Specifically, NSAIDs are believed to wipe out the entire inflammatory mediated proliferative phase of healing associated with WBC actions (days 0–4). Various studies have also shown that NSAIDs can delay muscle regeneration and may reduce ligament, tendon, and cartilage healing. By locking COX-1, which also normally acts to protect the gastrointestinal mucosa, nonselective NSAIDs and aspirin can cause significant gastric tissue damage. Nonselective NSAIDs’ major side effects include significant gastrointestinal upset, gastritis, ulceration, hemorrhage, and even death. The major push to develop the selective COX-2 inhibitors has been the recognition of significant complications associated with the nonselective COX-1 and COX-2 NSAIDs. NSAIDs have evolved from blocking both COX-1 and COX-2 to selectively only blocking COX-2 in order to inhibit the inflammatory response and reduce the production of inflammatory prostaglandins and thromboxanes. Both the enzymes act similarly, but selective inhibition (as accomplished by selective COX-2 inhibiting NSAIDs) can make a difference in terms of side effects.Īcetylsalicylic acid works by irreversibly disabling the COX enzymes to block the cascade. There are two types of COX enzymes, COX-1 and COX-2. Membrane-based arachidonic acid is transformed into prostaglandins and thromboxanes partly through the enzymatic action of cyclooxygenase (COX). A major component of the inflammatory pathway is called the arachidonic acid pathway because arachidonic acid is immediately released from traumatized cellular membranes. The inflammatory pathway is a complex biochemical pathway which, once stimulated by injury, leads to the production of these and other inflammatory mediators whose initial effect is pain and tissue destruction, followed by healing and recovery. Thromboxanes, which are also hormone activators, can regulate blood vessel tone, platelet aggregation, and clot formation to increase the inflammatory response. Prostaglandins act as short-lived localized hormones that can be released by any cell of the body during tissue, chemical, or traumatic injury, and can induce fever, inflammation, and pain, once they are present in the intercellular space. Increased concentrations of TNF-α are believed to cause the cardinal signs of inflammation to occur. NSAID mechanisms are primarily through interaction with proinflammatory cytokines interleukin (IL)-1a, IL-1b, IL-6 and tumor necrosis factor (TNF-α). The use of non-steroidal anti-inflammatory drug (NSAID) medication is still the mainstay of most classically taught clinicians for joint and spine related inflammatory pain, despite their commonly known side effects. With the elucidation of the role of inflammatory cytokines, there is now a clear understanding of the pathways by which many anti-inflammatory drugs can alleviate inflammation and relieve pain. In most cases, the genesis of pain is inflammatory, regardless of the etiology. Typically, patients will not require immediate surgical intervention, and therefore require treatments to reduce pain and enhance quality of life activities. Abnormalities of the joints of the spine, associated muscles, tendons, ligaments and bone structural abnormalities can all result in pain and need for neurosurgical consultations. Pain, heat, redness, and swelling (dolor, calor, rubor, tumor) are the classic manifestations of the inflammatory process.
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