Traumatic Lumbar Fractures Research Articles

The clinical results and function of the intersegmental disc after posterior-only partial corpectomy for lumbar burst fractures.

We treated the burst spinal fracture with posterior subtotal corpectomy and reconstruction. In some cases, the endplate and the adjacent disc can be preserved during the operation. The adjacent disc retained its mobility after the removal of the posterior pedicle screws. This study evaluated the clinical results and function of the intersegmental caudal disc after the removal of posterior pedicle screws for lumbar burst fractures. The study analyzed retrospectively 36 patients with acute burst traumatic lumbar fractures who underwent posterior partial subtotal corpectomy and reconstruction with preservation of the inferior endplate of the fractured vertebral body and the adjacent caudal disc, and sequential removal of the posterior pedicle screw 1 year after the second surgery from March 2015 to December 2021. All patients were followed for approximately 1 year after pedicle screw removal. Demographic data, anterior vertebral body height, local kyphosis, motion, caudal disc degeneration, and clinical outcomes were evaluated. After removal of the posterior pedicle screws, the intersegmental disc retained a range of motion of 10.55 ± 5.58°, and the disc degeneration was graded by Pfirrmann criteria from 2.21 ± 1.15 before first surgery to 3.18 ± 1.46 at last follow-up after second surgery. There were 2 cases of superficial wound infection, and 5 cases of postoperative neuralgia recovering after 3 months. Anterior fusion was achieved, although postoperative subsidence of the mesh was observed in 6 cases and screw loosening in 9 cases. Posterior-only partial subtotal corpectomy with preservation of the adjacent caudal disc not only achieved a good clinical effect, but also preserved intersegmental caudal disc function after removal of posterior pedicle screws approximately 1 year later. This technique is a promising alternative for cases in which the endplate obviates injury.

TsRNA-04002 alleviates intervertebral disk degeneration by targeting PRKCA to inhibit apoptosis of nucleus pulposus cells

BackgroundIntervertebral disk degeneration (IDD) is a degenerative disease that underlies various musculoskeletal and spinal disorders and is positively correlated with age. tRNA-derived small RNAs (tsRNA), as a new small noncoding RNAs, its function in IDD is unclear. Herein, our goal was to find the key tsRNA that affects IDD independently of age and explore the underlying mechanisms.MethodsSmall RNA sequencing was performed in nucleus pulposus (NP) tissues of traumatic lumbar fracture individuals, young IDD (IDDY) patients, and old IDD (IDDO) patients. The biological functions of tsRNA-04002 in NP cells (NPCs) were investigated by qRT-PCR, western blot, and flow cytometry analysis. The molecular mechanism of tsRNA-04002 was demonstrated by luciferase assays and rescue experiments. Furthermore, the therapeutic effects of tsRNA-04002 on IDD rat model were used and evaluated in vivo.ResultsCompared with fresh traumatic lumbar fracture patients, a total of 695 disordered tsRNAs is obtained (398 down-regulated tsRNAs and 297 up-regulated tsRNAs). These disordered tsRNAs were mainly involved in Wnt signaling pathway and MAPK signaling pathway. tsRNA-04002 was an age-independent key target in IDD, which was both lower expressed in IDDY and IDDO groups than control group. Overexpression of tsRNA-04002 restrained inflammatory cytokines IL-1β and TNF-α expression, increased the COL2A1, and inhibited the NPCs apoptosis. Furthermore, we determined that PRKCA was the target gene of tsRNA-04002 and was negatively regulated by tsRNA-04002. The rescue experiment results suggested that the high expression of PRKCA reversed the inhibitory effect of tsRNA-04002 mimics on NPCs inflammation and apoptosis, and promotive effect of COL2A1. Moreover, tsRNA-04002 treatment dramatically ameliorated the IDD process in the puncture-induced rat model, together with the blockade of PRKCA in vivo.ConclusionCollectively, our results substantiated that tsRNA-04002 could alleviate IDD by targeting PRKCA to inhibit apoptosis of NPCs. tsRNA-04002 may be a novel therapeutic target of IDD progression.

Necroptosis of nucleus pulposus cells involved in intervertebral disc degeneration through MyD88 signaling.

Background contextLow back pain, affecting nearly 40% of adults, mainly results from intervertebral disc degeneration (IVDD), while the pathogenesis of IVDD is still not fully elucidated. Recently, some researches have revealed that necroptosis, a programmed necrosis, participated in the progression of IVDD, nevertheless, the underlying mechanism remains unclear.PurposeTo study the mechanism of necroptosis of Nucleus Pulposus (NP) cells in IVDD, focusing on the role of MyD88 signaling.Study designThe expression and co-localization of necroptotic indicators and MyD88 were examined in vivo, and MyD88 inhibitor was applied to determine the role of MyD88 signaling in necroptosis of NP cells in vitro.MethodsHuman disc specimens were collected from patients receiving diskectomy for lumbar disc herniation (LDH) or traumatic lumbar fractures after MRI scanning. According to the Pfirrmann grades, they were divided into normal (Grades 1, 2) and degenerated groups (4, 5). Tissue slides were prepared for immunofluorescence to assess the co-localization of necroptotic indicators (RIP3, MLKL, p-MLKL) and MyD88 histologically. The combination of TNFα, LPS and Z-VAD-FMK was applied to induce necroptosis of NP cells. Level of ATP, reactive oxygen species (ROS), live-cell staining and electron microscope study were employed to study the role of MyD88 signaling in necroptosis of NP cells.Results In vivo, the increased expression and co-localization of necroptotic indicators (RIP3, MLKL, p-MLKL) and MyD88 were found in NP cells of degenerated disc, while very l low fluorescence intensity in tissue of traumatic lumbar fractures. In vitro, the MyD88 inhibitor effectively rescued the necroptosis of NP cells, accompanied by increased viability, ATP level, and decreased ROS level. The effect of MyD88 inhibition on necroptosis of NP cells was further confirmed by ultrastructure of mitochondria shown by Transmission Electron Microscope (TEM).ConclusionOur results indicated that the involvement of MyD88 signaling in the necroptosis of NP cells in IVDD, which will replenish the pathogenesis of IVDD and provide a novel potential therapeutic target for IVDD.

MicroRNA-155-3p attenuates intervertebral disc degeneration via inhibition of KDM3A and HIF1α.

Intervertebral disc degeneration (IDD) is a key element resulting in low back pain, but the mechanisms underlying IDD remain largely unknown. The purpose of the study was to investigate the influence of microRNA-155-3p (miR-155-3p) on proliferation and autophagy of nucleus pulposus (NP) cells in IDD with the involvement of hypoxia-inducible factor 1 α (HIF1α)/histone lysine demethylase 3A (KDM3A) axis. IDD NP tissues of patients with lumbar disc herniation and traumatic intervertebral disc NP tissues from patients with traumatic lumbar fracture were collected. Apoptosis in NP tissues was observed, and autophagy marker proteins in NP tissues were detected. NP cells in IDD were transfected with miR-155-3p mimic or KDM3A-siRNA to explore their roles in cell proliferation, autophagy and apoptosis. MiR-155-3p, KDM3A and HIF1α expression in NP tissues and cells were detected. Decreased miR-155-3p, and elevated HIF1α and KDM3A were presented in NP tissues and cells of IDD. Elevated miR-155-3p or silenced KDM3A promoted the proliferation and autophagy, and inhibited the apoptosis of NP cells of IDD. Moreover, elevated miR-155-3p decreased KDM3A and HIF1α expression, while silenced KDM3A decreased HIF1α expression in NP cells with IDD. The study concludes that up-regulated miR-155-3p or silenced KDM3A promotes the proliferation, autophagy, and restrains the apoptosis of NP cells of IDD via inhibition of HIF1α, which may be a promising approach for the treatment of IDD.

Unilateral Biportal Endoscopic-Guided Transcorporeal Vertebroplasty with Neural Decompression for Treating a Traumatic Lumbar Fracture of L5

Lumbar burst fractures (complete or incomplete) of L5 have a low incidence, accounting for 1.2% of all spinal burst fractures. Treatment for these fractures remains controversial. Decompression of neural elements and stabilization of the spine to preserve lordosis and avoid kyphotic deformity are recommended when a patient has a neurological deficit and an unstable fracture. Otherwise, the fracture could be managed conservatively. We report a detailed step-by-step unilateral biportal endoscopy technique used in a patient with an L5 incomplete burst fracture and neurological deficit. The patient had an acceptable immediate postoperative course; lower back pain and radicular symptoms improved significantly after surgery. Our unilateral biportal endoscopy technique for L5 incomplete burst fractures offers the capability to perform enough decompression of neural elements and assist other procedure-related maneuvers under direct endoscopic visualization. This technique could be considered another minimally invasive spine surgery option for treating selected patients with L5 incomplete burst fractures.

Downregulation of microRNA-125a is involved in intervertebral disc degeneration by targeting pro-apoptotic Bcl-2 antagonist killer 1.

Objective(s):To investigate the role of the microRNA-125a (miR-125a) and BAK1 in intervertebral disc degeneration (IDD).Materials and Methods:Degenerative lumbar nucleus pulposus (NP) tissues were obtained from 193 patients who underwent resection, and normal controls consisted of normal NP tissues from 32 patients with traumatic lumbar fracture in our hospital. All patients were graded according to the Pfirrmann criteria. QRT-PCR was used to detect the expression of miR-125a and BAK1, and apoptosis of NP tissues detected by TUNEL staining. After isolation of non- degenerative and degenerative nucleus pulposus cells (NPCs), the targeting relationship between miR-125a and BAK1 was verified by dual luciferase reporter gene assay. Flow cytometry was determined the NPCs apoptosis, and Western blot to measure the expressions of BAK1, Caspase-3, Bax and Bcl-2.Results:MiR-125a was reduced while BAK1 was elevated in IDD patients with the increase of Pfirrmann grade. Besides, miRNA-125a was negatively correlated to the NPCs apoptosis, while BAK1 mRNA was positively correlated to cell apoptosis. Additionally, BAK1 is the target gene of miRNA-125a. When transfection of miR-125a mimics in vitro, the apoptosis of NPCs were inhibited, with the down-regulation of BAK1, Caspase-3, and Bax, and the upregulation of Bcl-2. In addition, siBAK1 can reverse the pro-apoptosis function of miR-125a inhibitors in NPCs.Conclusion:miRNA-125a may regulate the apoptosis status of the NPCs by inhibiting the expression of its target gene BAK1, which provided a potential strategy for further development of IDD therapies.

MicroRNA‑96 regulates the proliferation of nucleus pulposus cells by targeting ARID2/AKT signaling.

The aberrant proliferation of nucleus pulposus (NP) cells has been reported to be implicated in the pathogenesis of intervertebral disc degeneration (IDD). Previous studies have demonstrated that microRNAs (miRNAs), which are a group of small noncoding RNAs, are critical regulators of cell proliferation in various pathologies. However, the role of miRNA‑96 (miR‑96) in the proliferation of NP cells remains to be determined. In the present study, reverse transcription‑quantitative polymerase chain reaction was used to investigate the expression of miR‑96 in NP tissues from patients with IDD and healthy tissues from patients with traumatic lumbar fracture as the control. A dual‑luciferase reporter assay was used to investigate whether AT‑rich interaction domain 2 (ARID2) may be a direct target gene for miR‑96. Furthermore, isolated NP cells from patients with IDD were transfected with miR‑96 mimics and ARID2‑targeting small interfering RNAs; cell proliferation, and the protein expression of Akt, phosphorylated Akt and ARID2 were examined, whereas the effects of an Akt inhibitor on NP cell proliferation were also evaluated. The present results demonstrated that miR‑96 expression was significantly upregulated in IDD samples, and the level of miR‑96 expression was positively associated with disc degeneration grade, which was evaluated by a modified Pfirrmann grading system. In addition, the current study identified ARID2 as a direct gene target of miR‑96. Furthermore, it was demonstrated that ARID2 mRNA expression was inversely correlated with the expression of miR‑96 in NP tissues. In addition, miR‑96 overexpression promoted NP cell proliferation and induced Akt phosphorylation, which led to increased cyclin D1 translation. Notably, overexpression of ARID2 or treatment with an Akt inhibitor decreased the effect of miR‑96 on NP cell proliferation. In conclusion, the results of the present study indicate that miR‑96 may promote the proliferation of human degenerated NP cells by targeting ARID2 via activation of the Akt pathway, and potentially serves as a therapeutic target for IDD.

Nonunion of Traumatic Lumbar Fracture: Case Report

Nonunion of flexion-distraction thoracolumbar fractures has few been described previously. The case report discussed a case of nonunion of traumatic lumbar fracture. A 30-year-old man suffered a traumatic L1-2 flexion-distraction fracture and no paraplegia. After complete bed rest 2 months, then hyperextension thoracolumbar cast 3 months, he still felt back pain when out-of-bed activity. X-ray images demonstrated the fracture was not united. At last, the patient underwent open reduction of the fracture nonunion and L1-2 posterior fusion using short segmental pedicle screw instrumentation with autogenous iliac crest graft. The patient gained an excellent functional restoration at 5 months after operation. This suggests that the disease entity may require surgical treatment as early as possible. Spinal fusion combined instrumentation fixation and bone graft may be the best treatment.

Lumbar corpectomy via retroperitoneal approach: a case series of 42 patients with traumatic lumbar fracture

INTRODUCTION: Epidural anesthesia has traditionally been considered the gold standard for pain control in patients with multiple rib fractures. And while it reduces pulmonary complications, pneumonia rates are still reported as high as 18%. Epidural anesthesia generally requires hospital resources such as a pain management team that are not always available. Additionally, polytrauma can often preclude the use of epidural anesthesia. Therefore, we sought to evaluate our institution’s pain control protocol for multiple rib fractures centered on infusion of low-dose ketamine. We hypothesize that ketamine is safe alternative to epidural pain management.

Transpedicular vertebral body augmentation reinforced with pedicle screw fixation in fresh traumatic A2 and A3 lumbar fractures: comparison between two devices and two bone cements

This retrospective study compares efficacy and safety of balloon kyphoplasty (BK) with calcium phosphate (Group A) versus KIVA implant with PMMA (Group B) reinforced with three vertebrae pedicle screw constructs for A2 and A3 single fresh non-osteoporotic lumbar (L1-L4) fractures in 38 consecutive age- and diagnosis-matched patient populations. Extracanal leakage of both low-viscosity PMMA and calcium phosphate (CP) as well as the following roentgenographic parameters: segmental kyphosis (SKA), anterior (AVBHr) and posterior (PVBHr) vertebral body height ratio, spinal canal encroachment (SCE) clearance, and functional outcome measures: VAS and SF-36, were recorded and compared between the two groups. All patients in both groups were followed for a minimum 26 (Group A) and 25 (Group B) months. Extracanal CP and PMMA leakage was observed in four (18%) and three (15%) vertebrae/patients of group A and B, respectively. Hybrid fixation improved AVBHr, SKA, SCE, but PVBHr only in group B. VAS and SF-36 improved postoperatively in the patients of both groups. Short-segment construct with the novel KIVA implant restored better than BK-fractured lumbar vertebral body, but this had no impact in functional outcome. Since there was no leakage difference between PMMA and calcium phosphate and no short-term adverse related to PMMA use were observed, we advice the use of PMMA in fresh traumatic lumbar fractures.