Pullout force of minimally invasive surgical and open pedicle screws-a biomechanical cadaveric study.

BACKGROUND: To assess whether lumbar pedicle screw placement with a minimally invasive surgical (MIS) vs. open technique imparts different biomechanical parameters and thus may affect failure rates. METHODS: Human cadaveric disarticulated lumbar vertebrae 1-5 were stabilised in cement. Pedicle screws were inserted either via the 'MIS' or 'open' technique, based on previously described anatomical landmarks. Each vertebra had one 'MIS' and one 'open' technique screw. Specimens were tested with an Instron mechanical testing machine, positioned to allow for testing of direct coaxial force. Load was applied until failure occurred, and load-displacement curves generated for each screw. RESULTS: Average failure load was found to be 685±399 N for MIS, versus 661±323 N for open technique (P=0.75). The average ultimate failure load was 748±421 N for MIS, versus 772±326 N for open (P=0.74). Average displacement until failure was 0.95±0.49 mm for MIS as compared to 0.95±0.62 mm for open (P=0.996). Axial stiffness was 936±217 N/mm for MIS and 1,016±263 N/mm for open (P=0.19). Average work required to result in failure was 0.84±1.09 J for MIS and 0.82±1.05 J for open (P=0.94). CONCLUSIONS: There was no significant difference in the biomechanical properties of the MIS as compared with open lumbar pedicle screws, when tested until failure under direct coaxial force. The clinical implication may be that there is no significant advantage in the biomechanical properties of MIS versus open lumbar pedicle screw insertion techniques.

Pedicle length and degree of slip in lumbosacral isthmic spondylolisthesis.

OBJECTIVE: The present retrospective study was performed to assess the anatomical features of the pedicle in isthmic spondylolisthesis and to correlate this with degree of slip. METHODS: Twenty-six patients with isthmic spondylolytic spondylolisthesis were studied. Relevant patient variables, length, width, height of the L5 pedicle, and the product of height and angle between pedicle and vertebral midline were measured. The length of the posterior compartment of the pedicle was calculated as the product of the pedicle length and angle. RESULTS: With measurements comparable to those reported in previous publications, the L5 pedicle was found to be longer, and the height and width of the body shorter, than published values for patients without spondylolysis. The difference between the length of the posterior compartment of the pedicle and height of body is significantly proportional to the degree of slip and may reflect an adaptive response for stabilizing the vertebral body with posterior elements. CONCLUSIONS: The pedicle anatomy was found to be altered in patients with L5 S1 spondylolytic spondylolisthesis. These anatomical changes have implications for surgeons performing fusion operations in terms of length of screw, landmarks used and entry approach.

Mesenchymal stem cell conditioned media attenuates in vitro and ex vivo myocardial reperfusion injury.

BACKGROUND: Previous studies have suggested that implantation of mesenchymal stem cells (MSC) or their conditioned media (MSC CM) improves heart function after myocardial infarction. We sought to determine whether MSC and MSC CM added at the onset of reperfusion attenuates myocardial reperfusion injury. METHODS: Rat MSC and neonatal rat cardiomyocytes (NRC) were isolated and cultured separately. NRC were subjected to simulated in vitro ischemia/reperfusion (I/R). At the onset of reperfusion, NRC received either fresh medium (control group) or one of the following treatments: MSC in fresh medium; MSC CM alone (without MSC); MSC CM + inhibitors of PI3K (LY294002 or Wortmannin); MSC CM + antibodies neutralizing IGF-1 or VEGF; MSC + inhibitors of PI3K; or cyclosporine. Cell injury was assessed by LDH activity and MTT staining at the end of reperfusion. VEGF, IGF-1 and HGF were measured in each experimental treatment preparation. Ex vivo experimentation on isolated rat hearts subjected to I/R were performed to evaluate the protective effects of MSC CM on myocardial reperfusion injuries measured through CK release and infarct size after TTC staining. RESULTS: In vitro cell injury was significantly reduced by MSC, MSC CM and CsA. PI3K inhibitors significantly attenuated the protection afforded by MSC CM but not growth factor inhibitors. Ex vivo experimentation showed that MSC CM significantly reduced myocardial I/R injury. CONCLUSION: Our data suggest that MSC CM added at the onset of reperfusion can protect myocardium from I/R injury. In vitro data suggest a protection mediated by paracrine activation of the PI3K pathway.