Evidence update-association between CILP and degeneration of the intervertebral disc: a meta-analysis.
Ontology highlight
ABSTRACT:
SUBMITTER: Campbell RJ
PROVIDER: S-EPMC5067264 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Background: The relationship between CILP (1184T>C) and IL-1α(+889C/T) polymorphisms and intervertebral disc degeneration (IDD) have been explored in several studies but the results were conflicting. The aim of the study was to evaluate and synthesize the currently available data on the association between CILP (1184T>C) and IL-1α(+889C/T) polymorphisms and susceptibility of phenotype-dependent radiologic IDD (RIDD) and symptomatic intervertebral disk herniation (SIDH). Methods: A computerized literature search was in PubMed, Cochrane Library, Embase, China National Knowledge Infrastructure database, and Web of Science. The pooled results were presented as odds ratios (ORs) with 95% confidence intervals (CIs). Moreover, the false-positive report probability (FPRP) test and trial sequential analysis (TSA) were applied to estimate the significant results. Results: Our evidence demonstrated that IL-1α(+889C/T) was significant associated with RIDD (allele model: OR = 1.34, 95%CI 1.03-1.74, p = 0.029) and SIDH (allele model: OR = 1.28, 95% CI 1.03-1.60, p = 0.028). However, the results were not noteworthy under the FPRP test and TSA analysis. Additionally, CILP (1184T>C) polymorphism was significantly associated with RIDD with adequate evidence (allele model: OR = 1.27, 95% CI 1.09-1.48, p = 0.002) instead of SIDH. Conclusion: The current meta-analysis illustrated firm evidence that CILP (1184T>C) polymorphism was significantly associated with the susceptibility of RIDD. However, the significant associations between IL-1α(+889C/T) and RIDD and SIDH were less credible. Thus, more multi-center studies with diverse populations were required to verify the results.
| S-EPMC9582649 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-04-05 | GSE230809 | GEO
Project description:STUDY DESIGN:Meta-analysis to collect all the relevant studies to further investigate whether or not the FAS ligand (FASL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) genetic polymorphisms are associated with susceptibility to intervertebral disc degeneration (IDD) in Chinese Han population. OBJECTIVE:To investigate whether or not the FASL and TRAIL genetic polymorphisms are associated with susceptibility to IDD in Chinese Han population. SUMMARY OF BACKGROUND DATA:FASL and TRAIL are both apoptotic gene. Several studies have assessed the associations of FASL and TRAIL gene with risk of IDD in Chinese Han population, but the results are inconsistent. METHODS:We systematically searched the PubMed, EMBASE, Medline, Scopus, Web of Science, CBM, and the Cochrane Library databases. Eligible studies assessing the polymorphisms in the FASL and TRAIL gene and risk of IDD were incorporated. The pooled odds ratio (OR) with its 95% confidence intervals (95% CI) was used. RESULTS:Six studies with a total of 1766 IDD cases and 1533 controls were finally included in the meta-analysis. Meta-analysis of FASL-844C/T (rs763110) polymorphism was statistically associated with decreased IDD risk under all genetic models (allele model: OR?=?0.68, 95% CI 0.59-0.80, P?=?0.000; homozygote model: OR?=?0.35, 95% CI 0.25-0.53, P?=?0.000; dominant model: OR?=?0.38, 95% CI 0.25-0.58, P?=?0.000; recessive model: OR?=?0.69, 95% CI 0.58-0.84, P?=?0.000). There was a significant association between TRAIL-1595C/T (rs1131580) polymorphism with increased IDD risk under each genetic model (allele model: OR?=?1.77, 95% CI 1.47-2.13, P?=?0.000; homozygote model: OR?=?2.44, 95% CI 1.70-3.51, P?=?0.000; dominant model: OR?=?1.67, 95% CI 1.22-2.29, P?=?0.002; recessive model: OR?=?3.13, 95% CI 2.40-4.08, P?=?0.000). In addition, the association between TRAIL-1525G/A (rs1131568) polymorphism and the susceptibility of IDD was statistically significant under all genetic models. CONCLUSION:The present meta-analysis demonstrated that FASL and TRAIL polymorphisms were significantly associated with susceptibility to IDD in Chinese Han population. LEVEL OF EVIDENCE:1.
| S-EPMC6250249 | biostudies-literature
Project description:The aim of this study is to determine the contribution of 2 single nucleotide polymorphisms (SNPs) in thrombospondin 2 (THBS2) gene to the development of intervertebral disc degeneration (IDD) in a Chinese Han population.We studied 138 patients with radiographically proven IDD and 136 healthy volunteers with no history of back problems. Magnetic resonance images (MRIs) were obtained for all the patients and controls. Image evaluation for IDD was performed to evaluate the severity of IDD. All patients and controls were genotyped for rs6422747 and rs6422748. Associations between genotypes and development of IDD were analyzed.We found that 2 SNPs in the intron region of THBS2 gene (rs6422747 and rs6422748) were associated with susceptibility of IDD. However, they were not related with severity of IDD, including the total number of degenerative disc and level of IDD. G allele in both SNPs was associated with a higher risk of IDD.The 2 SNPs (rs6422747 and rs6422748) in the THBS2 gene were associated with susceptibility of IDD but not severity of IDD in a Chinese Han population. Our results indicated that THBS2 gene polymorphisms might be the risk factors for IDD. More studies with larger sample size need to be perfected to make sure the functions of THBS2 gene polymorphisms in IDD development.
| S-EPMC5943876 | biostudies-literature
Project description:OBJECTIVE:We performed a meta-analysis to assess association between interleukin 1 (IL-1) polymorphisms and the risk of Intervertebral Disc Degeneration (IDD). BACKGROUND:A series of studies have investigated the association between common single nucleotide polymorphisms in IL-1 and IDD risk; however, the overall results are inconclusive. METHODS:Two independent investigators conducted a systematic search for relevant available studies. Allele frequencies were extracted from each study. The association between the IL-1? (+889C/T) or IL-1? (+3954C/T) polymorphism and IDD risk was measured by odds ratios (OR) with 95% confidence intervals (95% CI). RESULTS:Five and six studies, respectively, were ultimately included in the meta-analysis for the IL-1? (+889C/T) and IL-1? (+3954C/T) polymorphism. The combined results showed that the IL-1? (+889C/T) polymorphism was significantly associated with increased susceptibility to IDD, particularly in Caucasians (TT versus CC: OR = 2.95, 95% CI: 1.45, 6.04; Pheterogeneity = 0.82; TT versus CC/CT:OR = 2.29, 95% CI: 1.18, 4.47; Pheterogeneity = 0.20). In contrast, the IL-1? (+3954C/T) polymorphism showed a trend towards increased risk in Caucasians but no association in Asians. CONCLUSION:This meta-analysis suggested that the IL-1? (+889C/T) polymorphism is significantly associated with risk of IDD, especially in Caucasian populations.
| S-EPMC4890740 | biostudies-literature
Project description: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.
| S-EPMC9251272 | biostudies-literature
Project description:BACKGROUND: Lumbar disc disease (LDD) is one of the leading causes of disability in the working-age population. A functional single-nucleotide polymorphism (SNP), +1184T-->C, in exon 8 of the cartilage intermediate layer protein gene (CILP) was recently identified as a risk factor for LDD in the Japanese population (odds ratio (OR) 1.61, 95% CI 1.31 to 1.98), with implications for impaired transforming growth factorbeta1 signalling. AIM: To validate this finding in two different ethnic cohorts with LDD. METHODS: This SNP and flanking SNPs were analysed in 243 Finnish patients with symptoms of LDD and 259 controls, and in 348 Chinese subjects with MRI-defined LDD and 343 controls. RESULTS AND CONCLUSION: The results showed no evidence of association in the Finnish (OR = 1.35, 95% CI 0.97 to 1.87; p = 0.14) or the Chinese (OR = 1.05, 95% CI 0.77 to 1.43; p = 0.71) samples, suggesting that cartilage intermediate layer protein gene is not a major risk factor for symptoms of LDD in Caucasians or in the general population that included individuals with or without symptoms.
| S-EPMC2598035 | biostudies-literature
Project description:Purpose of reviewThis review aims to highlight recent advances in understanding the genetic basis of intervertebral disc degeneration (IDD).Recent findingsIt has been known for some time that IDD is highly heritable. Recent studies, and in particular the availability of agnostic techniques such as genome-wide association studies, have identified new variants in a variety of genes which contribute to the risk of IDD and to back pain.SummaryA variety of genetic variants are involved in IDD. Some are shared with variants predisposing to back pain, but few have been identified reliably in either phenotype. Further research is required to explain fully the high heritability and how the genetic variants influence cell biology to lead to IDD.
| S-EPMC6223888 | biostudies-literature
Project description:In this study, we used microarray analysis to investigate the biogenesis and progression of intervertebral disc degeneration. The gene expression profiles of 37 disc tissue samples obtained from patients with herniated discs and degenerative disc disease collected by the National Cancer Institute Cooperative Tissue Network were analyzed. Differentially expressed genes between more and less degenerated discs were identified by significant analysis of microarray. A total of 555 genes were significantly overexpressed in more degenerated discs with a false discovery rate of < 3%. Functional annotation showed that these genes were significantly associated with membrane-bound vesicles, calcium ion binding and extracellular matrix. Protein-protein interaction analysis showed that these genes, including previously reported genes such as fibronectin, COL2A1 and β-catenin, may play key roles in disc degeneration. Unsupervised clustering indicated that the widely used morphology-based Thompson grading system was only marginally associated with the molecular classification of intervertebral disc degeneration. These findings indicate that detailed, systematic gene analysis may be a useful way of studying the biology of intervertebral disc degeneration.
| S-EPMC3795174 | biostudies-literature
Project description:Low back pain (LBP), as a leading cause of disability, is a common musculoskeletal disorder that results in major social and economic burdens. Recent research has identified inflammation and related signaling pathways as important factors in the onset and progression of disc degeneration, a significant contributor to LBP. Inflammatory mediators also play an indispensable role in discogenic LBP. The suppression of LBP is a primary goal of clinical practice but has not received enough attention in disc research studies. Here, an overview of the advances in inflammation-related pain in disc degeneration is provided, with a discussion on the role of inflammation in IVD degeneration and pain induction. Puncture models, mechanical models, and spontaneous models as the main animal models to study painful disc degeneration are discussed, and the underlying signaling pathways are summarized. Furthermore, potential drug candidates, either under laboratory investigation or undergoing clinical trials, to suppress discogenic LBP by eliminating inflammation are explored. We hope to attract more research interest to address inflammation and pain in IDD and contribute to promoting more translational research.
| S-EPMC7846842 | biostudies-literature