Though Canadian researchers found evidence contradicting the use of NSAIDs to prevent heart attack, these analgesics are still commonly used to reduce pain and inflammation for athletes and patients with arthritis. The mechanism of action which makes NSAIDs effective pain relievers also inhibits platelet aggregation via the cyclooxygenase-arachidonic acid pathway. This means that PRP prepared while patients are taking NSAIDs will not achieve therapeutic potential because platelet function is impaired.
Without proper aggregation, platelets won’t be able to release growth factors such as platelet derived growth factor, vascular endothelial growth factor and transforming growth factor beta, among others. These tiny bioactive proteins are at the heart of successful PRP therapy. They promote tissue regeneration by direct surrounding cells to increase mitogenesis, chemotaxis and angiogenesis.⁶ As such, patients who abstain from the use of NSAIDs for two weeks prior to PRP preparation will benefit from increased platelet function and growth factor release.