Fracture healing is a unique multifaceted process requiring the presence of cells, molecular mediators, and angiogenic factors. The state of inflammation dominates the initial phase, but the ideal magnitude and duration of the process for an optimal outcome remains obscure. Biological response modifiers, such as platelet-rich plasma (PRP) preparations, have been used to reconstitute the desirable early inflammatory state, but the results obtained remain inconclusive. Ongoing research to characterize and quantify the inflammatory response after bone fracture is essential in order to better understand the molecular insights of this localized reaction and to expand our armamentarium in the management of patients with an impaired fracture healing response. Non-steroidal anti-inflammatory drugs frequently administered for analgesia after trauma procedures continue to be a cause of concern for a successful bone repair response.

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