RESUMEN
BACKGROUND: Intramedullary nail (IMN) fixation of the fibula in malleolar ankle fractures has been shown to result in less wound complications then plate fixation. Therefore, IMN fibula fixation may also be associated with lower rates of wound complications when used for higher-risk pilon fractures. The purpose of this study was to compare complications of fibula IMN fixation in pilon versus malleolar ankle fractures. METHODS: A retrospective cohort comparison was performed at an urban level one trauma center involving fibula fractures in 47 patients with AO/Orthopaedic Trauma Association (OTA) type 43 fractures and 48 patients with AO/OTA type 44 fractures being treated with fibula IMN fixation. Complications, fibula-specific complications, revision surgeries, and implant removals were reviewed. RESULTS: There was no detectable difference in complications (27% vs. 23%, 95% confidence interval of the odds ratio (CIOR) 0.5 to 3.2), fibular-specific complications (6% vs. 10%, CIOR 0.1 to 3.5), revision surgeries (4% vs. 4%, CIOR 0.1 to 7.5), or symptomatic fibula implant removals (13% vs. 21%, CIOR 0.1 to 1.6) between pilon and ankle fracture groups, respectively. There was one (2%) fibular nonunion and one wound complication (2%) in each of the fracture groups. CONCLUSION: Fibula IMN fixation of pilon versus ankle fractures resulted in a similar number of complications. Comparative studies of fibula IMN and plate fixation are necessary to determine if the benefits of fibula IMN in ankle fractures extends to pilon fractures. LEVEL OF EVIDENCE: Level III, retrospective cohort.
RESUMEN
BACKGROUND: Muscle hypertrophy in the mdx mouse model of Duchenne muscular dystrophy (DMD) can partially compensate for the loss of dystrophin by maintaining peak force production. Histopathology examination of the hypertrophic muscles suggests the hypertrophy primarily results from the addition of myofibers, and is accompanied by motor axon branching. However, it is unclear whether an increased number of innervated myofibers (myofiber hyperplasia) contribute to muscle hypertrophy in the mdx mice. METHODS: To better understand the cellular mechanisms of muscle hypertrophy in mdx mice, we directly compared the temporal progression of the dystrophic pathology in the extensor digitorum longus (EDL) muscle to myofiber number, myofiber branching, and innervation, from 3 to 20 weeks of age. RESULTS: We found that a 28% increase in the number of fibers in transverse sections of muscle correlated with a 31% increase in myofiber branching. Notably, the largest increases in myofiber number and myofiber branching occurred after 12 weeks of age when the proportion of myofibers with central nuclei had stabilized and the mdx mouse had reached maturity. The dystrophic pathology coincided with profound changes to innervation of the muscles that included temporary denervation of necrotic fibers, fragmentation of synapses, and ultra-terminal axon sprouting. However, there was little evidence of synapse formation in the mdx mice from 3 to 20 weeks of age. Only 4.4% of neuromuscular junctions extended ultra-terminal synapses, which failed to mature, and the total number of neuromuscular junctions remained constant. CONCLUSIONS: Muscle hypertrophy in mdx mice results from myofiber branching rather than myofiber hyperplasia.