Acute Soft Tissue Injuries And Nsaids Biology Essay

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Acute soft tissue injuries in athletes are routinely treated with nonsteroidal anti-inflammatory drugs (NSAIDs), yet their efficacy is unproven in the scientific literature. While NSAIDs are often prescribed for their anti-inflammatory, analgesic, and antipyretic effects after acute injury, there is little evidence to support the claim that NSAIDs speed up the return of injured athletes to competition. Additionally, separating the anti-inflammatory effects from the analgesic effects is not easy. Recent evidence from studies using animal models suggests that the short-term benefits of NSAIDs may be outweighed by long-term compromise of the structure and function of the injured tissue. NSAIDs are a family of drugs that have achieved widespread use in sports medicine in both prescription and over-the-counter (OTC) forms.

Soft tissue injuries and role of NSAIDs.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are used to speed up the return of injured athletes to compete early after injury. Evidence demonstrates that although, NSAIDs accelerates recovery after acute soft tissue injuries, long-term healing is compromised. An attempt is made to assess the healing associated with acute soft tissue injury and effects of NSAIDs on inflammation and According to Dalton et al (2006), NSAIDs are often administered after acute soft tissue injury in an effort to minimize pain and inflammation and thus hasten an injured athlete's return to competition. However, recent evidence suggests that the short-term benefits of NSAID therapy may adversely affect the long-term healing of injured soft tissues.

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We will discuss the classification of NSAIDs, the acute inflammatory process, the mechanisms of action of NSAIDs, and the positive and negative effects of NSAIDs on soft tissue healing. Majority of sports injuries, present muscle pain as a primary symptom. Depending upon the onset of the injury, injury to the soft tissues of the body such as muscles, tendons, ligaments, and pain are typically classified as either acute or chronic injuries. Most soft-tissue injuries are painful because of the swelling and inflammation that occurs after an injury. Pain relief is often the main reason that people turn to over-the-counter (OTC) anti-inflammatory medications that work by reducing the inflammation that occurs because of the injury. According to Smith et al (2008), contusions and muscle strains are very common in sport and responsible for substantial time loss. The healing process is sluggish, and it is common to be reinjured. In general, NSAIDs are administered orally and are broken down in the gastrointestinal system. The kidneys or the liver metabolizes the drug after circulation, depending on the individual properties of the NSAID.

Can treatment accelerate muscle healing? There have been many attempts to speed muscle healing. Traditionally, ice, rest, anti-inflammatory medications, and rehabilitation have been the mainstays of treatment. The use of non-steroidal anti-inflammatory drugs (NSAIDs) has been questioned. NSAIDs increase the expression of TGF β1 and decrease prostaglandin E2, which has a key role in the proliferation and differentiation of satellite cells. Recent studies have shown that NSAIDs likely tip the delicate balance of regeneration versus fibrosis toward fibrosis or scarring. The platelet-rich plasma (PRP) is used to improve healing has been highlighted lately. (Schnabel et al). The damaged tissues are directly injected with PRP extract, the aim being to improve the wound healing through growth factors delivery and theoretical optimizing the healing environment. Because it is an autologous sample, there is a negligible risk of allergy or the introduction of exogenous infection (Anitua et al).

According to Chan et al (2005), muscle strain is the most common complaint to be treated by physicians and account for the majority of all sport-related injuries. Except for complete ruptures of muscles, displaced avulsions, and recalcitrant symptoms from myositis ossificans, almost all muscle injuries are uniformly treated with nonoperative therapy. Standard nonoperative therapy for acute muscle injuries usually involves rest, ice, compression, and elevation (RICE). Beyond the principle of short-term rest and ice, there is no clear consensus on treatment of muscle injuries.

Aspirin (acetylsalicylic acid), originally derived from the bark of the willow tree, was the first NSAID, and has been used in various forms to treat human ailments for centuries. Originally marketed in the United States by the Bayer Corpo­ration in the late 1800s, aspirin was heralded as a panacea.' However, the primary physiologic mechanism of action of aspirin was not discovered until 1971, when it was reported that prostaglandin production was inhibited by aspirin. Numer­ous side effects associated with ingestion of aspirin led to the development of other chemically similar drugs, now known as NSAIDs that have clinical properties similar to aspirin but fewer adverse side effects. NSAIDs are mainly administered for their analgesic, antipyretic, anti-inflammatory, and antico­agulant effects. NSAIDs may also be delivered via topical gels, phonophoresis, iontophoresis, or intramuscular injection, although the efficacy of these routes of administration is not as well studied as the oral route of administration. Acetaminophen is a drug that is not an NSAID but deserves special mention. Acetaminophen (commonly marketed as Ty­lenol) renders analgesic and antipyretic effects but not anti-inflammatory or anticoagulant effects. It appears to operate independently of the cyclooxygenase pathway by which NSAlDs work. Acetaminophen is commonly administered for its analgesic effects after acute injury. Inhibition of COX-3 in the brain and the spinal cord may be mechanism of action of acetaminophen (SOURCE: Proceedings of the National Academy of Sciences 002;10.1073/pnas.162468699.)

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NSAlDs are classified by half-life, the time necessary to eliminate half of the ingested amount of drug from the body. The half-lives of NSAlDs vary from less than an hour to more than 24 hours. Peak plasma concentra­tions and peak clinical effects are seen after 3 to 5 half-lives when the patient is consistently taking the medication. Drugs with short half-lives normally are taken three to six times per day to achieve anti-inflammatory effects. Peak plasma concentrations and peak clinical effects can be seen sooner with short half-life NSAlDs. In contrast, drugs with longer half-lives are taken only once or twice per day and are slower in eliciting the desired clinical effects. However, patients who are prescribed drugs with longer half-lives tend to be more compliant in taking their medication. It is interesting to note that all but one of the OTC NSAIDs (naproxen sodium) is in the short half-life category.

Anti-inflammatory Drugs (NSAIDs) - Studies show no beneficial effect of NSAIDS in patients with tendon conditions (not surprising, as it is not an inflammatory condition). In fact, the 'pain killing' effect of NSAIDs may permit patients to ignore early symptoms thus allowing further tendon damage. In a recent study in the American Journal of Sports Medicine, it was found that the use of NSAID drugs may increase levels of leukotriene B4 thus potentially contributing to the development of tendonosis (Chan et al).

The inflammatory process, after acute injury, inflammation is the body's method of limiting the amount of tissue damage and protecting against further insult. Injury to soft tissue results in a nonspecific physiologic response that activates a series of proinflarnmatory events. Immediate vasoconstriction limits local hemorrhage and is followed by subsequent vasodilation and an increase in vascular permeability near the site of injury. Platelets quickly adhere to one another at the site of capillary damage to provide a mechanical plug to prevent further bleeding. Simultaneously, the clotting cascade is activated and results in the formation of fibrin and fibronectin; which form cross-links with collagen to reinforce the temporary plug and stop hemorrhage.

The zone of primary injury is defined by the extent of the initial hematoma. Prostaglandins, especially PGE2, play an integral role in the inflammatory process and may be produced by all cells in the human body except erythrocytes. They signal a plethora of proinflammatory events including induction of vasodilation, increased vascular permeability, increased local blood flow, and increased body temperature via actions on the hypothal­amus. Prostaglandins also serve to increase the sensation of pain by decreasing the sensitivity of nociceptors and poten­tiating the effects of bradykinin and histamine. More cell damage can occur from the edema and tissue hypoxia that are the result of the acute vascular inflammatory response. This subsequent tissue damage is often referred to as the "secondary zone of injury," in contrast to the initial damage caused by the actual mechanism of injury. The retarded healing of injured soft tissues after the administration of NSAIDs may be due to limiting development of the secondary zone of injury. If neutrophil and phagocyte migration are limited after injury, fibroblast and granulocyte activity may also be diminished in the days after injury. This may result in impaired scar tissue formation, thus leading to a subsequent decreased tensile strength of the mature scar tissue.

The primary mechanism of action of NSAIDs has been identified as inhibition of prostaglandin synthesis by blocking the cyclooxygenase pathway of the arachidonic acid cascade. NSAIDs also have anti-inflammatory effects unrelated to arachidonic acid. NSAIDs are known to inhibit neutrophil aggregation and migration to sites of inflammation. Other alterations of neutrophil function are also affected, including the slowing of lysosomal enzyme release, decreased oxidative phosphorylation, and decreased production of substances that are chemotactic for other leukocytes. Oxygen free-radical production by neutrophils and phagocytes is also decreased in the presence of NSAIDs. The effects of NSAIDs on human muscle inflammation have been studied using the induction of delayed-onset muscle soreness (DOMS) after repetitive eccentric contractions as a model of muscle injury in humans. Bouts of eccentric exercise generate small amounts of muscle fiber damage and result in significant pain in the days after eccentric exercise.

According to Kearney et al, combination of traditional non-steroidal anti-inflammatory drugs and some selective cyclo-oxygenase-2 inhibitors increase the risk of atherothrombosis; selective COX 2 inhibitors are associated with a moderate increase in the risk of vascular events, as are high dose regimens of ibuprofen and diclofenac, but high dose naproxen is not associated with such an excess. Clinical studies of the efficacy of NSAIDs on acute soft tissue injuries in the sports medicine setting have been highly criticized in previous literature reviews. It is difficult to separate the anti-inflammatory and analgesic effects of NSAIDs in the treatment of acute injuries. Analgesia may allow increased range of motion earlier in the rehabilitation process and thus hasten the recovery process, regardless of the anti-inflammatory effects. Further research is needed to examine the effects of analgesics without anti-inflammatory effects, such as acetaminophen, in the treatment of acute athletic injuries.

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Researchers utilizing animal models to study the histologic effects of NSAIDs on muscle and ligament injury have shown that NSAIDs yield short-term improvements in muscle healing and function, but either no long-term benefits or potentially deleterious long-term effects on muscle structure and function. As mentioned previously, aspirin was the original NSAID, but it was found to cause numerous adverse systemic effects in addition to its target analgesic, antipyretic, and anti-inflammatory effects. The other members of the NSAID class, while producing fewer adverse effects than aspirin, are also not free of side effects.

In conclusion, Because of the numerous adverse effects associated with NSAIDs, athletic trainers must be aware of the potential benefits and liabilities of NSAID use by injured athletes. Further research must address the effectiveness of NSAIDs in clinical trials involving injured athletes. Current research demonstrates that NSAIDs may be beneficial in hastening the return to competition by injured athletes but also that NSAIDs should be only one part of the total treatment plan. NSAIDs do not take the place of therapeutic modalities and exercise and must be considered as an adjunct to rehabilitation rather than the most direct route to recovery.