The benefits of elective spinal implant removal: a retrospective study of 137 patients.

PURPOSE: While spinal instrumentations are becoming more common, the advantages of elective spinal implant removal remain ambiguous. We hypothesized that elective implant removal of the posterior spine is beneficial. METHODS: A retrospective study evaluated 137 consecutive trauma patients with elective implant removal of the posterior spine. If additional cages were present, they were not removed. Primary outcomes were the change in pre- and post-operative pain, fingertip-floor distance (FFD), and Cobb angles. Some secondary outcomes consisted of complications, work disability, and pelvic incidence (PI). Different stabilization approaches and cage sizes were compared. RESULTS: The presence and amount of pain as well as the FFD showed significant improvement. There was no loss of reduction. Delayed wound healing was observed in 9%, but only 3% needed revision. Thoracic fascial dehiscences were seen only in patients (9%) that had stand-alone posterior surgery. Larger cages were associated with increased work disability. An increased PI was associated with less post-operative pain and decreased FFD. CONCLUSIONS: In this study, trauma patients benefited from elective implant removal of the posterior spine due to lower presence and level of pain, improved function and low revision rates; irrespective of an initial combined or stand-alone posterior approach or varying cage sizes. However, stand-alone posterior instrumentation may be accompanied by increased rates of fascial dehiscence surgeries and larger cages may lead to increased work disability. Increased PI may be associated with less pain after spinal implant removal.

Endothelial Rictor is crucial for midgestational development and sustained and extensive FGF2-induced neovascularization in the adult.

To explore the general requirement of endothelial mTORC2 during embryonic and adolescent development, we knocked out the essential mTORC2 component Rictor in the mouse endothelium in the embryo, during adolescence and in endothelial cells in vitro. During embryonic development, Rictor knockout resulted in growth retardation and lethality around embryonic day 12. We detected reduced peripheral vascularization and delayed ossification of developing fingers, toes and vertebrae during this confined midgestational period. Rictor knockout did not affect viability, weight gain, and vascular development during further adolescence. However during this period, Rictor knockout prevented skin capillaries to gain larger and heterogeneously sized diameters and remodeling into tortuous vessels in response to FGF2. Rictor knockout strongly reduced extensive FGF2-induced neovascularization and prevented hemorrhage in FGF2-loaded matrigel plugs. Rictor knockout also disabled the formation of capillary-like networks by FGF2-stimulated mouse aortic endothelial cells in vitro. Low RICTOR expression was detected in quiescent, confluent mouse aortic endothelial cells, whereas high doses of FGF2 induced high RICTOR expression that was associated with strong mTORC2-specific protein kinase Cα and AKT phosphorylation. We demonstrate that the endothelial FGF-RICTOR axis is not required during endothelial quiescence, but crucial for midgestational development and sustained and extensive neovascularization in the adult.