For many years the prescription of NSAIDs for all kind of sport injuries (soft tissue injuries, tendon injuries and bone fractures) has been a staple of sports medicine. NSAIDs have well established analgesic effects, but also proven side effects, most prominent among them being the risk of gastric ulcer and renal failure (especially in long term administration). And in the case of COX-2 inhibitors, CVS damage. Despite the risk of side effects, the medical community has considered the safety/efficiency ratio satisfying enough to accept the administration of NSAIDs. With recent data however (both on the biological mechanisms of NSAIDs action and in vivo studies regarding their ability to impair healing), such a practice should be seriously scrutinized.

NSAIDs Mechanism of Action

Since the discovery of aspirin in 1899 there has been very detailed research on the mechanism of NSAID action. NSAIDs work by blocking the formation of prostaglandins (PGEs) from arachidonic acid. They do this by inhibiting the enzyme Cyclooxygenase. Although it was previously believed that only one type of the cyclooxygenase enzyme existed, recent research has proved that there are two types of cyclooxygenase enzyme, COX-1and COX-2.

COX-1 is stimulated continuously by normal body physiology. The COX-1 enzyme is constitutive, meaning that its concentration in the body remains stable. It is present in most tissues and converts arachidonic acid into prostaglandins. These prostaglandins in turn stimulate normal body functions, such as stomach mucus production and kidney water excretion, as well as platelet formation. The location of the COX-1 enzyme dictates the function of the prostaglandins it releases. Thus, COX-1 produced prostaglandins in the stomach cause regeneration of the gastric mucus. This is believed to be the primary ulcer-inducing mechanism of NSAIDS, although some scientists believe that aspirin can also have a direct corroding effect on the gastric mucus, especially if it is undiluted. Inhibition of COX-1 also causes a drop in renal water excretion and reduces kidney blood flow, thus inducing renal damage in long term NSAID usage. In contrast to COX-1, the COX-2 enzyme is induced, meaning it is not naturally present in the body, but its expression can be greatly increased by macrophages: the scavenging white blood cells. COX-2’s most important role is in inflammation, where PGEs along with leucotrienes, interleukins and prostacyclins induce the usual symptoms of inflammation, such as increased blood flow to the tissue, increased temperature, redness, swelling, pain and increased concentration of white blood cells.