NSAIDs impair fracture healing by disrupting neutrophil-mediated repair
Neutrophils are among the first immune cells recruited to fractures, yet their contribution to bone repair remains poorly understood. Using live imaging and neutrophil perturbation in adult zebrafish, we show that neutrophils establish the early fracture microenvironment. Neutrophils rapidly accumulated at fractures, underwent NETosis, and exhibited transcriptional programmes associated with…
A recent study has revealed that non-steroidal anti-inflammatory drugs (NSAIDs) can severely impact fracture healing by interfering with neutrophil-mediated repair processes. Neutrophils, immune cells that are among the first to reach fractures, play a crucial role in establishing the initial fracture microenvironment. In adult zebrafish, researchers observed that neutrophils rapidly accumulate at fracture sites, undergo a process called NETosis, and exhibit transcriptional programs associated with matrix remodeling.
The study found that compromising neutrophil recruitment through the use of ibuprofen treatment or other perturbations significantly increased fracture non-union, delayed osteoblast differentiation, impaired mineralisation, and altered callus architecture. The researchers discovered that neutrophils actively interacted with extracellular matrix proteins, such as laminin, fibronectin, and collagen I, through uptake, trafficking, and secretion-associated pathways.
These findings provide a mechanistic explanation for how early NSAID exposure can lead to impaired skeletal regeneration, highlighting the essential role neutrophils play in the early stages of fracture repair.
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