European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society
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To investigate whether exogenous tumor necrosis factor-α (TNF-α) will initiate a degenerative process in intervertebral disc in vivo. ⋯ Intradiscal injection of exogenous TNF-α caused early stage disc degeneration in a porcine model. It may thus support the hypothesis of exogenic TNF-α being an important early pathogenetic factor in disc degeneration.
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Stromal vascular fraction (SVF), an adipose tissue-derived heterogeneous cell mixture containing, among others, multipotent adipose stromal cells (ASCs) and erythrocytes, has proved beneficial for a wide range of applications in regenerative medicine. We sought to establish intervertebral disc (IVD) regeneration by injecting SVF intradiscally during a one-step surgical procedure in an enzymatically (Chondroitinase ABC; cABC) induced goat model of disc degeneration. Unexpectedly, we observed a severe inflammatory response that has not been described before, including massive lymphocyte infiltration, neovascularisation and endplate destruction. ⋯ However, upon intradiscal injection of an identically processed SVF mixture into our goat IVD degeneration model during a fourth study, the adverse effects surprisingly occurred again. Despite our quest for the responsible agent, we eventually could not identify the mechanism through which the observed destructive responses occurred. Although we cannot exclude that the adverse effects are species-dependent or model-specific, we advertise caution with the clinical application of autologous SVF injections into the IVD until the responsible agent(s) are identified.
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To analyze the effects of mobility of degenerated disc in the lower lumbar discs (L4-5 and L5-S1) on both whole lumbar motion and adjacent segment ROM. ⋯ Degenerated lumbar discs did not show hypermobility within functional ROM. Loss of segmental ROM from advanced disc degeneration did not cause an increase in the ROM of the superior adjacent segment in vivo. When the LLS had motion-lost, advanced disc degeneration, whole lumbar motion was significantly decreased and compensatory increase in ROM was accomplished by the ULS.
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Chronic inflammation is thought to cause ligamentum flavum (LF) degeneration and hypertrophy in lumbar spinal canal stenosis (LSCS). Angiopoietin-like protein 2 (Angptl2) is highly expressed in hypertrophied LF. Because Angptl2 regulates interleukin-6 (IL-6) expression in various tissues, we investigated whether IL-6 is expressed in hypertrophied LF and, if so, does Angptl2 induce IL-6 expression in LF fibroblasts. ⋯ Angptl2 promotes inflammation in LF tissue by activating IL-6 expression, leading to LF degeneration and hypertrophy.
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The ratio of notochordal (NC) cells to mature nucleus pulposus (MNP) cells in the nucleus pulposus varies with species, age and health. Studies suggest that loss of NC cells is a key component of intervertebral disc degeneration. However, few studies have examined the phenotypes of these two cell populations. Therefore, this study aimed to isolate NC and MNP cells from the same intervertebral disc and study phenotypic differences in extracellular matrix production and cell morphology in 3D culture over 7 days. ⋯ NC and MNP cells can be isolated from the same bovine disc and maintain their distinct phenotypes in 3D culture.