细胞因子IL-1a、IL -6、TNF-a、MMP3与颈椎间盘退变机制的相关性研究

[目的]探讨细胞因子在颈椎间盘退变机制中的作用及其与神经功能的相关性.[方法]实验组椎间盘组织取自46例颈椎病患者,根据术前颈椎MRI及术中椎间盘突出情况分为两组:退变组(24例)和突出组(22例).对照组椎间盘组织取自15例无颈椎病病史的颈椎外伤患者.根据颈椎病患者术前JOA评分分为三组:轻度组(17例),中度组(15例)和重度组(14例).采用酶联免疫吸附法(ELISA法)分别检测不同退变程度颈椎间盘中IL-1a、IL -6、TNF -a和MMP3的表达水平.[结果]对照组、退变组和突出组三组之间比较,IL -1a、IL -6、TNF-a和MMP3的表达有统计学意义(P＜0.05),其表达水平与颈椎间盘退变呈正相关趋势;轻度组、中度组和重度组三组之间比较,MMP3、TNF -a的表达有统计学意义(P＜0.05),其表达水平与JOA评分呈负相关趋势.[结论]IL -1、IL -6、TNF -a和MMP3与颈椎间盘退变密切相关,其表达水平与椎间盘退变呈正相关趋势;TNF -a与神经功能有关,可能在神经损伤中起主导作用;MMP3与椎间盘突出有关,对TNF -a的神经功能损伤可能起促进作用.     

Autologous fibroblasts induce fibrosis of the nucleus pulposus to maintain the stability of degenerative intervertebral discs

Lumbar degenerative disc diseases cause low back pain(LBP). The maintenance of the height and stability of the intervertebral disc(IVD) space is an effective treatment for LBP. The following study evaluated the effects of fibroblast injection on intervertebral disc degeneration(IDD) in a preclinical setting. Compared with the IDD group, the fibroblast treatment group demonstrated effective maintenance of IVD height, reduced endplate degeneration, and improved nuclear magnetic resonance signals and overall histological structure. In doing so, fibrotic IVDs maintained the stability and biomechanics of the vertebra. This finding is in agreement with clinical findings that human nucleus pulposus(NP) fibrosis is essential for the maintenance of IVD height and mechanical properties in patients following percutaneous endoscopic lumbar discectomy(PELD). Mechanistically, we demonstrated that injected fibroblasts not only proliferated but also induced NP cells to adopt a fibrotic phenotype via the secretion of TGF-β.Finally, to better mimic human conditions, the efficacy of autologous fibroblast injection in the treatment of IDD was further examined in a nonhuman primate cynomolgus monkey model due to their capacity for upright posture. We showed that the injection of fibroblasts could maintain the IVD height and rescue IVD signals in cynomolgus monkeys. Taken together, the results of our study reveal that autologous fibroblast injection can enhance the natural process of fibrosis during acute and subacute stages of stress-induced IDD. Fibrotic IVDs can maintain the stability, biological activity, and mechanical properties of the intervertebral space, thus providing a new direction for the treatment of intervertebral space-derived lumbar degenerative diseases.     

Joint analysis of IVD herniation and degeneration by rat caudal needle puncture model

Intervertebral disc (IVD) degeneration is responsible for various spine pathologies and present clinical treatments are insufficient. Concurrently, the mechanisms behind IVD degeneration are still not completely understood, so as to allow development of efficient tissue engineering approaches. A model of rat IVD degeneration directly coupled to herniation is here proposed in a pilot study. Disc injury is induced by needle puncture, using two different needles gauges: a low caliber 25‐G needle and a high caliber 21‐G needle. Histological, biochemical, and radiographic degeneration was evaluated at 2 and 6 weeks post‐injury. We show that the larger caliber needle results in a more extended histological and radiographic degeneration within the IVD, compared to the smaller one. TUNEL quantification indicates also increased cell death in the 21‐G group. Analyses of collagen type I (Picrosirius red staining), collagen type II (immunofluorescence), and GAG content (Blyscan assay) indicate that degeneration features spontaneously recover from 2 to 6 weeks, for both needle types. Moreover, we show the occurrence of hernia proportional to the needle gauge. The number of CD68+ macrophages present, as well as cell apoptosis within the herniated tissue are both proportional to hernia volume. Moreover, hernias formed after lesion tend to spontaneously diminish in volume after 6 weeks. Finally, MMP3 is increased in the hernia in the 21‐G group at 2 weeks. This model, by uniquely combining IVD degeneration and IVD herniation in the same animal, may help to understand mechanisms behind IVD pathophysiology, such as hernia formation and spontaneous regression. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 35:258–268, 2017.

     

Functional Self‐Assembled Peptide Nanofibers for Bone Marrow Mesenchymal Stem Cell Encapsulation and Regeneration in Nucleus Pulposus

Low back pain (LBP) is mainly caused by intervertebral disc degeneration (IDD). Recent studies have demonstrated that the transplantation of mesenchymal stem cells (MSCs) can regenerate regions that have undergone degeneration, and the regenerative effect can be enhanced by using a hydrogel carrier. This article describes an injectable functional hydrogel system manufactured by combining RADA16‐I and RADA‐KPSS (RADA‐KPSS was manufactured by conjugating a bioactive motif derived from BMP‐7 [KPSS] onto the C terminal of RADA16‐I) at a volume ratio of 1:1. This hydrogel system can enhance the proliferation, differentiation, and chemotactic migration of BMSCs. In addition, the encapsulation of BMSCs with this system maintains cell viability for a long period after transplantation into an ex vivo cultured disc model. In conclusion, KPSS‐conjugated RADKPS is an ideal encapsulation system for BMSCs in intervertebral disc (IVD) regeneration.     

The Mechanisms and Functions of GDF‐5 in Intervertebral Disc Degeneration

Intervertebral disc degeneration (IDD) is widely recognized as the main cause of low back pain, which leads to disability in aging populations and induces great losses both socially and economically worldwide. Unfortunately, current treatments for IDD are aimed at relieving symptoms instead of preserving disc structure and function. Researchers are forged to find new promising biological therapeutics to stop, and even reverse, IVD degeneration. Recently, the injection of growth factors has been shown to be a promising biological therapy for IDD. A number of growth factors have been investigated to modulate the synthesis of the extracellular matrix (ECM) through a variety of pathogenetic biological mechanisms, including suppressing inflammatory process and down‐regulating degrading enzymes. However, growth factors, including Transforming Growth Factor‐β (TGF‐β), Fibroblast Growth Factor (FGF), and Insulin‐like Growth Factor‐1 (IGF‐1), may induce unwanted blood vessel in‐growth, which accelerates the process of IDD. On the contrary, studies have demonstrated that injection of GDF‐5 into the intervertebral disc of mice can effectively alleviate the degeneration of the intervertebral disc, which elicits their response via BMPRII and will not induce blood vessel in‐growth. This finding suggests that GDF‐5 is more suitable for use in IDD treatment compared with the three other growth factors. Substantial evidence has suggested that GDF‐5 may maintain the structure and function of the intervertebral disc (IVD). GDF‐5 plays an important role in IDD and is a very promising therapeutic agent for IDD. This review is focused on the mechanisms and functions of GDF‐5 in IDD.     

Treatment of Intervertebral Disc Degeneration

Intervertebral disc degeneration (IDD) causes a variety of signs and symptoms, such as low back pain (LBP), intervertebral disc herniation, and spinal stenosis, which contribute to high social and economic costs. IDD results from many factors, including genetic factors, aging, mechanical injury, malnutrition, and so on. The pathological changes of IDD are mainly composed of the senescence and apoptosis of nucleus pulposus cells (NPCs), the progressive degeneration of extracellular matrix (ECM), the fibrosis of annulus fibrosus (AF), and the inflammatory response. At present, IDD can be treated by conservative treatment and surgical treatment based on patients'' symptoms. However, all of these can only release the pain but cannot reverse IDD and reconstruct the mechanical function of the spine. The latest research is moving towards the field of biotherapy. Mesenchymal stem cells (MSCs) are regard as the potential therapy of IDD because of their ability to self‐renew and differentiate into a variety of tissues. Moreover, the non‐coding RNAs (ncRNAs) are found to regulate many vital processes in IDD. There have been many successes in the in vitro and animal studies of using biotherapy to treat IDD, but how to transform the experimental data to real therapy which can apply to humans is still a challenge. This article mainly reviews the treatment strategies and research progress of IDD and indicates that there are many problems that need to be solved if the new biotherapy is to be applied to clinical treatment of IDD. This will provide reference and guidance for clinical treatment and research direction of IDD.     

非手术治疗无骨折脱位型颈脊髓损伤预后的多因素分析

目的 :探讨影响非手术治疗无骨折脱位型颈脊髓损伤预后的因素。方法 :回顾性分析2009年1月至2012年12月接受非手术治疗的122例无骨折脱位型颈脊髓损伤患者的临床资料,其中男84例,女38例;平均年龄(52.37±13.27)岁(18~83岁)。选择年龄、性别、受伤原因、受伤至治疗时间、脊髓损伤ASIA分级、MRI脊髓损伤类型、脊髓损伤范围、有效颈椎管率、椎间盘突出Pfirrmann分级、椎间盘突出节段、椎间盘韧带复合体损伤、大剂量甲基强的松龙冲击治疗12个可能对非手术治疗预后产生影响的因素,应用单因素和多因素Logistic回归分析,研究其对预后的影响。结果:单因素分析显示MRI脊髓损伤类型、脊髓损伤范围、有效颈椎管率、椎间盘突出Pfirrmann分级、椎间盘突出节段及脊髓损伤ASIA分级均对预后有显著影响(P均0.05)。进一步行多因素分析,按照其作用强度,影响预后的主要因素依次为:MRI脊髓损伤类型、脊髓损伤范围、有效颈椎管率、椎间盘突出Pfirrmann分级、脊髓损伤ASIA分级(P均0.05)。结论 :影响非手术治疗无骨折脱位型颈脊髓损伤预后的主要因素是MRI脊髓损伤类型及范围,同时与有效椎管率、椎间盘突出程度及脊髓损伤ASIA分级相关。对于选择非手术治疗需谨慎,仅适用MRI检查提示脊髓信号无改变或水肿程度轻且范围局限者,其余则建议积极手术治疗。     

Long-term histological analysis of innervation and macrophage infiltration in a mouse model of intervertebral disc injury–induced low back pain

Low back pain (LBP) is a leading cause of global disability. Multiple anatomical, cellular, and molecular factors are implicated in LBP, including the degeneration of lumbar intervertebral discs (IVDs). We previously described a mouse model that displays behavioral symptoms of chronic LBP. Here, we investigated the development of pathological innervation and macrophage infiltration into injured IVDs following a puncture injury in mice over 12 months. 2-month old CD1 female mice underwent a single puncture of the ventral L4/5 IVD using a 30G needle, and were sacrificed 4 days and 0.5-, 3-, 6- and 12-months post-injury. Severity of disc degeneration was assessed using colorimetric staining. IVD innervation was measured by PGP9.5-immunoreactivity (-ir) and calcitonin gene-related peptide-ir (CGRP-ir). Macrophage accumulation into IVDs was detected by F4/80-ir. Mechanical IVD injury resulted in severe degeneration and increased PGP9.5-ir nerve fiber density starting at 4 days that persisted for up to 12 months and dorsal herniations began to occur at 3 months. CGRP-ir was also upregulated in injured IVDs, with the largest increase at 12 months after injury. Infiltration of F4/80-ir macrophages was observed in injured IVDs by day 4 both dorsally and ventrally, with the latter diminishing in the later stage. Persistent LBP is a complex disease with multiple underlying pathologies. By highlighting pathological changes in IVD innervation and inflammation, our study suggests that strategies targeting these mechanisms might be useful therapeutically.     

Needle puncture injury of the rat intervertebral disc affects torsional and compressive biomechanics differently

Needle puncture is a common method of inducing intervertebral disc (IVD) degeneration in small animal models and may have some similarities to IVD injury conditions such as herniation. Yet, the influence of puncture injuries on IVD biomechanics is not well understood. This study quantified the acute effects of anular injury on the biomechanics of rat caudal IVDs in compression and torsion following puncture with 30, 25 and 21 G needles. In compression, puncture injury reduced elastic stiffness by 20% for all needle sizes, but differences between control and punctured discs did not remain after compressive overload. In contrast, torsional parameters associated with anular fiber tension were affected proportionally with needle size. We conclude that IVD injuries that penetrate through the thickness of the annulus affect IVD biomechanics through different mechanisms for compression and torsion. Anular injuries affect torsional properties in a manner directly related to the amount of fiber disruption and compressive properties in a manner that affects pressurization.     

Galectins‐1 and ‐3 in Human Intervertebral Disc Degeneration: Non‐Uniform Distribution Profiles and Activation of Disease Markers Involving NF‐κB by Galectin‐1

Degeneration of the human intervertebral disc (IVD) is assumed to underlie severe clinical symptoms, in particular chronic back pain. Since adhesion/growth‐regulatory galectins are linked to arthritis/osteoarthritis pathogenesis by activating a pro‐degradative/‐inflammatory gene expression signature, we hypothesized a similar functional involvement of galectins in IVD degeneration. Immunohistochemical evidence for the presence of galectins‐1 and ‐3 in IVD is provided comparatively for specimens of spondylochondrosis, spondylolisthesis, and spinal deformity. Immunopositivity was detected in sections of fixed IVD specimens in each cellular compartment with age‐, disease‐, and galectin‐type‐related differences. Of note, presence of both galectins correlated with IVD degeneration, whereas correlation with age was seen only for galectin‐3. In addition, staining profiles for these two galectins showed different distribution patterns in serial sections, an indication for non‐redundant functionalities. In vitro, both galectins bound to IVD cells in a glycan‐dependent manner. However, exclusively galectin‐1 binding triggered a significant induction of functional disease markers (i.e., IL6, CXCL8, and MMP1/3/13) with involvement of the nuclear factor‐kB pathway. This study thus gives direction to further network analyses and functional studies on galectins in IVD degeneration. © 2019 The Authors. Journal of Orthopaedic Research® published by Wiley Periodicals, Inc. on behalf of Orthopaedic Research Society. J Orthop Res 37:2204–2216, 2019     

The Effects of Platelet‐Rich Plasma on Halting the Progression in Porcine Intervertebral Disc Degeneration

Disc degeneration and the subsequent herniation and/or rupture of the intervertebral disc (IVD) are due to a failure of the extracellular matrix of the annulus to contain the contents of the nucleus. This results from inadequate maintenance of the matrix components as well as the proteolytic activity of matrix metalloproteinases (MMPs) that degrade matrix molecules. Arresting progression of disc degeneration in the annulus holds greater clinical potential at this point than prevention of its onset in the nucleus. Therefore, in this study, we have therapeutic aims that would decrease levels of the cytokines and growth factors that indirectly lead to disc degeneration via stimulating MMP and increase levels of several beneficial growth factors, such as transforming growth factor‐β, with the addition of platelet‐rich plasma (PRP) that would stimulate cell growth and matrix synthesis. For this study, we attempted to address these imbalances of metabolism by using tumor necrosis factor‐α treated annulus fibrosus cells isolated from porcine IVD tissue and incubating the cells in a growth factor rich environment with PRP. These results indicate that the PRP in vitro increased the production of the major matrix components (type II collagen and aggrecan) and decreased the inhibitory collagenase MMP‐1. This application will address a therapeutic approach for intervening early in the degenerative process.     

Age‐related spontaneous lumbar intervertebral disc degeneration in a mouse model

The pathogenesis of intervertebral disc degeneration is unclear, but it is a major cause of several spinal diseases. Animal models have historically provided an appropriate benchmark for understanding the human spine. However, there is little information about when intervertebral disc degeneration begins in the mouse or regarding the relationship between magnetic resonance imaging and histological findings. The aim for this study was to obtain information about age‐related spontaneous intervertebral disc degeneration in the mouse lumbar spine using magnetic resonance imaging and a histological score regarding when the intervertebral disc degeneration started and how rapidly it progressed, as well as how our histological score detected the degeneration. The magnetic resonance imaging index yielded a moderate correlation with our Age‐related model score. The Pfirrmann grade and magnetic resonance imaging index had moderate correlations with age. However, our Age‐related model score had a high correlation with age. Intervertebral disc level was not a significant variable for the severity of disc degeneration. Both Pfirrmann grade and the Age‐related model score were higher in the ≥14‐month‐old group than in the 6‐month‐old group. The present results indicated that mild but significant intervertebral disc degeneration occurred in 14‐month‐old mice, and the degree of degeneration progressed slowly, reaching a moderate to severe condition for 22‐month‐old mice. At least a 14‐month follow‐up is mandatory for evaluating spontaneous age‐related mouse intervertebral disc degeneration. The histological classification score can precisely detect the gradual progression of age‐related spontaneous intervertebral disc degeneration in the mouse lumbar spine, and is appropriate for evaluating it. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:224–232, 2018.     

NF-κB inhibitor,NEMO-binding domain peptide attenuates intervertebral disc degeneration

BACKGROUND CONTEXTNonphysiological mechanical loading and inflammation are both critically involved in intervertebral disc (IVD) degeneration, which is characterized by an increase in cytokines and matrix metalloproteases (MMPs) in the nucleus pulposus (NP). This process is known to be mediated by the NF-κB pathway.CLINICAL SIGNIFICANCECurrent clinical treatments for IVD degeneration focus on the alleviation of symptoms rather than targeting the underlying mechanism. Injection of an NF-κB inhibitor may attenuate the progression of IVD degeneration.PURPOSETo investigate the ability of the NF-κB inhibitor, NEMO binding domain peptide (NBD), to alter IVD degeneration processes by reducing IL-1β- and mechanically-induced cytokine and MMP levels in human nucleus pulposus cells in vitro, and by attenuating IVD degeneration in an in vivo rat model for disc degeneration.STUDY DESIGNExperimental in vitro and animal model.PATIENT SAMPLEDiscarded specimens of lumbar disc from 21 patients, and 12 Sprague Dawley rats.OUTCOME MEASURESGene and protein expression, cell viability, µMRI and histology.METHODSIL-1β-prestimulated human nucleus pulposus cells embedded into fibrin constructs were loaded in the Flexcell FX-5000 compression system at 5 kPa and 1 Hz for 48 hours in the presence and absence of NBD. Unloaded hNPC/fibrin constructs served as controls. Cell viability in loaded and unloaded constructs was quantified, and gene and protein expression levels determined. For in vivo testing, a rat needle disc puncture model was employed. Experimental groups included injured discs with and without NBD injection and uninjured controls. Levels of disc degeneration were determined via µMRI, qPCR and histology. Funding sources include $48,874 NASS Young Investigator Research Grant and $119,174 NIH 5K01AR071512-02. There were no applicable financial relationships or conflicts of interest.RESULTSMechanical compression of hNPC/fibrin constructs resulted in upregulation of MMP-3 and IL-8. Supplementation of media with 10 μM NBD during loading increased cell viability, and decreased MMP-3 gene and protein levels. IVD injury in rat resulted in an increase in MMP-3, IL-1β and IL-6 gene expression. Injections of 250 µg of NBD during disc injury resulted in decreased IL-6 gene expression. µMRI analysis demonstrated a reduction of disc hydration in response to disc needle injury, which was attenuated in NBD-treated IVDs. Histological evaluation showed NP and AF lesion in injured discs, which was attenuated by NBD injection.CONCLUSIONSThe results of this study show NBD peptide's capacity to reduce IL-1β- and loading-induced MMP-3 levels in hNPC/fibrin constructs while increasing the cells’ viability, and to attenuate IVD degeneration in rat, involving downregulation of IL-6. Therefore, NBD may be a potential therapeutic agent to treat IVD degeneration.     

极外侧型腰椎间盘突出症的诊治

目的了解极外侧型腰椎间盘突出症的诊断方法及治疗效果。方法 手术治疗经ＣＴ诊断的４例极外侧型腰椎间盘突出症。结果 ４例患者经６个月－４年随访效果优良。结论极外侧腰椎间盘突出症以ＣＴ扫描确诊率较高，一经确诊，手术治疗为首选。     

Disc degeneration of cervical spine on MRI in patients with lumbar disc herniation: comparison study with asymptomatic volunteers

An association between progression of cervical disc degeneration and that of lumbar disc degeneration has been considered to exist. To date, however, this association has not yet been adequately studied. Age-related changes in the cervical intervertebral discs were evaluated by magnetic resonance imaging (MRI) in patients with lumbar disc herniation, and compared with the MRI findings of healthy volunteers without lower back pain. The purpose of this study was to clarify whether the prevalence of asymptomatic cervical disc degeneration is higher in patients with lumbar disc herniation than in healthy volunteers. The study was conducted on 51 patients who were diagnosed as having lumbar disc herniation and underwent cervical spine MRI. The patients consisted of 34 males and 17 females ranging in age from 21–83 years (mean 46.9 ± 14.5 years) at the time of the study. The control group was composed of 113 healthy volunteers (70 males and 43 females) aged 24–77 years (mean 48.9 ± 14.7 years), without neck pain or low back pain. The percentage of subjects with degenerative changes in the cervical discs was 98.0% in the lumbar disc herniation group and 88.5% in the control group (p = 0.034). The presence of lumbar disc herniation was associated significantly with decrease in signal intensity of intervertebral disc and posterior disc protrusion in the cervical spine. None of the MRI findings was significantly associated with the gender, smoking, sports activities, or BMI. As compared to healthy volunteers, patients with lumbar disc herniation showed a higher prevalence of decrease in signal intensity of intervertebral disc and posterior disc protrusion on MRI of the cervical spine. The result of this study suggests that disc degeneration appears to be a systemic phenomenon.     

Interleukin‐6 and interleukin‐6 receptor expression,localization, and involvement in pain‐sensing neuron activation in a mouse intervertebral disc injury model

The pathological mechanism of intractable low back pain is unclear. However, intervertebral disc (IVD) degeneration is a primary cause of low back pain, and pain‐related mediators, such as interleukin‐6 (IL‐6), have been correlated with discogenic pain. The objective of this study is to elucidate the mechanism of local IL‐6 and IL‐6 receptor (IL‐6R) expression after IVD injury as well as determine the involvement of IL‐6/IL‐6 signaling in discogenic pain. To do this, quantitative and immunohistological analyses in a mouse model of IVD injury were performed. Firstly, we measured the local expression levels of IL‐6 and IL‐6R in IVDs by enzyme‐linked immunosorbent assay (ELISA). Secondly, we immunohistochemically confirmed their localization in injured IVDs. Lastly, we evaluated the effects of intradiscal injection of an IL‐6 inhibitor by evaluating pain‐related protein, calcitonin gene‐related peptide (CGRP), expression in dorsal root ganglia (DRG) neurons that innervate IVDs. Injured IVDs showed increased production of IL‐6 and IL‐6R. IL‐6 and IL‐6R expression in the injured IVD were predominantly localized in the annulus fibrosus and endplate, and intradiscal injection of the IL‐6 inhibitor suppressed CGRP expression in the DRG neurons. These results show that IL‐6 and IL‐6R expression levels are responsive to IVD injury and that inhibition of IL‐6/IL‐6R signaling may be a promising analgesic treatment for degenerative disc diseases. © 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 33:1508–1514, 2015.     

Use of Allogeneic Hypoxic Mesenchymal Stem Cells For Treating Disc Degeneration in Rabbits

Intervertebral discs (IVDs) are important biomechanical components of the spine. Once degenerated, mesenchymal stem cell (MSC)‐based therapies may aid in the repair of these discs. Although hypoxic preconditioning enhances the chondrogenic potential of MSCs, it is unknown whether bone marrow MSCs expanded under hypoxic conditions (1% O₂, here referred to as hypoxic MSCs) are better than bone marrow MSCs expanded under normoxic conditions (air, here referred to as normoxic MSCs) with regards to disc regeneration capacity. The purpose of this study was to compare the therapeutic effects of hypoxic and normoxic MSCs in a rabbit needle puncture degenerated disc model after intra‐disc injection. Six weeks after needle puncture, MSCs were injected into the IVD. A vehicle‐treated group and an un‐punctured sham‐control group were included as controls. The tissues were analyzed by histological and immunohistochemical methods 6 and 12 weeks post‐injection. At 6 and 12 weeks, less disc space narrowing was evident in the hypoxic MSC‐treated group compared to the normoxic MSC‐treated group. Significantly better histological scores were observed in the hypoxic MSC group. Discs treated with hypoxic MSCs also demonstrated significantly better extracellular matrix deposition in type II and XI collagen. Increased CD105 and BMP‐7 expression were also observed upon injection of hypoxic MSCs. In conclusion, hypoxic MSC injection was more effective than normoxic MSC injection for reducing IVD degeneration progression in vivo. © 2019 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 37:1440–1450, 2019.     

椎间盘疝入胸腰段骨折椎体导致骨折畸形愈合及椎间隙高度下降

目的：分析损伤且疝入胸腰段骨折椎体的椎间盘组织对骨折愈合、椎体骨缺损体积变化及椎间隙高度影响的临床特点。方法：自2016年4月至2020年4月，行椎弓根钉棒系统复位内固定治疗140例胸腰段单椎体骨折合并上邻椎间盘损伤患者，男83例，女57例，年龄19~58（39.33±10.26）岁。术后6、12、18个月定期门诊复诊随访。损伤椎间盘组织未疝入骨折椎体患者为对照组，椎间盘损伤且疝入骨折椎体患者为观察组。通过不同回访时间下胸腰段正侧位X线片、CT及MRI扫描图像，分析计算骨折椎体楔变角、矢状位后凸角和上邻椎间隙高度变化，椎体复位后骨折愈合及骨缺损体积的变化以及椎间盘退变等级变化；并通过视觉模拟评分（visual analogue scale，VAS）、日常生活功能障碍指数（Oswestry disability index，ODI）评估患者预后；最后综合分析不同组别之间上述结果的差异性。结果：所有患者术后伤口正常愈合，无并发症发生。共87例患者获得完整回访资料，至少回访至内固定术后18个月。胸腰段正侧位X线发现观察组患者在复位内固定手术18个月后，椎体楔变角、矢状位后凸角增加及上邻椎间隙高度下降均大于对照组（P<0.05）。CT扫描发现观察组患者椎体复位术后12个月骨折畸形愈合并形成与椎间隙相通的骨缺损"空腔"，且其体积较前明显增大（P<0.05）。MRI扫描发现术后12个月观察组损伤椎间盘退变率较对照组严重且差异具有统计学意义（P<0.05）。但各时间下腰背部疼痛VAS及ODI差异无统计学意义。结论：损伤椎间盘组织疝入骨折椎体，使骨折周围骨质吸收骨缺损体积增大，形成与椎间隙相通的畸形愈合"空腔"，这可能是内固定装置去除后椎体楔变角、矢状面后凸角增加和椎间隙高度下降的主要原因。