What is the mechanism of action of NSAIDs for the treatment of supraspinatus tendonitis?

Updated: Dec 03, 2018
  • Author: Thomas M DeBerardino, MD; Chief Editor: Sherwin SW Ho, MD  more...
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NSAIDs mechanism of action

The major mechanism of action of NSAIDs is inhibition of the synthesis of prostaglandin (PG), specifically PGE2, via blocking cyclooxygenase (COX), which is the enzyme that converts arachidonic acid into PG. PGs lower the threshold to noxious stimuli by sensitizing the nociceptors to the actions of other noxious endogenous substances (eg, bradykinin, histamine, substance P, serotonin). In soft tissue, PGE2 causes pain and inflammation. In the GI tract, it is cytoprotective and increases the secretion of mucus and bicarbonates and decreases the secretion of gastric acids and digestive enzymes. In the renal system, PGE2 enhances renal salt and water excretion by acting as a vasodilator of small arterial blood vessels.

The COX pathway is subdivided into COX-1, which is responsible for PGE2 production in the GI tract and kidneys, and COX-2, which is responsible for inflammatory PG synthesis during soft tissue injury. NSAIDs serve as competitive inhibitors of COX activity and either selectively inhibit the COX-2 enzymes or nonselectively inhibit both the COX-1 and the COX-2 enzymes, making the nonselective NSAIDs a higher risk for potential ulcerogenic and other adverse effects.

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