Academic journal article International Journal of Child and Adolescent Health

Adolescence, Musculoskeletal Disorders and Sports Injuries

Academic journal article International Journal of Child and Adolescent Health

Adolescence, Musculoskeletal Disorders and Sports Injuries

Article excerpt

Introduction

Musculoskeletal injuries account for most sports-related injuries (1). Overuse musculoskeletal injuries account for more than half of all sport-related injuries in adolescents and young adults. Overuse injuries can result in chronic or intermittent symptoms depending on the athlete's level of activity. Acute muscle injuries (i.e., strains, contusions, and lacerations) can lead to significant structural or functional damage to the muscle (1-11). Delayed-onset muscle soreness (DOMS) (exercise-induced muscle damage [EIMD]), typically associated with new or unaccustomed exercise, often results from intense eccentric muscle activity and manifests with pain, discomfort, and decreased performance 24 to 48 hours after exercise (1,4).

Nonpharmacological approaches are often considered as first-line treatment for musculoskeletal injuries and may include relative rest, ice, compression, and elevation (3). Moderate to severe injuries to the athlete may result in several weeks of an inability to train or compete. Even after resuming the physical activity or sport, the athlete may continue to experience difficulties with muscle weakness and decreased flexibility (1). As a result, treatment is often sought to alleviate pain, restore function, and allow the athlete to resume activities more quickly. Treatment options include analgesics such as nonsteroidal anti-inflammatory drugs (NSAIDs), acetaminophen, and topical over-the-counter (OTC) preparations. These classes of drugs are reviewed in this chapter, including their mechanisms of action, side effects, and efficacy in treating pain and inflammation associated with acute and overuse musculoskeletal injuries.

Mechanism of action

Arachidonic acid is released from cellular membranes as a result of tissue injury. Arachidonic acid is broken down by cyclooxygenase (COX) to produce prostaglandins and thromboxane A2, and by lipoxygenase (LOX) enzymes to produce leukotrienes. Prostaglandins are localized hormones that, once released within the intracellular space, can produce fever, inflammation, and pain (12). Thromboxanes are released in response to tissue injury and are responsible for producing platelet aggregation as well as clot formation, and for regulation of vascular tone (12). Pain relief and decreased inflammation occur from the blockade of COX enzymes, thereby inhibiting prostaglandin E2 and prostacyclin (PGI2) formation (12, 13).

Two forms of COX enzymes are cyclooxygenase- 1 (COX-1) and cyclooxygenase-2 (COX-2). COX-1 is expressed in most normal tissues and cells, and is the predominant form within gastric epithelial cells (12,14). Prostaglandin production within the gastrointestinal tract protects the gastrointestinal mucosa from gastric acidity. COX-2 is expressed when tissue damage occurs, and its release is induced by cytokines and inflammatory mediators during inflammation (12, 14). NSAIDs are a heterogeneous class of medications that are chemically unrelated but known to have similar therapeutic effects, including antipyretic, analgesic, and anti-inflammatory activity. Their primary therapeutic effect is due to inhibition of prostaglandin synthesis by inhibiting COX-2 activity, and a correlation exists between COX-2 inhibition and anti-inflammatory activity (15). Bradykinin and cytokines (ie, tumor necrosis factor-a [TNF-a] and interleukin-1 [IL-1]) are thought to be responsible for inducing pain with inflammation and releasing prostaglandins that enhance pain sensitivity (16). Other mediators, such as neuropeptides (ie, substance P) are also involved in inducing pain. The gastrointestinal adverse effects of NSAIDs are predominantly, but not exclusively, due to inhibition of COX-1 enzyme (Fig. 2). NSAIDs are considered competitive, reversible inhibitors of COX enzymes (unlike aspirin, which is considered an irreversible inhibitor of COX enzymes) and do not affect the LOX pathway (17).

Salicylated NSAIDs

Derivatives of salicylic acid include aspirin (acetylsalicylic acid), diflunisal (difluorophenyl derivative), salsalate, magnesium salicylate, and choline magnesium salicylate (tables 1 and 2). …

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