Acute muscle injuries go through a predictable cycle of healing and repair. Exercise-induced muscle injury first causes fiber disruption and local microhemorrhage, followed by extravasation of inflammatory cells and a phagocytic phase to remove injured tissue, and finally a regenerative phase of muscle fiber healing occurs (Armstrong et al., 1991). Limiting overall inflammation decreases pain and minimizes secondary tissue injury caused by hypoxia and inflammatory mediators. However, some amount of inflammation is required in the healing process to remove necrotic muscle fibers and allow scar tissue to bridge the defect (Almekinders and Gilbert, 1986), but how far to limit this inflammation through pharmacotherapy remains uncertain.

In contrast to acute muscle injuries, the pathologic findings in most tendon injuries are consistent with tendinosis, a degenerative condition of the tendon, and not a tendinitis involving inflammation, as was formerly believed. Healthy tendon contains parallel bundles of tightly packed collagen fibers, with little extracellular matrix (ground substance) and no fibroblasts or myofibroblasts. In contrast, symptomatic tendons contain disorganized collagen fibers, increased mucoid ground substance, prominent capillary proliferation, and increased numbers of fibroblasts and myofibroblasts (Khan et al., 1999). Histopathologic examination is notably devoid of inflammatory cells. Animal models have also suggested that inflammatory cells are absent by 1 week after induced overuse injury (Zamora and Marini, 1988). These findings are present in the most common tendon injuries, including the patella, Achilles, rotator cuff, and extensor carpi radialis brevis tendons, and have important implications in the treatment of tendon disorders (Khan et al., 1999). Use of the term tendinopathy, rather than tendinitis, is recommended to describe a painful tendon condition.

The generation of pain in chronic tendon injuries appears to involve more than just inflammation. A biochemical hypothesis to explain tendon pain states that biochemical agents are leaked from a degenerated tendon and irritate nociceptors (pain receptors) on adjacent structures (Khan and Cook, 2000). In patellar tendinopathy, higher levels of glycosaminoglycans have been found in the infrapatellar fat pad (Khan et al., 1996), and in patients with partial rotator cuff tears higher levels of substance P were found in the adjacent subacromial bursa and were significantly associated with pain (Gotoh et al., 1998).

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