Abstract
Simple SummaryPostfracture treatment with nonsteroidal anti-inflammatory drugs might result in delayed healing. This study was aimed to evaluate and compare the effects of flunixin meglumine (FM) and ketoprofen on bone fracture healing in rabbits. A simple unilateral diaphyseal fracture was made and followed by fixation by K-wire. Healing was evaluated with radiography, histopathology, and immunohistochemistry. Interestingly, the results revealed that FM enhanced bone fracture healing combined with the activation of early collagen deposition, marked angiogenesis, and enhanced vascular endothelial growth factor. However, ketoprofen delayed bone fracture healing. These findings provide novel baseline information about the potential beneficial effects of FM on bone fracture healing cases.Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most commonly used postoperative analgesics, antipyretics, and anti-inflammatories, and they help prevent blood clotting. However, most NSAIDs delay bone healing. This study was aimed to investigate bone healing in a rabbit animal model by assessing the ability of flunixin meglumine (FM) and ketoprofen to induce fracture healing by examining histology, radiological changes, and vascular endothelial growth factor (VEGF) immunostaining during bone healing. For this purpose, 24 New Zealand rabbits were assigned to three groups: the control group, the FM group, and the ketoprofen group. Our results revealed that there were no intraoperative complications, and all surviving rabbits achieved full-weight bearing. Significant periosteal reaction and callus formation were confirmed at 2 postoperative weeks. Interestingly, FM enhanced callus formation, bone union, and remodeling in the FM group compared to the control and ketoprofen groups. FM enhanced bone healing through early collagen deposition and marked angiogenesis process activation by increasing the expression of VEGF. Our findings demonstrated, for the first time, the potential imperative action of FM in the bone healing process rather than other NSAIDs in animals.
Highlights
The bone healing process involves multi-sequential events associated with numerous cellular functions that promote mineralization of the fracture site followed by remodeling to return the affected bone to its original structure [1]
(1 specimen/animal) time points radiographic findings of the control group at postoperative weeks showed mild soft treatment, the specimens were subjected to the histopathological examination of osteogenecallus formation, with the noncomplete bridging bone union increasing over time
The first this study has revealed the potential of flunixin meglumine (FM), on bone fracture healing by enhancing angiogenesis at the fracture of the oneNSAIDs, of the Nonsteroidal anti-inflammatory drugs (NSAIDs), FM, on bone fracture healing by enhancing angiogenesis at the site, as reflected
Summary
The bone healing process involves multi-sequential events associated with numerous cellular functions that promote mineralization of the fracture site followed by remodeling to return the affected bone to its original structure [1]. Anti-inflammatory drugs have been extensively used as a painkiller to ensure fracture site immobility. Numerous studies have demonstrated that steroidal and nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit healing in soft and hard tissues [3,4]. Various reports have suggested that NSAIDs interfere with bone healing, though others have contradicted these findings [7]. Celecoxib [8,9] and aspirin [10] inhibit bone healing [11,12], while ibuprofen [13] and parecoxib [14] do not affect bone healing
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