NSAIDs effect on bone healing

Abstract

The extensive use of non-steroidal anti-inflammatory drugs (NSAIDs) for the treatment of severe pain associated with bone fractures raises concerns regarding their impact on fracture healing. While NSAIDs are favored for their anti-inflammatory properties, long-term administration has been associated with adverse effects on fracture healing. Despite the recognized risks, conflicting information exists regarding the effects of NSAIDs on fracture healing. Fracture healing is a complex process involving mechanisms of repair, including direct and indirect bone healing pathways. The inflammatory phase plays a crucial role in initiating the healing, with immune cells secreting cytokines and growth factors essential for healing. Prostaglandins, synthesized by COX enzymes, are key mediators, exerting stimulatory effects on bone formation and resorption. However, NSAIDs inhibit prostaglandin synthesis by blocking COX activity, disrupting the fracture-healing process. NSAIDs also have an inhibitory effect on the differentiation of chondrocytes into mature hypertrophied chondrocytes, crucial for endochondral ossification. Collagen X, expressed by hypertrophied chondrocytes, serves as a vital marker of fracture healing and has been implicated in the successful union of fractures. A comprehensive understanding of the interplay between NSAIDs, prostaglandins, and fracture healing mechanisms is essential for optimizing treatment strategies and minimizing adverse outcomes in patients with bone fractures.