scholarly journals Validity and interobserver agreement of a new radiographic grading system for intervertebral disc degeneration: Part III. Thoracic spine

Author(s):  
Christian Liebsch ◽  
Youping Tao ◽  
Annette Kienle ◽  
Hans-Joachim Wilke

Abstract Purpose The aim of this study was to assess the validity and objectivity of a new quantitative radiographic grading system for thoracic intervertebral disc degeneration. Methods The new grading system involves the measurement variables “Height loss” and “Osteophyte formation”, which are determined from lateral radiographs, resulting in the “Overall degree of degeneration” on a four-point scale from 0 (no degeneration) to 3 (severe degeneration). Validation was performed by comparing the radiographic degrees of degeneration of 54 human intervertebral discs to the respective macroscopic degrees, which were defined as the “real” degrees of degeneration. Interobserver agreement was examined using radiographs of 135 human thoracic intervertebral discs. Agreement was quantified by means of quadratically weighted Kappa coefficients with 95% confidence limits (CL). Results Validation revealed almost perfect agreement between the radiographic and the macroscopic overall degrees of degeneration (Kappa 0.968, CL 0.944–0.991), while the macroscopic grades tended to be underestimated in low degeneration grades. Radiographic grading of two independent observers also exhibited almost perfect agreement (Kappa 0.883, CL 0.824–0.941) as well as tendencies towards rater-dependent differences in low degeneration grades. Conclusion The new quantitative radiographic grading scheme represents a valid, reliable, and almost objective method for assessing the degree of degeneration of individual thoracic intervertebral discs. Potential effects of interindividual variations and the radiographic superimposition of anatomical structures represent a limitation of this method should be taken into account when using the grading system for clinical and experimental purposes, especially with regard to specific morphological as well as patient- and donor-specific characteristics.

2005 ◽  
Vol 15 (6) ◽  
pp. 720-730 ◽  
Author(s):  
Hans-Joachim Wilke ◽  
Friederike Rohlmann ◽  
Cornelia Neidlinger-Wilke ◽  
Karin Werner ◽  
Lutz Claes ◽  
...  

2006 ◽  
Vol 15 (6) ◽  
pp. 731-731 ◽  
Author(s):  
Hans-Joachim Wilke ◽  
Friederike Rohlmann ◽  
Cornelia Neidlinger-Wilke ◽  
Karin Werner ◽  
Lutz Claes ◽  
...  

2006 ◽  
Vol 15 (6) ◽  
pp. 732-741 ◽  
Author(s):  
Annette Kettler ◽  
Friederike Rohlmann ◽  
Cornelia Neidlinger-Wilke ◽  
Karin Werner ◽  
Lutz Claes ◽  
...  

Spine ◽  
2007 ◽  
Vol 32 (24) ◽  
pp. E708-E712 ◽  
Author(s):  
James F. Griffith ◽  
Yi-Xiang J. Wang ◽  
Gregory E. Antonio ◽  
Kai Chow Choi ◽  
Alfred Yu ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Shaoyi Wang ◽  
Jianlu Wei ◽  
Jie Shi ◽  
Qiting He ◽  
Xiaocong Zhou ◽  
...  

Background. Inflammation plays an important role in intervertebral disc degeneration (IDD). The protein follistatin-like 1 (FSTL1) plays a proinflammatory role in a variety of inflammatory diseases. Objectives. The purpose of this study was to investigate whether IDD could be delayed by inhibiting FSTL-1 expression. Methods. We established a puncture-induced IDD model in wild-type and FSTL-1+/- mice and collected intervertebral discs (IVDs) from the mice. Safranin O staining was used to detect cartilage loss of IVD tissue, and HE staining was used to detect morphological changes of IVD tissue. We measured the expression of FSTL-1 and related inflammatory indicators in IVD tissues by immunohistochemical staining, real-time PCR, and Western blotting. Results. In the age-induced model of IDD, the level of FSTL-1 increased with the exacerbation of degeneration. In the puncture-induced IDD model, FSTL-1-knockdown mice showed a reduced degree of degeneration compared with that of wild-type mice. Further experiments showed that FSTL-1 knockdown also significantly reduced the level of related inflammatory factors in IVD. In vitro experiments showed that FSTL-1 knockdown significantly reduced TNF-α-induced inflammation. Specifically, the expression levels of the inflammatory factors COX-2, iNOS, MMP-13, and ADAMTS-5 were reduced. Knockdown of FSTL-1 attenuated inflammation by inhibiting the expression of P-Smad1/5/8, P-Erk1/2, and P-P65. Conclusion. Knockdown of FSTL-1 attenuated inflammation by inhibiting the TNF-α response and Smad pathway activity and ultimately delayed IDD.


2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Zhaohui Zhai ◽  
Zhaoxin Li ◽  
Zhonglei Ji ◽  
Xiaosheng Lu

Objective. Polygonatum sibiricum polysaccharide (PSP) has antioxidant activity, immune enhancement, and other biological properties. However, the effect of PSP on intervertebral disc degeneration has not been reported. In this study, we mainly investigated the effect of PSP on the apoptosis, inflammation, and oxidative stress of nucleus pulposus cells (NPCs) during the process of intervertebral disc degeneration. Methods. A rat NPC model induced by H2O2 was constructed. The CCK8 method was used to measure the effects of PSP on the apoptosis of rat NPCs induced by H2O2. The effects on the activity of SOD and content of MDA were also determined. The rat model of intervertebral disc degeneration was treated with PSP for 1 month, and the mRNA expression levels of IL-1β, COX2, iNOS, Col2α1, Col10α1, and MMP3 were measured by qPCR in the tissue of intervertebral disc. NPCs from the degenerated intervertebral discs were separated, and the cell viability was measured by the CCK8 method. The contents of SOD and MDA in NPCs were determined as well. Results. PSP significantly reduced the apoptosis of NPCs induced by H2O2, significantly increased the SOD content, and decreased the content of MDA in H2O2-induced NPCs. The expression level of IL-1β, COX2, and iNOS in the rat model with intervertebral disc degeneration was significantly downregulated after 1 month of PSP treatment. PSP treatment increased the expression of Col2α1 type and significantly decreased the expression of Col10α1 type collagen and MMP3 in rats with disc degeneration. PSP treatment significantly reduced NPC apoptosis and increased its SOD content and reduced MDA content, which is consistent with the results from cell-level experiments. Conclusion. PSP can effectively reduce the apoptosis, inflammation, and oxidative stress of H2O2-induced NPCs in rats with intervertebral disc degeneration and mitigate the progression of intervertebral disc degeneration, which has the potential to be developed as new drugs for the treatment of intervertebral disc degeneration.


2018 ◽  
Vol 2018 ◽  
pp. 1-12 ◽  
Author(s):  
Yazhou Lin ◽  
Guoqing Tang ◽  
Yucheng Jiao ◽  
Ye Yuan ◽  
Yuehuan Zheng ◽  
...  

Accumulating evidence suggests that Propionibacterium acnes (P. acnes) is a novel pathogenic factor promoting intervertebral disc degeneration (IVDD). However, the underlying mechanisms by which P. acnes induces IVDD have been unclear. In this study, we quantified the severity of IVDD, as well as the expressions of inducible nitric oxide synthase (iNOS)/nitric oxide (NO) and cyclooxygenase (COX-2)/prostaglandin (PGE2) in human intervertebral discs (IVDs) infected with P. acnes. Compared with P. acnes-negative IVDs, P. acnes-positive IVDs showed increased iNOS/NO and COX-2/PGE2 activity concomitant with more severe IVDD. In order to detect the potential correlation between iNOS/NO expression, COX-2/PGE2 expression, and IVDD, we developed a P. acnes-induced IVDD rat model and found that the upregulation of iNOS/NO and COX-2/PGE2 was essential to the occurrence of P. acnes-induced IVDD. This finding was supported by the fact that the inhibition of iNOS/NO and COX-2/PGE2 activity ameliorated IVDD significantly, as evidenced by restored aggrecan and collagen II expression both in vivo and in vitro. Mechanistically, we found that P. acnes induced iNOS/NO and COX-2/PGE2 expressions via a reactive oxygen species- (ROS-) dependent NF-κB cascade. Furthermore, NADPH oxidase participated in P. acnes-induced ROS, iNOS/NO, and COX-2/PGE2 expressions. Overall, these findings further validated the involvement of P. acnes in the pathology of IVDD and provided evidence that P. acnes-induced iNOS/NO and COX-2/PGE2 activation via the ROS-dependent NF-κB pathway is likely responsible for the pathology of IVDD.


Author(s):  
Yu Song ◽  
Saideng Lu ◽  
Wen Geng ◽  
Xiaobo Feng ◽  
Rongjin Luo ◽  
...  

AbstractIntervertebral disc degeneration (IDD) is a common and early-onset pathogenesis in the human lifespan that can increase the risk of low back pain. More clarification of the molecular mechanisms associated with the onset and progression of IDD is likely to help establish novel preventive and therapeutic strategies. Recently, mitochondria have been increasingly recognized as participants in regulating glycolytic metabolism, which has historically been regarded as the main metabolic pathway in intervertebral discs due to their avascular properties. Indeed, mitochondrial structural and functional disruption has been observed in degenerated nucleus pulposus (NP) cells and intervertebral discs. Multilevel and well-orchestrated strategies, namely, mitochondrial quality control (MQC), are involved in the maintenance of mitochondrial integrity, mitochondrial proteostasis, the mitochondrial antioxidant system, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis. Here, we address the key evidence and current knowledge of the role of mitochondrial function in the IDD process and consider how MQC strategies contribute to the protective and detrimental properties of mitochondria in NP cell function. The relevant potential therapeutic treatments targeting MQC for IDD intervention are also summarized. Further clarification of the functional and synergistic mechanisms among MQC mechanisms may provide useful clues for use in developing novel IDD treatments.


Sign in / Sign up

Export Citation Format

Share Document