Effect of a transpositional muscle flap on VEGF mRNA expression in a canine fracture model.
The effect of sepsis on neovascularization in fractures that follows open fractures is important to the understanding of bone and soft-tissue healing. An animal model was designed that mimics the open fracture and the clinical repair of the human, high-energy open fracture. Vascular endothelial growth factor (VEGF) mRNA levels in canine bone samples were determined in samples from days 0 and 7. Canine right tibiae were fractured with a penetrating, captive-bolt device and then repaired in a standard clinical fashion using an interlocking intramedullary nail. Animals were subject to one of the following experimental protocols: tibial fracture (group I, n = 3); tibial fracture and Staphylococcus aureus inoculation at the fracture site (group II, n = 3); and tibial fracture and S. aureus inoculation with a rotational gastrocnemius muscle flap (group III, n = 3). Bone samples were harvested on days 0 and 7 and prepared for reverse transcriptase polymerase chain reaction assay. Primers for VEGF were commercially prepared and assay products were sequenced. The assay products were associated with Genebank VEGF mRNA sequences. VEGF mRNA levels increased significantly in the fracture-alone group from day 0 to day 7 (n = 3, p < 0.05). In the fracture and S. aureus group (group I), VEGF mRNA expression decreased 79 percent (p < 0.05). In animals with fractures inoculated with S. aureus and a transpositional muscle flap (group III), VEGF mRNA expression was increased 38 percent from day 0 to day 7 (p < 0.05) and was similar to the increase observed in the fracture-alone group. These results demonstrate that S. aureus decreased the normal increase of VEGF mRNA expression during bone wound healing. Use of the transpositional muscle flap in the presence of S. aureus increased VEGF mRNA expression over time to the expression pattern observed in the fracture-alone group. This experimental model demonstrates that specific biological signals and cellular pathways are influenced by bacterial infection and type of surgical closure.
Khodaparast
Omeed
O
Department of Plastic Surgery, University of Texas Southwestern Medical Center, Dallas 75390, USA.
Coberly
Dana M
DM
Mathey
Jonathon
J
Rohrich
Rod J
RJ
Levin
L Scott
LS
Brown
Spencer A
SA
D000818:Animals; D001842:Bone and Bones / Q000378:metabolism*; D004285:Dogs; D016228:Endothelial Growth Factors / Q000235:genetics / Q000378:metabolism*; D005594:Fracture Fixation, Intramedullary; D017102:Fracture Healing / Q000502:physiology; D005597:Fractures, Open / Q000378:metabolism* / Q000601:surgery; D015870:Gene Expression; D006614:Hindlimb; D036341:Intercellular Signaling Peptides and Proteins / Q000235:genetics / Q000378:metabolism*; D008222:Lymphokines / Q000235:genetics / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013203:Staphylococcal Infections / Q000378:metabolism; D013524:Surgical Flaps; D013978:Tibial Fractures / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D014946:Wound Infection / Q000378:metabolism
D016228:Endothelial Growth Factors; D036341:Intercellular Signaling Peptides and Proteins; D008222:Lymphokines; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors