The aim of this study was to retrospectively analyze and evaluate the effect of treatment employing pedicle subtraction osteotomy for chronic, posttraumatic thoracolumbar kyphosis. This study included 19 patients, 11 males and 8 females, with chronic, posttraumatic thoracolumbar kyphosis. Pre-operative kyphosis ranged from 31° to 63°. The history of trauma ranged from 8 to 63 months. All patients were treated with pedicle subtraction osteotomy. A mean 40.2° improvement in sagittal alignment was achieved with a mean correction rate of 85.8 %. Perioperative complications were encountered in two patients, one with cerebrospinal fluid leakage followed by encephalitic infection and one with a wound infection. Both were treated conservatively with antibiotics and local wound care. There were no other severe complications. The average follow-up period was 15 months (range 6-41 months). At the last follow-up, clinical symptoms and neurological function were significantly improved. Of 14 patients presenting with intractable back pain, VAS scores improved from a preoperative mean of 6.7 (range 5.0-8.0) to an average 2.0 (range 0-3.0) at final follow-up. No significant loss of correction was observed (loss of 1.7°), and solid fusion was achieved in all 19 patients. A single-stage posterior pedicle subtraction osteotomy is a safe and effective procedure for correction of posttraumatic thoracolumbar kyphosis. Using this technique, it is possible to safely obtain no greater than 55° of correction at a single level.
To our knowledge, this is the first report of pinealectomy in nonhuman primates. Of the 18 monkeys, 10 had a loss of melatonin secretion, for a mean of 29 months after surgery. Because none of the monkeys had scoliosis develop, this study strongly suggests that the possible etiologic factors producing idiopathic scoliosis in lower animals are different from primates, and findings in lower animals cannot necessarily be extrapolated to human beings.
The present study examined the effects of transforming growth factor (TGF)-β3, connective tissue growth factor (CTGF) and tissue inhibitor of metalloproteinase 1 (TIMP1) gene transduction, using a lentiviral vector, on rabbit intervertebral disc degeneration , with the intention of investigating their potential use in gene therapy. A model of lumbar intervertebral disc degeneration was created by needle puncture into the annulus fibrosus of 15 New Zealand white rabbits. Empty lentivirus or recombinant lentiviral plasmid lenti-TGFβ3-P2A-CTGF-T2A-TIMP1 was injected into degenerative lumbar intervertebral discs (representing the control and experimental groups, respectively), whilst untreated degenerative lumbar intervertebral discs served as the puncture group. After 16 and 20 weeks, magnetic resonance imaging (MRI) was conducted and the changes in intensity on micrographs of degenerative intervertebral discs were measured. The mRNA levels of aggrecan and type II collagen in nucleus pulposus tissue were determined by reverse transcription-polymerase chain reaction, and protein expression levels of type II collagen and aggrecan were determined by western blot analysis. MRI results indicated that intervertebral disc degeneration was ameliorated in the experimental group when compared with the control and the puncture group. Furthermore, the expression levels of type II collagen and aggrecan in the puncture and control groups were significantly lower than in the experimental group (P<0.05). In conclusion, lenti-TGFβ3-P2A-CTGF-T2A-TIMP1 co-transduction can promote synthesis of aggrecan and type II collagen in degenerative intervertebral discs, thereby delaying intervertebral disc degeneration. These results indicate the potential of gene therapy in treatment of intervertebral disc degeneration.
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