The spine journal : official journal of the North American Spine Society
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Central cord syndrome (CCS) is a common cause of incomplete spinal cord injury. However, to date, national trends in the management and mortality after CCS are not fully understood. ⋯ Elderly patients with medical comorbidities are associated with a lower surgical rate and a higher mortality rate. Surgical management was more prevalent in the south and large hospitals. Mortality was higher in rural hospitals. It is important for surgeons to understand how patient, surgical, and institutional factors influence surgical management and mortality.
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During the past decade, a disproportionate increase of spinal fusion procedures has been observed. Along with this trend, image-guided spine surgery has been experiencing a renaissance in the recent years. A wide range of different navigation systems are available on the market today. However, only few published studies assess the learning curves concerning these new spinal navigation techniques. So far, a study on the learning curve for intraoperative three-dimensional fluoroscopy (3DFL)-navigated pedicle screw (PS) placement is still lacking. ⋯ We could demonstrate significant learning effects for 3DFL-navigated PS placement with regard to intraoperative 3D scan acquisition, PS placement time, and PS accuracy.
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Insertion of intervertebral fusion devices between consecutive Smith-Peterson osteotomies (SPOs) provides an anterior fulcrum during compression, which has been documented to improve achievable Cobb angle correction. Extension of these principles to an expandable device would theoretically provide greater surgical adjustment for flatback and scoliotic cases than a static cage. ⋯ The expandable interbody did have a slight effect on lordotic correction; each additional millimeter in height expansion yielded approximately 1° in correction across the three SPO levels. Even without significant differences between the states, an expandable device may allow the surgeon more control of lordotic correction within the operating room than a static spacer alone.
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Previous studies have demonstrated the use of bone marrow mesenchymal stem cells (BMSCs) in tissue-engineering treatments to slow or reverse diseased intervertebral discs. Several approaches have successfully used the coculturing of stem cells with disc-native nucleus pulposus cells (NPCs) with the evidence of transformed BMSCs into NP-like cells, increased activity and matrix production by NPCs, or elements of both. The influence of the cytokine transforming growth factor-beta (TGF-β) in the differentiation of BMSCs into NP-like cells and its upregulation in coculture to increase matrix production are well established. However, the role of the inflammatory signaling molecule nuclear factor kappa B (NF-κB) in intervertebral disc degeneration is far less clear, although there is some existing evidence suggesting its role in the pathogenesis and progression of disc disease. A limited number of studies in other pathologies have alluded to the antagonistic relationship between both proteins. To date, there is no such investigation of their dynamic role in coculture of BMSCs and NPCs. ⋯ Coculture of BMSCs may be able to delay NPC matrix degeneration potentially through the concomitant upregulation of TGF-β and the downregulation of NF-κB pathway.
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Intervertebral disc (IVD) degeneration, a major cause of low back pain, is considered to be induced by daily mechanical loading. Mechanical stress is widely known to affect cell survival and extracellular matrix metabolism in many cell types. Although the involvement of integrin α5β1 transmembrane mechanoreceptor in IVD degeneration has been reported, the precise function of integrin α5β1 remains obscure. ⋯ The dynamic loading organ culture system simulated cellular responses to mechanical loading of the IVD. Our results suggest that IVD cells recognize the mechanical stress through RGD integrins, particularly the α5β1 subtype that is highly expressed in NP and AF cells. Further experiments using this system will provide information about pathomechanisms of IVD degeneration through the mechanotransduction pathways.