Osteoarthritis (OA) is an age-related degenerative disease of the synovial joints. From a global perspective, OA is a local manifestation of systemic aging in the joints, while from the joints themselves, it is the result of changes in the intra-articular environment, which involves both biochemical changes in all tissues and structures of the joints, and may be related to local changes in the mechanical structure of the joints. The biochemical and biomechanical factors are mutually influential and causal. It can be seen that the development of OA is the result of many factors acting together, therefore, in terms of treatment strategy, it is necessary to adopt a variety of integrated treatment, and at the same time, it is necessary to integrate individualized treatment measures as much as possible for the different characteristics of each patient. Broadly speaking, we can divide the existing treatments into three major categories, including non-pharmacological, pharmacological, and surgical treatments. Let’s talk about the general principles of drug treatment. Humans have known OA for a long time, but the research and understanding of it has only just begun, and there are really very few therapeutic drugs that can be used clinically. The International Osteoarthritis Research Institute (OARSI) treatment guidelines published in 2008 recommended eight drug treatment measures, and in 2010, some amendments were made. The first category is painkillers. There is a great deal of prejudice against pain medications among patients in this country, mainly because of concerns about their addictive nature and side effects. However, studies have shown that as far as addiction is concerned, if a pain response does exist within the body, reasonable use of pain medication will not cause addiction, and even when chronic pain is chronic and requires long-term use of pain medication, it will rarely cause addiction. Moreover, in OA patients, the preferred clinical pain medication is not narcotic analgesics, but acetaminophen, followed by non-steroidal anti-inflammatory analgesics (NASIDs), and again narcotic analgesics, which are often needed for surgical treatment when narcotic analgesics are often needed, so addiction is really not a problem. Acetaminophen is a very old classic, and is the first-line drug of choice in many national guidelines for the treatment of inflammatory joint disease. It has a very wide safety range, with a maximum daily dose of about 3.6 grams, and low side effects and high long-term safety. The safety profile is even better at smaller doses (under 3 grams per day) and when long-term use is avoided when possible. NASIDs are also classical anti-inflammatory and analgesic drugs, and we should note that the word “inflammation” in this anti-inflammatory term usually refers to a sterile inflammatory reaction, not related to bacteria. In OA, it refers to the abnormal biochemical reaction of the intra-articular environment mentioned above, which causes pain, and NASIDs drugs are used to relieve pain by inhibiting this inflammatory reaction, and they do not act directly on the nervous system. The common feature is that they have a high gastrointestinal and cardiovascular risk and are usually not recommended for long-term high dose use, but rather for short-term use at the lowest effective dose. In particular, patients over 65 years of age and those with a history of peptic ulcers, bleeding and perforation should be avoided to avoid rebleeding, and in patients without gastrointestinal risk factors, use with a gastric mucosal protector is also recommended. Cilobal belongs to a new class of NASIDs drugs with much less gastrointestinal risk, but still has a higher risk of cardiovascular complications and should still be used with caution in patients of advanced age and in patients with risk factors for heart attack/cerebral infarction/stroke. Because of the high incidence of side effects of oral NASIDs, some manufacturers have made them into topical creams or compresses to allow the drug to work locally, which can provide pain relief and avoid systemic side effects, among which the more famous is Fotarim emulsion. mild pain. Of course, we have a wide variety of traditional Chinese ointments, as well as capsaicin ointments in western medicine, which work in a similar way. The second major group of drugs are the glycosaminoglycans, including sodium hyaluronate, glucosamine, and chondroitin sulfate, which are three high-profile drugs. In fact, although they are similar in chemical structure, the glycosaminoglycans themselves are so varied and diverse that differences in chemical structure inevitably lead to differences in clinical action. Sodium hyaluronate is a large molecular weight glycosaminoglycan that is present in the joint fluid of both normal and OA joints. Many studies and literature analyses have demonstrated its effectiveness in the treatment of OA, but the drawback is that it cannot be taken orally, but only as an intra-articular injection, known as viscoelastic supplementation therapy. Because intra-articular injection is an invasive operation, its application is somewhat limited. Moreover, the hip joint is not easily injected because of its deep location, so it is usually most commonly used in the knee joint, while other joints are relatively less used. When glucocorticoids are injected into the knee joint for OA, their pain-relieving effect generally lasts only about 4 weeks and does not contribute to functional improvement. Unlike hormones, sodium hyaluronate has a slower onset of action, generally taking about 2-3 weeks, but its efficacy can last for as long as 2-3 months. Because of the large amount of glycosaminoglycans in cartilage and cartilage matrix, glucosamine and chondroitin sulfate are used extensively as nutritional supplements, and the name “chondroprotective agent” has been suggested to refer specifically to these two drugs. However, because OA is a multi-causal, total joint disease, the lesions are not limited to cartilage and subchondral bone, but involve all components of the joint, and the abnormal mechanical environment, such a narrow name as “chondroprotective agent” is clearly inappropriate. The other side of the coin is that new therapeutic agents for OA are difficult to discover or invent, and the therapeutic mechanism of action of glycosaminoglycans remains poorly understood. Studies have shown that there is no evidence to date that supplements containing glucosamine and chondroitin sulfate have a therapeutic effect on osteoarthritis, and a new meta-analysis published in 2010 showed that the results of glucosamine action differed between preparations, even those produced by different manufacturers. While many previous studies have used supplements with a mixture of both ingredients for therapeutic use and found no significant therapeutic effect, the new study used pharmaceutical-grade glucosamine as the study drug and found not only a weak therapeutic effect of chondroitin sulfate, but also a stronger effect of glucosamine sulfate than glucosamine hydrochloride. Of course, these results remain to be further observed and confirmed by additional clinical studies, and the complexity of OA and the diversity of glycosaminoglycans dictate that this is a long and costly process to explore.