Recently a patient told me that his knee arthritis of many years had returned with severe pain and asked me what he should do. When he asked me, I wondered how the pain could still be so bad after taking painkillers. It turned out that he was afraid of always take painkillers have harm to the body, eat a few days will not dare to eat. So eat painkillers in the end how much harm to the body? Specifically, as an orthopedic surgeon, I generally recommend that these patients take selective COX-2 inhibiting non-steroidal anti-inflammatory analgesics, so what exactly is this drug? Is there anything to be aware of when using them? First of all, how does pain actually come about? The production of pain can be imaginatively understood as a firefighting process, when there is an injury somewhere in the human body is equivalent to a fire, the human body will release local inflammatory mediators act as firefighters, firefighters on the one hand to control the fire, on the one hand, the fire will be reported to the fire level by level, in the passage of the spinal cord, the spinal cord will be the firefighters of the report and the inhibitory signals of the cerebral command comparison, only in the peripheral nociceptive signals are too strong, exceeding the threshold of centralized threshold of the downward inhibitory system, then nociception occurs. Thus, there are two critical points in the regulation of pain: inflammatory mediators in the periphery and control systems within the spinal cord. Accordingly, pain medications are divided into two categories, those that act on peripheral inflammatory mediators and those that act on nociceptive centers. For pain caused by inflammation and tissue damage such as degenerative osteoarthritis, rheumatoid arthritis, fasciitis, chronic strain injuries, muscle sprains, etc., orthopedic surgeons most commonly choose the first type of painkillers, that is, painkillers that act on peripheral inflammatory mediators. These painkillers that act on peripheral inflammatory mediators, also known as nonsteroidal anti-inflammatory drugs (NSAIDs), are commonly used in the treatment of acute and chronic pain, and the anti-inflammatory, analgesic, and antipyretic effects of these drugs are achieved through the inhibition of the enzyme cyclooxygenase (COX). The human body contains two types of COX, COX-1 and COX-2. COX-1 is mainly found in the stomach, kidneys and platelets, and has the function of regulating peripheral vascular resistance, maintaining renal blood flow, protecting gastric mucosa and regulating platelet aggregation.COX-2 is one of the key enzymes that cause inflammatory reactions, which can be promoted to lead to tissue damage. Traditional non-selective NSAIDs painkillers gastrointestinal damage is quite common, such as ibuprofen, diclofenac, etc., the long-term use of which can easily lead to adverse symptoms of the digestive tract, ulcers, bleeding and other complications, mainly as a result of inhibition of COX-1, and selective COX-2 inhibitors it can selectively inhibit COX-2 activity, with less impact on COX-1, and fewer and milder gastrointestinal adverse reactions to Selective COX-2 inhibitor celecoxib, for example, the results of clinical trials found an annual ulcer complication rate of 0.2%, compared with an annual ulcer rate of 1.7% for non-selective NSAIDs. Admittedly, there is no consensus on the difference in cardiovascular disease risk between the two NSAIDs painkillers, and in addition, there is a potential risk of renal damage if applied in large quantities over a long period of time, both with conventional NSAIDs and COX-2 inhibitors. However, overall the safety of selective COX-2 inhibiting NSAIDs is still superior to that of traditional NSAIDs, and as long as the indications are mastered, the safety of NSAIDs can still be guaranteed.