背景:椎体终板缺损通常与椎间盘退行性疾病有关,然而,它们与患者报告的症状的联系仍不清楚.COX-2和PGE-2因其在炎症和疼痛中的作用而闻名。EP-4受体参与疼痛信号传导。检查它们在椎体终板组织中的表达可以提供对下腰痛的病理机制的见解。
目的:探讨终板缺损与患者报告症状的关系,进一步阐明COX-2/PGE-2/EP-4轴在慢性下腰痛发病机制中的作用。
方法:回顾性研究患者样本:本研究共纳入71例接受单级L4/5或L5/S1改良椎板切除减压保留近端上椎板和经椎间孔腰椎椎间融合术的患者,包括18例诊断为腰椎间盘突出症的患者,19伴有退行性腰椎管狭窄症的腰椎间盘突出症,34例退行性腰椎滑脱.
方法:人口统计数据,Pfirrmann等级,修改更改,终板缺陷评分,背部和腿部疼痛的视觉模拟量表(VAS),术前Oswestry残疾指数(ODI),3个月和6个月随访,和终板组织切片中免疫阳性细胞(COX-2,PGE-2和EP-4)的百分比。
方法:根据腰椎MR终板形态将患者分为缺损组和非缺损组。所有术中终板标本立即用10%甲醛固定,3天后包埋在石蜡中用于组织切片。比较缺陷组和非缺陷组的结局指标。数据采用独立t检验和χ²检验进行分析。使用Pearson等级相关检验评估患者报告的症状与组中免疫阳性细胞百分比之间的相关性。使用正向逐步似然比方法的多变量逻辑回归模型来识别与终板缺陷独立相关的因素。
结果:缺陷组的年龄明显高于非缺陷组(52.5±7.7vs.57.2±9.1。P=0.024)。性别差异不显著,诊断,BMI,合并症,或两组之间的手术水平。缺损组患者的Modic改变(Ⅱ型/Ⅲ型)比非缺损组患者更常见(38.5%vs.11.1%,P<0.001),椎间盘退变(PfirrmannⅣ/Ⅴ级)也是如此(69.2%vs.33.3%,P<0.001)。缺陷组的VAS-Back明显较高(6.5±2.0vs.4.9±1.6,P<0.001)和ODI评分(62.9±10.7vs.45.2±14.8,P<0.001)比非缺陷组,而在术后3个月和6个月的随访中,两组之间没有显着差异。组织学上,缺损组的特征是终板组织切片中COX-2,PGE-2和EP-4的上调。在缺陷组和非缺陷组中,VAS-Back与COX-2的表达呈中度正相关(r=0.643;r=0.558,p均<0.001)。PGE-2(r=0.611;r=0.640,p均<0.001),和EP-4(r=0.643;r=0.563,p均<0.001)。多因素回归分析显示,COX-2阳性细胞百分比与终板缺损相关(OR=1.509,95CI[1.048~2.171],P=0.027),以及PGE-2阳性的百分比(OR=1.291,95CI[1.106~1.508],P=0.001)和EP-4阳性细胞(OR=1.284,95CI[1.048~2.171],P=0.003)。
结论:终板缺损患者的生活质量较差,更严重的椎间盘退变和Modic改变,并上调终板缺损患者软骨终板COX-2/PGE-2/EP-4轴表达。炎症因子可能显著促进终板缺损患者慢性下腰痛的发生和进展。因此影响患者报告的症状。
BACKGROUND: Vertebral endplate defects are often implicated in degenerative disc disorders, yet their connection to patient-reported symptoms remains unclear. COX-2 and PGE-2 are known for their roles in inflammation and pain, with EP-4 receptor involvement in pain signaling. Examining their expression in vertebral endplate tissues may provide insights into pathomechanism of low back pain.
OBJECTIVE: To investigate the association between endplate defects and patient-reported symptoms and to further clarify the role of the COX-2/PGE-2/EP-4 axis in the pathogenesis of chronic low back pain.
METHODS: Retrospective study.
METHODS: A total of 71 patients who had undergone single-level L4/5 or L5/S1 modified laminectomy decompression preserving proximal upper laminae and transforaminal lumbar interbody fusion surgery were included in this study, including 18 patients diagnosed with lumbar disc herniation, 19 with lumbar disc herniation accompanied by degenerative lumbar spinal stenosis, and 34 with degenerative spondylolisthesis.
METHODS: Demographic data, Pfirrmann grade, Modic changes, endplate defect score, visual analog scale (VAS) for back and leg pain, and Oswestry Disability Index (ODI) before surgery, 3-month and 6-month follow-up, and the percentage of immune-positive cells (COX-2, PGE-2, and EP-4) in endplate tissue sections.
METHODS: Patients were divided into defect and nondefect groups according to endplate morphology on lumbar MR. All intraoperative endplate specimens were immediately fixed in 10% formaldehyde, and then embedded in paraffin 3 days later for tissue sections. The outcome measures were compared between the defect group and nondefect group. Data were analyzed using independent t-tests and χ² tests. Pearson\'s rank correlation test was used to assess correlations between patient-reported symptoms and the percentage of immune-positive cells in the groups. Multivariable logistic regression models using the forward stepwise likelihood ratio method were used to identify the factors that were independently associated with endplate defects.
RESULTS: The age of Defect group was significantly higher than that of nondefect group (52.5±7.7 vs 57.2±9.1. p=.024). There were no significant differences in gender, diagnosis, BMI, comorbidities, or surgical level between the two groups. Modic changes (Type Ⅱ/Type Ⅲ) were more common in patients of Defect group than nondefect group (38.5% vs 11.1%, p<.001), and so was disc degeneration (Pfirrmann grade Ⅳ/Ⅴ) (69.2% vs 33.3%, p<.001). Defect group had significantly higher VAS-Back (6.5±2.0 vs 4.9±1.6, p<.001) and ODI scores (62.9±10.7 vs 45.2±14.8, p<.001) than nondefect group, while there was no significant differences between the two groups during the 3 and 6-month follow-up after surgery. Histologically, Defect group was characterized by upregulation of COX-2, PGE-2, and EP-4 in endplate tissue sections. Both in defect and nondefect groups, VAS-Back showed moderate positive correlations with the expressions of COX-2 (r=0.643; r=0.558, p both<.001), PGE-2 (r=0.611; r=0.640, p both<.001), and EP-4 (r=0.643; r=0.563, p both<.001). Multivariate regression analyses reveled that percentage of COX-2-positive cells was associated with endplate defects (OR=1.509, 95%CI [1.048-2.171], p=.027), as well as percentage of PGE-2-positive (OR=1.291, 95%CI [1.106-1.508], p=.001) and EP-4-positive cells (OR=1.284, 95%CI [1.048∼2.171], p=.003).
CONCLUSIONS: Patients with endplate defects had worse quality of life, more severe disc degeneration and Modic changes, and up-regulated COX-2/PGE-2/EP-4 axis expression in cartilage endplates in patients with defected endplates. Inflammatory factors may significantly contribute to the onset and progression of chronic low back pain in patients with endplate defects, consequently impacting patient-reported symptoms.