RESUMEN
FGF2 is a potent stimulator of vascular growth; however, even with a deficiency of FGF2 (Fgf2-/-), developmental vessel growth or ischaemia-induced revascularization still transpires. It remains to be elucidated as to what function, if any, FGF2 has during ischaemic injury. Wildtype (WT) or Fgf2-/- mice were subjected to hindlimb ischaemia for up to 42 days. Limb function, vascular growth, inflammatory- and angiogenesis-related proteins, and inflammatory cell infiltration were assessed in sham and ischaemic limbs at various timepoints. Recovery of ischaemic limb function was delayed in Fgf2-/- mice. Yet, vascular growth response to ischaemia was similar between WT and Fgf2-/- hindlimbs. Several angiogenesis- and inflammatory-related proteins (MCP-1, CXCL16, MMPs and PAI-1) were increased in Fgf2-/- ischaemic muscle. Neutrophil or monocyte recruitment/infiltration was elevated in Fgf2-/- ischaemic muscle. In summary, our study indicates that loss of FGF2 induces a pro-inflammatory microenvironment in skeletal muscle which exacerbates ischaemic injury and delays functional limb use.
Asunto(s)
Factor 2 de Crecimiento de Fibroblastos/metabolismo , Músculo Esquelético/metabolismo , Neovascularización Fisiológica , Daño por Reperfusión/metabolismo , Animales , Quimiocina CCL2/genética , Quimiocina CCL2/metabolismo , Quimiocina CXCL16/genética , Quimiocina CXCL16/metabolismo , Factor 2 de Crecimiento de Fibroblastos/genética , Miembro Posterior/irrigación sanguínea , Metaloproteinasas de la Matriz/genética , Metaloproteinasas de la Matriz/metabolismo , Ratones , Músculo Esquelético/irrigación sanguínea , Músculo Esquelético/fisiología , Inhibidor 1 de Activador Plasminogénico/genética , Inhibidor 1 de Activador Plasminogénico/metabolismo , RegeneraciónRESUMEN
The goal of the present work was to perform a systematic review of the literature of the past 10 years regarding dynamic and static fixation of the distal tibiofibular syndesmosis to determine any clinical differences between the 2 procedures. A literature search of the PubMed MEDLINE database was conducted to identify relevant studies related to distal tibiofibular syndesmosis. Studies before January 1, 2007, were excluded to limit the project to the recent literature. Clinical outcomes, device removal rates, time to weightbearing after the initial procedure, and the cost effectiveness of each device were explored. In these 26 studies, 350 patients were treated using a dynamic technique and 845 were treated using a static technique. The weighted American Orthopedic Foot and Ankle Score was 91.70 (standard error [SE] 1.87) for dynamic fixation patients and the weighted average was 86.48 (SE 2.17) for static fixation patients (pâ¯=â¯.068). A secondary procedure to remove the fixation device was performed in 7.7% of dynamic fixation patients and in 39.4% of static fixation patients when studies with 100% device removal were excluded (p < .0001). The mean time to weightbearing was 5.96 (SE 0.72) weeks for patients who underwent dynamic fixation and 10.45 (SE 0.99) weeks for those who had static fixation (pâ¯=â¯.0002). The cost for dynamic fixation was found to be less than that for static fixation when secondary procedures for device removal were considered. Based on similar clinical functional scores, lower secondary procedure rates, faster time to full weightbearing, and lower costs to patients, dynamic fixation of the distal tibiofibular syndesmosis may be a superior option compared with static fixation.