Abstract
This article identifies the underlying molecular events responsible for fracture nonunions in a subset of fracture patients. Expression profiling of fracture callus tissue from both uneventful fracture repair and nonunion outcomes showed a decrease of COX-2 expression and an inability to mount an immune response in nonunion fractures. Validation in vitro with Saos-2 osteoprogenitor cell lines showed a decrease in osteogenesis potential after the cells were treated with celecoxib, a COX-2 specific inhibitor and anti-inflammatory agent. This article recapitulates that an initial immune response is crucial to fracture healing and suggests limited usage of COX-2 inhibitors in patients with healing fractures.
MeSH terms
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Adult
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Aged
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Aged, 80 and over
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Bone Morphogenetic Protein 2
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Bone Morphogenetic Proteins / pharmacology
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Bony Callus / cytology
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Bony Callus / metabolism
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Celecoxib
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Cell Line
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Cyclooxygenase 2 / drug effects
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Cyclooxygenase 2 / metabolism*
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Cyclooxygenase Inhibitors / pharmacology*
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Female
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Fracture Healing / drug effects*
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Fractures, Ununited / drug therapy
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Fractures, Ununited / metabolism*
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Humans
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Male
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Membrane Proteins / drug effects
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Membrane Proteins / metabolism*
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Middle Aged
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Osteogenesis / drug effects
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Pyrazoles / pharmacology*
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Recombinant Proteins / pharmacology
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Sulfonamides / pharmacology*
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Transforming Growth Factor beta / pharmacology
Substances
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Bone Morphogenetic Protein 2
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Bone Morphogenetic Proteins
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Cyclooxygenase Inhibitors
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Membrane Proteins
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Pyrazoles
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Recombinant Proteins
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Sulfonamides
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Transforming Growth Factor beta
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recombinant human bone morphogenetic protein-2
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Cyclooxygenase 2
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PTGS2 protein, human
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Celecoxib