse effect on the synthesis of cartilage matrix proteoglycans, and even have a role in promoting synthesis, which is suitable for selection. In recent years, there is evidence that the anti-inflammatory and analgesic effects of nsaids are due to the inhibition of selective cyclooxygenase 2 (cox-2), while cox-1 is associated with gastrointestinal adverse effects. Compared with conventional nsaids, cox-2 specific inhibitors such as celecoxib can significantly reduce gastrointestinal adverse effects due to cox-1 blockade, but adverse effects such as hypertension, water and sodium retention or congestive heart failure should be noted. Because of the gastrointestinal adverse effects of nsaids and its possible deleterious effects on articular cartilage metabolism, nsaids should be used with caution in elderly OA and should also be closely observed for its possible risk of promoting cardiovascular events when applied as a cox-2 selective inhibitor. Diacerein exerts anti-inflammatory and protective effects on articular cartilage by inhibiting the production and release of il-1 and oxygen free radicals, inhibiting the activity of mmp and stabilizing the lysosomal membrane, improving patient symptoms, promoting cartilage repair and improving the course of the disease. Its analgesic effect and improvement of joint function are similar to those of nsaids. The preparation does not affect the effects of phospholipase a, cyclooxygenase and lipoxygenase, and the common adverse effects of nsaids occur less frequently in diacerein. Hormone generally line intra-articular injection, not more than 3 to 4 times a year. 2, improve the structure of the slow-acting drugs, that is, specific drugs, also known as articular cartilage protective drugs, generally slow onset of action, including hyaluronic acid, glucosamine, etc.. Its basic focus is not to control the symptoms, but to protect the articular cartilage, to prevent its structural damage to normal joints can reduce the occurrence of OA, while the OA joints can stall or slow down the further deterioration of the disease. Its mechanism of action ① promotes the synthesis of proteoglycans in cartilage to repair and rebuild articular cartilage. Increased synthesis of proteoglycans indicates that the articular cartilage is undergoing active repair. Since 1956, when lennart roden of Karolinska Institute in Sweden first published that “glucosamine” could significantly increase the synthesis of chondroitin sulfate, many experiments have confirmed that glucosamine can stimulate the synthesis of proteoglycans. ②Inhibit the activity of mmp and phospholipase a 2 (pla 2), block the inhibitory effect of il-1β, prevent the production of NO and superoxide radicals, and prevent the further degeneration of cartilage. Cartilage degradation is closely related to mmp and il-1. mmp, such as the activation of matrix degrading enzymes and collagenase, leads to the degradation of cartilage matrix; pla 2 is involved in mediating il-1 and activating collagenase; il-1 promotes the synthesis and activation of mmp, induces the production of prostaglandin e2 and NO, and inhibits proteoglycan synthesis; NO and superoxide radicals inhibit the anabolism of cartilage matrix and promote catabolism. . Glucosamine significantly inhibited mmp activity, inhibited il-1β activity, blocked lps, rhil-1β-induced NO production, inhibited superoxide radical production in rat macrophages, inhibited chondrocyte pla 2 and collagenase activity in OA patients, and blocked degenerative changes in cartilage. OA is associated with reduced chondrocyte repair capacity, decreased adhesion to fibronectin, and inability of chondrocytes to migrate to damaged sites. The mutual adhesion of chondrocytes to matrix components, such as fibronectin, glass-linked proteins, platelet-reactive elements, and collagen, is a key factor in the process of tissue repair and cell migration. Protein kinase c blocks the inhibitory effect of il-1 on proteoglycan synthesis and is involved in cell adhesion. In vitro application of glucosamine significantly increased protein synthesis, promoted protein kinase c production, significantly improved the adhesion of OA chondrocytes to fibronectin, and promoted cartilage repair and regeneration. ④Anti-inflammatory effect: glucosamine inhibits the swelling of rat foot induced by carrageenan, dextran and formaldehyde, and has a protective effect on plasmacytosis and increased capillary permeability induced by carrageenan, formaldehyde and acetic acid; on inflammatory mediators such as bradykinin; hyaluronic acid hyaluronic acid is the main component of synovial fluid, maintaining the elasticity and viscosity of synovial fluid, and is composed of n-acetylamino glucuronic acid and glucuronic acid macromolecular proteoglycans. Exogenous hyaluronic acid can cover the surface of cartilage and synovial membrane to re-form a normal physiological barrier, and improve synovial fluid viscosity and reduce friction between cartilage and synovial membrane; promote the synthesis of hyaluronic acid in synovial fluid and promote the synthesis of proteoglycans; inhibit the expression of il-1β and mmp in OA synovial fluid, but not in articular cartilage; inhibit the production of prostaglandin e 2; inhibit nociceptive nerve It inhibits nociceptive neurotransmission, barriers the release and diffusion of inflammatory mediators, and decreases nociceptive sensitivity. Recently, it has been reported that intra-articular injections of hyaluronic acid, heparin, and chondroitin sulfate may be a potential trigger for rheumatoid arthritis, but more trials are needed to support this. Intra-articular injection of hyaluronic acid for OA treatment can relieve joint pain, improve joint flexibility, and have anti-inflammatory effects, and has a good safety profile. The results of clinical studies have shown that hyaluronic acid has similar therapeutic effects to standard nsaids and significantly reduces pain. In 2 well-designed rcts, the hyaluronic acid group was significantly more effective than the saline group. Chondroitin sulfate is the most abundant proteoglycan in the cartilage matrix. It is a long-chain polymer composed of n-acetylamino galactose and glucuronic acid, with a large molecular weight, easily hydrolyzed in the gastrointestinal tract, and as an important component of the cartilage matrix, it has a similar mechanism of action to It has a similar mechanism of action to glucosamine. Its mechanism of action includes anti-inflammation, promoting the synthesis of proteoglycans in the matrix and reducing their loss, maintaining the normal metabolic process of the matrix in combination with glucosamine, and delaying the degenerative changes of articular cartilage. Several clinical studies have shown that chondroitin sulfate relieves mild to moderate OA symptoms, is superior to the placebo group in reducing pain, is consistent with nsaids, and exhibits a good safety profile. The study showed that after 1 year of treatment in OA patients, the digital imaging analysis system showed that the joint gap between the tibia and femur was stable in the chondroitin sulfate group, while the joint gap tended to narrow in the placebo group, suggesting that it may slow down the degeneration of OA cartilage. It will take time before chondroitin sulfate is actually used clinically in OA, and there is a lack of sufficient evidence whether glucosamine is more effective in combination with chondroitin sulfate than alone. Other drugs include glucosaminoglycan, S-adenosylmethionine, and doxycycline, but the exact efficacy of these drugs remains to be further investigated. Biologic agents, joint cavity injections, and surgical treatment are also available. Conservative treatment should be used as much as possible in general treatment, and surgical treatment should be considered only when conservative treatment is ineffective. 3, joint cavity injection of hyaluronic acid is an important component of the joint fluid, has the role of protecting cartilage and reducing pain sensitivity; stimulate chondrocyte synthesis of proteoglycans, and inhibit the apoptosis of OA chondrocytes to improve joint function. Intra-articular injection of sodium hyaluronate can restore the normal viscoelasticity of synovial fluid, increase the lubrication function, activate the self-repair process of cartilage tissue, and inhibit the decomposition of cartilage matrix, which is particularly advantageous for the application of non-selective nsaids and cox-2 inhibitors in elderly OA patients with contraindications, poor results or adverse reactions, and is mostly used for knee OA. The analgesic effect of intra-articular hyaluronic acid injections was found to be similar to that of nsaids, while the improvement in joint function was better than that of nsaids alone; it was more effective in OA with mild cartilage wear, but less effective in OA with moderate to severe cartilage destruction. When there is acute synovitis in knee OA and acute inflammatory effusion in the bursa and tendons around the joint, intra-articular hormone injection can relieve the acute joint pain of OA and promote the local inflammation to subside, which can obtain satisfactory pain relief, but because it may cause crystal arthritis, it should not be used repeatedly and is not advocated for systemic use. The effect of hyaluronic acid in relieving pain appears later than that of hormone, but lasts longer. 4, is being studied in the treatment of drugs and means mmp inhibitors: in the pathogenesis of OA, mmp activity is enhanced, playing a key role in bone damage, a variety of drugs to improve the condition mainly through the inhibition of mmp role. Tissue-type matrix protease inhibitor (timps) is a natural inhibitor of mmp discovered in recent years, the concentration of timp in OA synovial fluid is significantly lower than normal, it is a group of multifunctional factors that can inhibit the activity of mmp, effectively preventing the degradation of connective tissue and OA disease development. Tetracyclines have the effect of inhibiting mmp, inhibit the secretion of inflammatory cytokines, reduce cartilage destruction, the representative drugs are doxycycline. Gene therapy: gene therapy is a new treatment method in recent years, the main application of il-1ra, il-10, il-13 and other experimental research on gene transfection, il-1ra gene therapy is the current hot spot of OA research. Once applied in the clinic, is a better way to treat senile OA. 5, other drug therapy: elderly OA patients, often accompanied by osteoporosis, subchondral bone plate quality changes may also accelerate the destruction of cartilage, which in turn causes compensatory osteophytes, so in the treatment of senile OA should be carried out at the same time anti-osteoporosis treatment. Local topical application of methyl salicylic acid or topical drugs containing nsaids, capsaicin and other drugs, can reduce OA joint pain. 6, surgical treatment: degenerative changes in the primary OA of the elderly, the disease usually develops slowly and can remain quite a period of quiescence. As far as possible, the use of non-surgical treatment, such as older patients with more severe persistent pain and joint activity disorders are significant, progressive restriction of daily activities, the need to consider surgical treatment. In addition to arthroscopic joint cavity cleaning, general orthopedic surgery such as arthroplasty, joint fusion, osteotomy, etc. is not suitable for elderly patients because of the need for external fixation after surgery. Arthroplasty can relieve joint pain and improve joint function for most OA patients, and is suitable for the elderly because artificial joints have a limited life span.