HIGHLIGHTED TOPIC Role of Inflammation in Skeletal Muscle, Connective Tissue, and Exertional Injuries: To Block or Not to Block? NSAID therapy effects on healing of bone, tendon, and the enthesis
نویسندگان
چکیده
Su B, O’Connor JP. NSAID therapy effects on healing of bone, tendon, and the enthesis. J Appl Physiol 115: 892–899, 2013. First published July 18, 2013; doi:10.1152/japplphysiol.00053.2013.—Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for the treatment of skeletal injuries. The ability of NSAIDs to reduce pain and inflammation is well-established. However, the effects of NSAID therapy on healing of skeletal injuries is less defined. NSAIDs inhibit cyclooxygenase activity to reduce synthesis of prostaglandins, which are proinflammatory, lipid-signaling molecules. Inhibition of cyclooxygenase activity can impact many physiological processes. The effects of NSAID therapy on healing of bone, tendon, and the tendon-to-bone junction (enthesis) have been studied in animal and cell culture models, but human studies are few. Use of different NSAIDs with different pharmacological properties, differences in dosing regimens, and differences in study models and outcome measures have complicated comparisons between studies. In this review, we summarize the mechanisms by which bone, tendon, and enthesis healing occurs, and describe the effects of NSAID therapy on each of these processes. Determining the impact of NSAID therapy on healing of skeletal tissues will enable clinicians to appropriately manage the patient’s condition and improve healing outcomes.
منابع مشابه
NSAID therapy effects on healing of bone, tendon, and the enthesis.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used for the treatment of skeletal injuries. The ability of NSAIDs to reduce pain and inflammation is well-established. However, the effects of NSAID therapy on healing of skeletal injuries is less defined. NSAIDs inhibit cyclooxygenase activity to reduce synthesis of prostaglandins, which are proinflammatory, lipid-signaling molecules....
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