Inhibiting tau protein improves the recovery of spinal cord injury in rats by alleviating neuroinflammation and oxidative stress.

After spinal cord injury, the concentrations of total and hyperphosphorylated tau in cerebrospinal fluid increase, and levels of both correlate with injury severity. Tau inhibition is considered effective therapy for many central nervous system diseases, including traumatic brain injury and Alzheimer's disease. However, whether it can play a role in the treatment of spinal cord injury remains unclear. In this study, the therapeutic effects of tau inhibition were investigated in a rat model of transection spinal cord injury by injecting the rats with a lentivirus encoding tau siRNA that inhibits tau expression. We found that tau inhibition after spinal cord injury down-regulated the levels of inflammatory mediators, including tumor necrosis factor-α, interleukin-6 and interleukin-1ß. It also led to a shift of activated microglial polarization from the M1 pro-inflammatory phenotype to the M2 anti-inflammatory phenotype, and reduced the amount of reactive oxygen species in the acute phase. Furthermore, the survival of residual neural cells around the injury epicenter, and neuronal and axonal regeneration were also markedly enhanced, which promoted locomotor recovery in the model rats. Collectively, our findings support the conclusion that tau inhibition can attenuate neuroinflammation, alleviate oxidative stress, protect residual cells, facilitate neurogenesis, and improve the functional recovery after spinal cord injury, and thus suggest that tau could be a good molecular target for spinal cord injury therapy.

Aerobic Glycolysis Induced by mTOR/HIF-1α Promotes Early Brain Injury After Subarachnoid Hemorrhage via Activating M1 Microglia.

M1 microglial activation is crucial for the pathogenesis of early brain injury (EBI) following subarachnoid hemorrhage (SAH), and there is growing evidence that glucose metabolism is frequently involved in microglial activation. However, the molecular mechanism of glycolysis and its role in M1 microglial activation in the context of EBI are not yet fully understood. In this study, firstly, the relationship between aerobic glycolysis and M1 microglial activation as well as SAH-induced EBI was researched in vivo. Then, intervention on mammalian target of rapamycin (mTOR) was performed to investigate the effects on glycolysis-dependent M1 microglial activation and EBI and its relationship with hypoxia-inducible factor-1α (HIF-1α) in vivo. Next, Hif-1α was inhibited to analyze its role in aerobic glycolysis, M1 microglial activation, and EBI in vivo. Lastly, both in vivo and in vitro, mTOR inhibition and Hif-1α enhancement were administered simultaneously, and the combined effects were further confirmed again. The results showed that aerobic glycolysis and M1 microglial polarization were increased after SAH, and glycolytic inhibition could attenuate M1 microglial activation and EBI. Inhibition of mTOR reduced glycolysis-dependent M1 microglial polarization and EBI severity by down-regulating HIF-1α expression, while enhancement had the opposite effects. Blockading HIF-1α had the similar effects as suppressing mTOR, while HIF-1α agonist worked against mTOR antagonist when administered simultaneously. In conclusion, the present study showed new evidence that aerobic glycolysis induced by mTOR/HIF-1α might promote EBI after SAH by activating M1 microglia. This finding provided new insights for the treatment of EBI.

Association of cerebrospinal fluid advanced oxidation protein products levels with early brain injury and prognosis of aneurysmal subarachnoid hemorrhage: A preliminary prospective study.

OBJECTIVES: In this study, we investigated the time course in the cerebrospinal fluid (CSF) advanced oxidation protein products (AOPPs) levels in patients with aneurysmal subarachnoid hemorrhage (aSAH), and ascertained the relationship between the levels of AOPPs and early brain injury (EBI), hydrocephalus and prognosis of patients with aSAH. METHODS: We measured the CSF AOPPs levels in 50 patients with aSAH at 1-3 d, 4-6 d, 7-9 d, and 10-12 d after hemorrhage. The modified Fisher grades, Hunt-Hess grades, CSF IL-6 levels, peripheral blood count of white blood cells, cerebral edema scores and hydrocephalus were used to assess the severity of brain injury. Modified Rankin Scale (mRS) scores were used to assess the prognosis. Patients with mRS scores greater than 2 were considered to have a poor outcome. RESULTS: CSF AOPPs levels were significantly higher in patients with aSAH with poor prognosis, compared to patients with good prognosis and peaked in the early stage. Among patients with aSAH, the levels of CSF AOPPs on days 1-3 were significantly correlated with modified Fisher grades, Hunt-Hess grades, CSF IL-6 levels, peripheral blood count of white blood cells, and cerebral edema scores. Also, in patients with hydrocephalus, early CSF AOPPs levels were significantly elevated. Levels of CSF AOPPs in aSAH patients on days 1-3, 4-6, and 7-9 were independently associated with poor prognosis at the 90-day follow-up, and the optimal area under the curve (AUC) values for CSF AOPPs levels were found on days 1-3. CONCLUSIONS: AOPPs may serve as the potential biomarker to assess the severity of EBI and prognosis in patients with aSAH.

Role of TREM-1 in the development of early brain injury after subarachnoid hemorrhage.

Triggering receptor expressed on myeloid cells-1 (TREM-1) was found to be induced in the context of subarachnoid hemorrhage (SAH) before. This study further investigates its role in the development of SAH-induced early brain injury (EBI). Firstly, rats were randomly divided into Sham and SAH groups for analysis of temporal patterns and cellular localization of TREM-1. Secondly, TREM-1 intervention was administrated to produce Sham, vehicle, antagonist and agonist groups, for analyzing TREM-1, Toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88) and NF-κB expressions at 24 h post-modeling, and EBI assessment at 24 h and 72 h. Thirdly, TLR4 inhibitor (TAK-242) was exploited to produce Sham, Sham+TAK-242, SAH, and SAH + TAK-242 groups to analyze the effects of TLR4 inhibition on TREM-1 induction and EBI evaluation at 72 h. Fourthly, the relationship of soluble TREM-1 (sTREM-1) levels in cerebrospinal fluid of SAH patients with Hunt-Hess grades were explored. The results showed that TREM-1 increased in the brain after experimental SAH (eSAH) early at 6 h and peaked at 48 h, which was found to be located in microglia and endothelial cells. TREM-1 inhibition attenuated EBI associated with TLR4/MyD88/NF-κB suppression, while enhancement had the opposite effects. Contrarily, TLR4 inhibition prevented TREM-1 induction and ameliorated EBI. In addition, sTREM-1 levels in SAH patients positively correlated with Hunt-Hess grades. Overall, the present study provides new evidence that TREM-1 increases dynamically in the brain after eSAH and it is located in microglia and endothelial cells, which may aggravate EBI by interacting with TLR4 pathway. And sTREM-1 in patients might act as a monitoring biomarker of EBI, providing new insights for future studies.

Oligodendrocyte differentiation from human neural stem cells: A novel role for c-Src.

Human neural stem cells (hNSCs) can differentiate into an oligodendrocyte lineage to facilitate remyelination in patients. Molecular mechanisms underlying oligodendrocyte fate specification remains unknown, hindering the development of efficient methods to generate oligodendrocytes from hNSCs. We have found that Neurobasal-A medium (NB) is capable of inducing hNSCs to oligodendrocyte progenitor cells (OPCs). We identified several signaling molecules are altered after cultivation in NB medium, including Akt, ERK1/2 and c-Src. While sustained activation of Akt and ERK1/2 during both NB induction and subsequent differentiation was required for OPC differentiation, c-Src phosphorylation was increased temporally during the period of NB induction. Both pharmacological inhibition and RNA interference confirmed that a transient elevation of phospho-c-Src is critical for OPC induction. Furthermore, inactivation of c-Src inhibited phosphorylation of Akt and ERK1/2. In summary, we identified a novel and critical role of c-Src in guiding hNSC differentiation to an oligodendrocyte lineage.

Radiosynthesis and Preliminary Biological Evaluation of 18F-Fluoropropionyl-Chlorotoxin as a Potential PET Tracer for Glioma Imaging.

Purposes: Chlorotoxin can specifically bind to matrix metalloproteinase 2 (MMP-2), which are overexpressed in the glioma. In this work, radiosynthesis of [18F]-fluoropropionyl-chlorotoxin ([18F]-FP-chlorotoxin) as a novel PET tracer was investigated, and biodistribution in vivo and PET imaging were performed in the C6 glioma model. Procedures: [18F]-FP-chlorotoxin was prepared from the reaction of chlorotoxin with [18F]-NFB (4-nitrophenyl 2-[18F]-fluoropropionate), which was synthesized from multistep reactions. Biodistribution was determined in 20 normal Kunming mice. Small-animal PET imaging with [18F]-FP-chlorotoxin was performed on the same rats bearing orthotopic C6 glioma at different time points (60 min, 90 min, and 120 min) after injection and compared with 2-deoxy-2-[18F] fluoro-D-glucose ([18F]-FDG). Results: [18F]-FP-Chlorotoxin was successfully synthesized in the radiochemical yield of 41% and the radiochemical purity of more than 98%. Among all the organs, the brain had the lowest and stable uptake of [18F]-FP-chlorotoxin, while the kidney showed the highest uptake. Compared with [18F]-FDG, a low uptake of [18F]-FP-chlorotoxin was detected in normal brain parenchyma and a high accumulation of [18F]-FP-chlorotoxin was found in the gliomas tissue. The glioma to normal brain uptake ratio of [18F]-FP-chlorotoxin was higher than that of [18F]-FDG. Furthermore, the uptake of [18F]-FP-chlorotoxin at 90 min after injection was better than that at 60 min after injection. Conclusions: Compared with [18F]-FDG, [18F]-FP-chlorotoxin has a low and stable uptake in normal brain parenchyma. [18F]-FP-Chlorotoxin seems to be a potential PET tracer with a good performance in diagnosis of the glioma.

Early administration of tumor necrosis factor-alpha antagonist promotes survival of transplanted neural stem cells and axon myelination after spinal cord injury in rats.

Neural stem cell (NSC) transplantation has been reported to be a leading strategy to stimulate neuroplasticity, repair neuronal loss and promote the morphologic and functional recovery of spinal cord injury (SCI). However, massive death of transplanted NSCs is still a problem, which is considered to be related to a series of pro-inflammatory cytokines that induce apoptosis, extensive demyelination and axonal destruction. Tumor necrosis factor alpha (TNF-α), as one of the major inflammation initiators, contributes to secondary neural cell death. We previously found that the administration of the TNF-α antagonist etanercept during the acute phase of SCI can reduce the apoptosis of neurons and oligodendrocytes. To investigate whether etanercept can suppress transplanted NSC apoptosis and promote NSC survival, axon myelination and functional recovery, we tested the combination strategy of the early administration of etanercept and NSC transplantation. First we observed that etanercept suppressed the TNF-α expression and apoptosis of transplanted NSCs by Western blot, TUNEL and immunofluorescence staining. The Basso, Beattle and Bresnahan scale and motor-evoked potential were used to evaluate functional recovery. The results suggest significantly better recovery after combination therapy. Further, histopathological alterations were evaluated by hematoxylin and eosin staining and Nissl staining. These procedures showed that the early administration of etanercept improved survival of neurons in the ventral horn, restored neural morphology and produced a smaller cavity area. We observed most abundant NF-positive fibers after the combination treatment, indicating that combination therapy retained and promoted neural regeneration. Finally, the early suppression of TNF-α reduced the occurrence of demyelination, and the combination therapy led to more myelinated axons, as shown by electron microscopy. These data suggest that this strategy significantly protected transplanted NSCs via the anti-inflammation and anti-apoptosis effects of etanercept, promoting re-myelination, neural regeneration and locomotor function.

[Comparative study of Kurokawa's double door laminoplasty and modified Kurokawa's double door laminoplasty for the treatment of cervical disorders].

OBJECTIVE: To observe and compare the medium-long-term efficacy of Kurokawa's and modified Kurokawa's double door laminoplasty for the treatment of cervical disorders. METHODS: A retrospective analysis was performed to compare the outcomes and complications between two kinds of operations on 172 cases from January 2002 to December 2010, including 106 cases of cervical spondylotic myelopathy, 52 cases of cervical stenosis, 21 cases of cervical ossification of the posterior longitudinal ligament. Patients were divided into two groups according to two surgical methods: traditional group, including 51 male and 18 female patients, with mean age of (56 ± 18) years (35-76 years); modified group, including 75 male and 28 female patients, with mean age of (58 ± 20)years (35-80 years). The two groups were comparable and compared according to different data using t test, χ(2) test and rank sum test. RESULTS: All patients were followed up continuously for (52 ± 33)months, 123 patients were followed up ≥ 2 years, 71 patients ≥ 5 years. All patients' Japanese Orthopaedic Association (JOA) score improved significantly at the latest follow-up(t = 3.420, P < 0.01); no significant difference between the patients' JOA score improvement rate of two groups. The postoperative incidence rate of axial symptoms in patients of modified group (3.9%) was significantly lower than the traditional group (14.5%) (χ(2) = 7.548, P < 0.05), and cervical intervertebral activity decreased in the modified group was better than the traditional group in the first 3 months postoperatively (27% ± 6% vs. 19% ± 4%,Z = 6.34, P < 0.05), but during the medium-long-term follow-up, no significant difference in the cervical intervertebral activity decreased between two groups. CONCLUSIONS: Medium-long-term efficacy of Kurokawa's and modified Kurokawa's double door laminoplasty is satisfied and reliable. Avoiding damaging of semispinalis cervicis insertion in spinous process of C2, the modified operation method can protect the extensor group of the neck muscle and reduce the incidence of postoperative axial symptoms better.

Blockade of interleukin 6 signaling improves the survival rate of transplanted bone marrow stromal cells and increases locomotor function in mice with spinal cord injury.

Bone marrow stromal cells (BMSCs) have the potential to improve functional recovery in patients with spinal cord injury (SCI); however, they are limited by low survival rates after transplantation in the injured tissue. Our objective was to clarify the effects of a temporal blockade of interleukin 6 (IL-6)/IL-6 receptor (IL-6R) engagement using an anti-mouse IL-6R monoclonal antibody (MR16-1) on the survival rate of BMSCs after their transplantation in a mouse model of contusion SCI. MR16-1 cotreatment improved the survival rate of transplanted BMSCs, allowing some BMSCs to differentiate into neurons and astrocytes, and improved locomotor function recovery compared with BMSC transplantation or MR16-1 treatment alone. The death of transplanted BMSCs could be mainly related to apoptosis rather than necrosis. Transplantation of BMSC with cotreatment of MR16-1 was associated with a decrease of some proinflammatory cytokines, an increase of neurotrophic factors, decreased apoptosis rates of transplanted BMSCs, and enhanced expression of survival factors Akt and extracellular signal-regulated protein kinases 1/2. We conclude that MR16-1 treatment combined with BMSC transplants helped rescue neuronal cells and axons after contusion SCI better than BMSCs alone by modulating the inflammatory/immune responses and decreasing apoptosis.

Serum levels of IL-33 is increased in patients with ankylosing spondylitis.

Interleukin-33 (IL-33) is implicated in rheumatoid arthritis with effects of promoting tumor necrosis factor-alpha (TNF-α) and interleukin-17 (IL-17) productions, which have been demonstrated to play a pivotal role in ankylosing spondylitis (AS). However, changes of IL-33 levels and its effects in AS have not been investigated. Eighty-nine and 178 healthy controls were included in the current study. Erythrocyte sedimentation rate, serum levels of C-reactive protein, IL-17, and IL-33 were determined. Effects of IL-33 on TNF-α and IL-6 productions were investigated. Effects of IL-33 on neutrophil migration were also evaluated. Serum levels of IL-33 were elevated in AS patients. Moreover, IL-33 was significantly higher in active AS patients according to Bath Ankylosing Spondylitis Disease Activity Index. IL-33 concentrations in serum were positively correlated with TNF-α and IL-17 levels (IL-33 and TNF-α, r = 0.54, P < 0.01; IL-33 and IL-17, r = 0.47, P < 0.01). IL-33 dose-dependently enhanced TNF-α and IL-6 productions by peripheral blood mononuclear cells (PBMCs) responding to lipopolysaccharide. IL-33 induced neutrophil migration only in higher doses (≥10 ng/ml). Serum levels of IL-33 were elevated in AS patients. IL-33 may play a role in AS development via enhancing TNF-α production by PBMCs and inducing neutrophil migration.

Adjacent segment degeneration after single-segment PLIF: the risk factor for degeneration and its impact on clinical outcomes.

PURPOSE: To investigate: (1) the risk factors for radiologic cranial adjacent segment degeneration (ASD) after single-segment PLIF at the same level, and (2) the impact of the ASD on the clinical outcomes. METHODS: From October 2004 to May 2009, 109 patients who underwent PLIF for degenerative instability at L4/5 and have more than 2 years follow-up were studied retrospectively. We measured the preoperative bone mineral density (BMD), lumbar lordosis, the lumbosacral joint angle, the lumbar inclination, the height and the dynamic angulation of the intervertebral space at the fused segments and the upper adjacent segment, the sliding displacement between L3 and L4. Clinical outcomes were evaluated using the Japanese Orthopedic Association (JOA) score and the Oswestry Disability Index (ODI). Patients were divided into two groups according to the progression of L3-L4 degeneration: Group A without progression of L3-L4 degeneration, Group B with progression of L3-L4 degeneration. Clinical outcomes and radiologic measurement index between the two groups were compared, and the risk factors for progression of L3-L4 degeneration were analyzed. The correlation between clinical outcomes and progression of L3-L4 degeneration were also investigated. RESULTS: There were 11 patients (22%) classified into Group A. No significant difference was found between the two groups in terms of the lordosis angle at L1 and S1, the laminar inclination at L3, the pre-existing L3-L4 disk degeneration, the lordosis angle of L4-L5, the lumbosacral joint angle and preoperative BMD (P > 0.05). Significant differences were found between the two groups in age. No significant difference was found between the two groups in the ODI and the JOA score at the final follow-up (P > 0.05). CONCLUSION: Radiologic degeneration of the cranial adjacent segment after single-segment PLIF did not significantly correlate with clinical outcomes. Age was a risk factor for radiologic degeneration, however, there was no significant correlation between degeneration and preoperative radiologic factors and bone mineral density (BMD).

High-mobility group box-1 and its receptors contribute to proinflammatory response in the acute phase of spinal cord injury in rats.

STUDY DESIGN: To examine the localization and expression of high-mobility group box-1 (HMGB-1) protein and its receptors after rat spinal cord injury. OBJECTIVE: To elucidate the contribution of HMGB-1 and its receptors as potential candidates in a specific upstream pathway to the proinflammatory response leading to a cascade of secondary tissue damage after spinal cord injury. SUMMARY OF BACKGROUND DATA: HMGB-1 was recently characterized as a key cytokine with a potential role in nucleosome formation and regulation of gene transcription. No studies have investigated the role of HMGB-1 in spinal cord injury. METHODS: Injured thoracic spinal cord from 62 rats aged 8 to 12 weeks and spinal cord from 20 control rats were examined. HMGB-1 was localized by immunofluorescence staining, costaining with cell markers, and by immunoelectron microscopy. The expression of HMGB-1 and its receptors, receptor for advanced glycation end products (RAGE), toll-like receptor (TLR)2, and TLR4 were also examined by immunohistochemistry. RESULTS: HMGB-1 expression appeared earlier than that of tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6 in the spinal cord injury rats, with the HMGB-1 produced by both macrophages and neurons. HMGB-1 translocated from nucleus to cytoplasm in some neurons at an early stage after neural injury. Increased expression of HMGB-1, RAGE, and TLRs was observed after injury, and interaction of HMGB-1 with RAGE or TLRs, particularly in macrophage, was confirmed at 3 days after injury. CONCLUSION: Our results demonstrated an earlier onset in the expression of HMGB-1 than in tumor necrosis factor-α, IL-1ß, and IL-6 after spinal cord injury. The release of HMGB-1 from neurons and macrophages is mediated through the HMGB-1/RAGE or TLR pathways. HMGB-1 seems to play at least some roles in the proinflammatory cascade originating the secondary damage after the initial spinal cord injury.

Tumor necrosis factor-α antagonist reduces apoptosis of neurons and oligodendroglia in rat spinal cord injury.

STUDY DESIGN: To examine the effects of a tumor necrosis factor (TNF)-α antagonist (etanercept) on rat spinal cord injury and identify a possible mechanism for its action. OBJECTIVE: To elucidate the contribution of etanercept to the pathologic cascade in spinal cord injury and its possible suppression of neuronal and oligodendroglial apoptosis. SUMMARY OF BACKGROUND DATA: Etanercept has been recently used successfully for treatment of inflammatory disorders. However, only a few studies have examined its role in suppressing neuronal and oligodendroglial apoptosis in spinal cord injury. METHODS: Etanercept or saline (control) was administered by intraperitoneal injection 1 hour after thoracic spinal cord injury in rats. The expressions and localizations of TNF-α, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2) were examined by immunoblot and immunohistochemical analyses. Spinal cord tissue damage between saline- and etanercept-treated groups was also compared after hematoxylin-eosin and luxol fast blue (LFB) staining. The Basso-Beattie-Bresnahan (BBB) scale was used to evaluate rat locomotor function after etanercept administration. Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL)-positive cells were counted and the immunoreactivity to active caspase-3 and caspase-8 was examined after etanercept administration. RESULTS: Immunoblot and double immunofluorescence staining revealed suppression of TNF-α, TNFR1, and TNFR2 expression after administration of etanercept in the acute phase of spinal cord injury. LFB staining demonstrated potential myelination in the etanercept-treated group from 2 week after spinal cord injury, together with an increased BBB locomotor score. Double immunofluorescence staining showed a significant decrease in TUNEL-positive neurons and oligodendroglia from 12 hour to 1 week in the gray and white matters after etanercept administration. Immunoblot analysis demonstrated overexpression of activated caspase-3 and caspase-8 after spinal cord injury, which was markedly inhibited by etanercept. CONCLUSION: Our results indicated that etanercept reduces the associated tissue damage of spinal cord injury, improves hindlimb locomotor function, and facilitates myelin regeneration. This positive effect of etanercept on spinal cord injury is probably attributable to the suppression of TNF-α, TNFR1, TNFR2, and activated caspase-3 and caspase-8 overexpressions, and the inhibition of neuronal and oligodendroglial apoptosis.

Transpedicular fixation in management of thoracolumbar burst fractures: monosegmental fixation versus short-segment instrumentation.

STUDY DESIGN: A prospective clinical trial was conducted. OBJECTIVE: To compare the clinical and radiologic late results of monosegmental transpedicular fixation versus short-segment pedicle instrumentation (SSPI) in management of thoracolumbar burst fractures and evaluate the efficacy of monosegmental transpedicular fixation. SUMMARY OF BACKGROUND DATA: SSPI (1 level above and 1 below the fracture level) are accepted by many surgeons as an accepted technique for the treatment of thoracolumbar burst fractures. To preserve more motion segments, some authors have advocated monosegmental pedicle instrumentation (MSPI). The recent developments showed that MSPI yielded good clinical results; however, there were no report about comparison of clinical outcome between monosegmental and biosegmental transpedicular fixation in management of thoracolumbar burst fractures. METHODS: Eighty-five patients with thoracolumbar burst fractures fulfilling the inclusion criteria were included in the study. The patients were randomized by a simple method into 2 groups. Group 1 were treated with monosegmental transpedicular fixation (n = 47), and group 2 were treated with biosegmental transpedicular fixation (n = 38). Clinical (Low Back Outcome Score and Oswestry Disability Index) and radiologic (load-sharing classification index, sagittal index, and percentage of anterior body height compression) outcomes were analyzed. RESULTS: The 2 groups were similar in age, follow-up period, and severity of the deformity and fracture. The postoperative and follow-up sagittal index, local kyphosis, percentage of anterior body height compression, and average correction loss in local kyphosis in both groups were not significantly different. The failure rate between the 2 surgical approaches was also not significantly different (group 1 = 6.38% and group 2 = 5.26%). Oswestry Disability Index improved in both groups by >25 points in a similar amount (P = 0.23). The average follow-up Low Back Outcome Score was 74.9 and 60.2 for group 1 and group 2, respectively (P = 0.033). CONCLUSION: In conclusion, radiologic parameters demonstrated that both MSPI and SSPI are the effective and reliable operative techniques for selected thoracolumbar burst fractures. MSPI shortened the operative time and decreased the amount of blood loss significantly and, thus, offered better clinical results. Nevertheless, long-term studies are supposed to be performed to support the outcomes.

Two kinds of posterior approach for Kvmmell's disease after osteoporotic thoracolumbar fracture.

OBJECTIVE: To compare the surgical results of two kinds of posterior approach for osteoporotic thoracolumbar Kvmmell's disease. METHODS: Clinical and radiographic results of 1-segmental pedicle screw fixation combined with vertebroplasty (Group A, n equal to 12) or posterior shortening osteotomy (Group B, n equal to 16) for osteoporotic thoracolumbar Kvmmell's disease were analyzed retrospectively. Japanese orthopedic association (JOA) and visual analogue scale (VAS) scores were used for clinical evaluation. Neurological status was judged by Frankel grades. X-ray was used to evaluate the radiographic results. Complications related to operation and devices were also considered. RESULTS: The follow-up period was 12-54 months (average 29 months). Pre-and post-operative VAS were 9.3 and 3.2 in Group A, 8.9 and 2.5 in Group B, respectively. The mean JOA score at the final follow-up was significantly higher than that of pre-operation (t equal to 5.306, P less than 0.001). There was no significant difference between Groups A and B (t equal to 0.618, P larger than 0.05). The kyphosis were corrected from preoperative 33.9 degree A)/37.3 degree B) to postoperative 10.3 degree A)/6.5 degree B), and 15.3 degree (A)/13.7 degree B) at the final follow-up. There was a significant difference between the two groups at the final follow-up. Frankel grade was improved from grade C preoperatively to postoperatively grade D or E in 7 cases of Group A and 5 cases of Group B, from grade D to E in 5 cases of Group A and 11 cases of Group B. The mean improvement was 1.6 and 1.7 grades for Groups A and B, respectively. There were no serious complications related to internal fixation. CONCLUSIONS: The similar clinical results can be obtained by the two kinds of posterior surgical methods for osteoporotic Kvmmell's disease. Posterior spinal shortening is a better choice for patients with serious kyphosis combined with neurological deficit than the other.