Lumbar Intervertebral Disc Degeneration Research Articles

Waterpipe Smoking and Lumbar Intervertebral Disc Degeneration: A Pilot Study.

Retrospective study. The objective of this study is to investigate the association of waterpipe smoking with lumbar intervertebral disc degeneration (IVDD). This is a retrospective chart review study. A total of 286 adults who underwent a lumbar magnetic resonance imaging (MRI) at a tertiary medical center were included and divided into three groups. Group 1 (n = 125) included non-smokers, group 2 (n = 80) smoked cigarettes only, and group 3 (n = 81) smoked waterpipe only. The intervertebral discs were graded using the Pfirmann disc degeneration grading system. The study showed higher lumbar disc degeneration scores for waterpipe and cigarette smokers compared to non-smokers at all spinal levels. Specifically, post hoc analysis showed that there was a significant difference at L1-L2 between cigarette smokers and non-smokers (P = 0.007) and between waterpipe smokers and non-smokers (P = 0.013), and a significant difference at L3-L4 and L4-L5 between non-smokers and cigarettes smokers (P < .001 and P = .029 respectively). Waterpipe smoking is associated with lumbar intervertebral disc degeneration.

The association of lumbar intervertebral disc degeneration with low back pain is modified by underlying genetic propensity to pain

The association of lumbar intervertebral disc degeneration with low back pain is modified by underlying genetic propensity to pain

THE ASSOCIATION BETWEEN INDIVIDUAL LUMBAR INTERVERTEBRAL DISC DEGENERATION FEATURES AND LOW BACK PAIN IS MODIFIED BY GENETIC PROPENSITY TO PAIN

BackgroundThe association between lumbar intervertebral disc degeneration (LDD) and low back pain (LBP) is modest. We have recently shown that genetic propensity to pain is an effect modifier of the LDD-LBP relationship when LDD is defined as a summary score of LDD (LSUM), suggesting the association may be driven by individuals with the greatest genetic predisposition to pain. This study examined the association between individual spine magnetic resonance imaging (MRI)-determined LDD features and LBP in subgroups defined by genetic predisposition to pain.MethodWe developed a polygenic risk score (PRS) for “genetic propensity to pain” defined as the number of non-back pain locations (head, face, neck/shoulder, stomach/abdomen, hip, and knee) with duration ≥3 months in 377,538 UK Biobank participants of European ancestry. This PRS was used to stratify TwinsUK MRI samples (n=645) into four strata of genetic propensity to pain. We examined the association between LBP and MRI features of lumbar disc height, disc signal intensity, disc bulge, and osteophytes with adjustments for age, sex, PRS strata, interaction terms for each MRI feature x PRS strata, and twin status.ResultsWe found significant effect modification of the LDD-LBP relationship by genetic propensity to pain for the lumbar MRI features of disc height (p=0.03 for the interaction term with highest quartile of genetically-predicted propensity to pain) and disc signal intensity (p=0.001), but not for disc bulge and osteophytes.ConclusionGenetic propensity to pain modifies the association between individual LDD features and LBP and should be considered in LBP clinical studies.Conflicts of interestNo conflicts of interestSources of fundingNo funding obtainedAcknowledgementUKBB data were obtained under the project #18219This paper is submitted to the Spine journal and is under review.

Application of network pharmacology and dock of molecules on the exploration of the mechanism of frankincense-myrrh for lumbar intervertebral disc degeneration: A review.

To investigate the efficacy of Frankincense-Myrrh in lumbar Intervertebral degenerative diseases (LIDD). The active components of frankincense-myrrh was retrieved with a unique system pharmacology platform for Traditional Chinese Medicine Systems Pharmacology (TCMSP). The LIDD-related target genes were screened with DisGeNET and Genecards databases. Then, STRING & Cytoscape were used for analyzing the Protein-Protein Interaction network. DAVID was used for analyzing Gene Ontology (GO) & Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Finally, molecules of AutoDockVina and Pymol were used for docking the molecules for verifying active ingredients and key targets' binding force. The 105 LIDD-related targets identified in Ruxiang (RX)-Moyao (MY) involve 53 active ingredients. In addition, topological analysis was conducted for identifying the 12 key targets. According to the analysis results of GO & KEGG, RX-MY is significant for treating LIDD through participating in many pathways and biological processes, such as signaling pathways of inflammatory response reactive process, MAP kinase activity, TNF, and MAPK, etc. According to the dock results, the active components oxo-tirucalic, acid, isofouquierone, (7S, 8R, 9S, 10R, 13S, 14S,17Z)-17-ethylidene-7-hydroxy-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15-decahydrocyclopenta [a] phenanthrene-3,16-dion in RX-MY binds actively. The basic pharmacological action and RX-MY-related mechanism in the treatment of LIDD was revealed in this study for the first time. It is predicted that the results may provide a treatment plan for RX-MY with replacement of NSAIDs and warrant investigation of new therapeutic alternatives for LIDD. However, these predictions should be validated by relevant pharmacological trials.

Advances in the interaction between lumbar intervertebral disc degeneration and fat infiltration of paraspinal muscles: critical summarization, classification, and perspectives.

More than 619 million people in the world suffer from low back pain (LBP). As two potential inducers of LBP, intervertebral disc degeneration (IVDD) and fat infiltration of paraspinal muscles (PSMs) have attracted extensive attention in recent years. So far, only one review has been presented to summarize their relationship and relevant mechanisms. Nevertheless, it has several noticeable drawbacks, such as incomplete categorization and discussion, lack of practical proposals, etc. Consequently, this paper aims to systematically summarize and classify the interaction between IVDD and fat infiltration of PSMs, thus providing a one-stop search handbook for future studies. As a result, four mechanisms of IVDD leading to fat infiltration of PSMs and three mechanisms of fat infiltration in PSMs causing IVDD are thoroughly analyzed and summarized. The typical reseaches are tabulated and evaluated from four aspects, i.e., methods, conclusions, benefits, and drawbacks. We find that IVDD and fat infiltration of PSMs is a vicious cycle that can promote the occurrence and development of each other, ultimately leading to LBP and disability. Finally, eight perspectives are proposed for future in-depth research.

Myricetin Restores Autophagy to Attenuate Lumbar Intervertebral Disk Degeneration Via Negative Regulation of the JAK2/STAT3 Pathway.

Autophagy is a critical player in lumbar intervertebral disk degeneration (IDD), and autophagy activation has been suggested to prevent the apoptosis of nucleus pulposus cells (NPCs). Myricetin has anti-cancer, anti-inflammatory, and antioxidant potentials and can activate autophagy. Thus, this study focused on the roles and mechanisms of myricetin in IDD. A puncture-induced rat IDD model was established and intraperitoneally injected with 20-mg/kg/day myricetin. Histopathological changes of intervertebral disks (IVDs) were assessed by hematoxylin and eosin staining and Safranin O/Fast Green staining. The isolated NPCs from IVDs of healthy rats were stimulated with IL-1β to mimic IDD-like conditions. The roles of myricetin in cell apoptosis, extracellular matrix (ECM) degradation, autophagy repression, and the JAK2/STAT3 pathway activation were examined by cell counting kit-8, flow cytometry, western blotting, real-time quantitative polymerase chain reaction, and immunofluorescence staining. Myricetin treatment attenuated the apoptosis and ECM degradation, and enhanced autophagy in the IL-1β-treated NPCs, whereas the myricetin-mediated protection was limited by autophagy inhibition. Mechanistically, myricetin activated autophagy through blocking the JAK2/STAT3 signaling. In vivo experiments revealed that intraperitoneal injection of myricetin activated NPC autophagy to relieve puncture injury in rats. Myricetin prevents IDD by attenuating NPC apoptosis and ECM degradation through blocking the JAK2/STAT3 pathway to enhance autophagy.

The association of lumbar intervertebral disc degeneration with low back pain is modified by underlying genetic propensity to pain

BACKGROUND CONTEXTAssociations between magnetic resonance imaging (MRI)-detected lumbar intervertebral disc degeneration (LDD) and LBP are often of modest magnitude. This association may be larger in specific patient subgroups. PURPOSETo examine whether the association between LDD and LBP is modified by underlying genetic predispositions to pain. STUDY DESIGNCross-sectional study in UK Biobank (UKB) and Twins UK. PATIENT SAMPLESA genome-wide association study (GWAS) of the number of anatomical chronic pain locations was conducted in 347,538 UKB participants. The GWAS was used to develop a genome-wide polygenic risk score (PRS) in a holdout sample of 30,000 UKB participants. The PRS model was then used in analyses of 645 TwinsUK participants with standardized LDD MRI assessments. OUTCOME MEASURESEver having had LBP associated with disability lasting ≥1 month (LBP1). METHODSUsing the PRS as a proxy for “genetically-predicted propensity to pain”, we stratified TwinsUK participants into PRS quartiles. A “basic” model examined the association between an LDD summary score (LSUM) and LBP1, adjusting for covariates. A “fully-adjusted” model also adjusted for PRS quartile and LSUM x PRS quartile interaction terms. RESULTSIn the basic model, the odds ratio (OR) of LBP1 was 1.8 per standard deviation of LSUM (95% confidence interval [CI] 1.4–2.3). In the fully-adjusted model, there was a statistically significant LSUM-LBP1 association in quartile 4, the highest PRS quartile (OR=2.5 [95% CI 1.7–3.7], p=2.6×10−6), and in quartile 3 (OR=2.0, [95% CI 1.3–3.0]; p=.002), with small-magnitude and/or nonsignificant associations in the lowest 2 PRS quartiles. PRS quartile was a significant effect modifier of the LSUM-LBP1 association (interaction p≤.05). CONCLUSIONSGenetically-predicted propensity to pain modifies the LDD-LBP association, with the strongest association present in people with the highest genetic propensity to pain. Lumbar MRI findings may have stronger connections to LBP in specific subgroups of people.

Allogeneic Disc Progenitor Cells Safely Increase Disc Volume and Improve Pain, Disability, and Quality of Life in Patients With Lumbar Disc Degeneration-Results of an FDA-Approved Biologic Therapy Randomized Clinical Trial.

Progenitor cells derived from intervertebral disc tissue demonstrated immunomodulatory and regenerative properties in preclinical studies. We report the safety and efficacy results of a US Food and Drug Administration-approved clinical trial of these cells for the treatment of symptomatic degenerative disc disease. Sixty patients with symptomatic single-level lumbar degenerative disc disease (mean age 37.9 years, 60% men) were enrolled in a randomized, double-blinded, placebo-controlled Phase I/Phase II study at 13 clinical sites. They were randomized to receive single intradiscal injections of either low-dose cells (N = 20), high-dose cells (N = 20), vehicle alone (N = 10), or placebo (N = 10). The primary endpoint was mean visual analog scale (VAS) pain improvement >30% at 52 weeks. Disc volume was radiologically assessed. Adverse events (AEs), regardless of whether they were related to treatment, were reported. Patients were assessed at baseline and at 4, 12, 26, 52, 78, and 104 weeks posttreatment. At week 52, the high-dose group had a mean VAS percentage decrease from baseline (-62.8%, P = 0.0005), achieving the endpoint of back pain improvement >30%; the mean change was also significantly greater than the minimal clinically important difference of a 20-point decrease (-42.8, P = 0.001). This clinical improvement was maintained at week 104. The vehicle group had a smaller significant decrease in VAS (-52.8%, P = 0.044), while the low-dose and placebo groups showed nonsignificant improvements. Only the high-dose group had a significant change in disc volume, with mean increases of 249.0 mm3 (P = 0.028) at 52 weeks and 402.1 mm3 (P = 0.028) at 104 weeks. A minority of patients (18.3%) reported AEs that were severe. Overall, 6.7% of patients experienced serious AEs, all in the vehicle (n = 1) or placebo (n = 3) groups, none treatment related. High-dose allogeneic disc progenitor cells produced statistically significant, clinically meaningful improvements in back pain and disc volume at 1 year following a single intradiscal injection and were safe and well tolerated. These improvements were maintained at 2 years post-injection. NCT03347708-Study to Evaluate the Safety and Preliminary Efficacy of Injectable Disc Cell Therapy, a Treatment for Symptomatic Lumbar Intervertebral Disc Degeneration.

Lumbar spine MRI annotation with intervertebral disc height and Pfirrmann grade predictions.

Many lumbar spine diseases are caused by defects or degeneration of lumbar intervertebral discs (IVD) and are usually diagnosed through inspection of the patient's lumbar spine MRI. Efficient and accurate assessments of the lumbar spine are essential but a challenge due to the size of the clinical radiologist workforce not keeping pace with the demand for radiology services. In this paper, we present a methodology to automatically annotate lumbar spine IVDs with their height and degenerative state which is quantified using the Pfirrmann grading system. The method starts with semantic segmentation of a mid-sagittal MRI image into six distinct non-overlapping regions, including the IVD and vertebrae regions. Each IVD region is then located and assigned with its label. Using geometry, a line segment bisecting the IVD is determined and its Euclidean distance is used as the IVD height. We then extract an image feature, called self-similar color correlogram, from the nucleus of the IVD region as a representation of the region's spatial pixel intensity distribution. We then use the IVD height data and machine learning classification process to predict the Pfirrmann grade of the IVD. We considered five different deep learning networks and six different machine learning algorithms in our experiment and found the ResNet-50 model and Ensemble of Decision Trees classifier to be the combination that gives the best results. When tested using a dataset containing 515 MRI studies, we achieved a mean accuracy of 88.1%.

Fully Automatic Fine-Grained Grading of Lumbar Intervertebral Disc Degeneration Using Regional Feature Recalibration Network.

Accurate fine-grained grading of lumbar intervertebral disc (LIVD) degeneration is essential for the diagnosis and treatment design of high-incidence low back pain. However, the grading accuracy is still challenged by lacking the fine-grained degenerative details, which is mainly due to the existing grading methods are easily dominated by the salient nucleus pulposus regions in LIVD, overlooking the inconspicuous degeneration changes of the surrounding structures. In this study, a novel regional feature recalibration network (RFRecNet) is proposed to achieve accurate and reliable LIVD degeneration grading. Detection transformer (DETR) is first utilized to detect all LIVDs and then input to the proposed RFRecNet for the fine-grained grading. To obtain sufficient features from both the salient nucleus pulposus and the surrounding regions, a regional cube-based feature boosting and suppression (RC-FBS) module is designed to adaptively recalibrate the feature extraction and utilization from the various regions in LIVD, and a feature diversification (FD) module is proposed to capture the complementary semantic information from the multi-scale features for the comprehensive fine-grained degeneration grading. Extensive experiments were conducted on a clinically collected dataset, which consists of 500 MR scans with a total of 10225 LIVDs. An average grading accuracy of 90.5%, specificity of 97.5%, sensitivity of 90.8%, and Cohen's kappa correlation coefficient of 0.876 are obtained, which indicate that the proposed framework is promising to provide doctors with reliable and consistent fine-grained quantitative evaluation results of the LIVD degeneration conditions for the optimal surgical plan design.

Role of Bushen Huoxue Formula and transplanted endothelial progenitor cells play in promoting endplate microcirculation and attenuating intervertebral disc degeneration

ObjectiveTo explore whether Bushen Huoxue Formula (BSHXF) improves the angiogenesis ability of transplanted endothelial progenitor cells (EPCs) in endplate and its potential mechanism in delaying intervertebral disc degeneration (IDD). MethodsBSHXF was analyzed via Ultra-High Performance Liquid Chromatography (UPLC). Rabbit axial compression lumbar IDD models were constructed and the effects of BSHXF, EPCs, and their combination in IDD were determined by MRI, histological evaluation, TUNEL, and immunofluorescence assays. Additionally, CCK-8 assay, flow cytometry, and tube formation assay were used to evaluate EPCs viability, proliferation, cell cycle and the angiogenesis ability of EPCs between groups. ResultsBSHXF and transplanted EPCs both attenuate the process of IDD in the rabbit model assessed by MRI, HE staining and Masson staining. TUNEL-positive NP cells were significantly reduced in the BSHXF group, EPCs group, and EPC + BSHXF group compared to the model group (P < 0.05), with the EPC + BSHXF group showing the most significant therapeutic effect. Immunofluorescence detection showed that VEGF, CD34 expression and quantity of microvessels in the endplate significantly increased in the EPC + BSHXF group compared to all the other groups (P < 0.05). Besides, the CCK-8 assay showed an upregulation of EPC viability and the tube formation assay demonstrated a significant increase in tube length and branching in EPCs cultured with BSHXF-containing serum (P < 0.05). Furthermore, BSHXF-containing serum increased VEGF expression in EPCs cultured in vitro (P < 0.05). ConclusionsBoth BSHXF and EPCs transplantation play an important role in increasing endplate angiogenesis and attenuating IDD. BSHXF can enhance the viability and tube-forming ability of EPCs and endplate microcirculation.

Study and analysis of the correlation between lumbar spondylolisthesis and Modic changes.

This study aimed to explore the risk factors of Modic changes in lumbar spondylolisthesis. The distribution of Modic changes in different types of lumbar spondylolisthesis, degree of spondylolisthesis, and degree of intervertebral disc degeneration in patients with lumbar spondylolisthesis was observed and analyzed. Statistical analysis was conducted to assess whether intervertebral disc degeneration, local mechanical changes, etc. affect the occurrence of Modic changes. The risk factors of Modic changes in lumbar spondylolisthesis were further illustrated. The age in the lumbar spondylolisthesis with Modic changes group was younger than that in the lumbar spondylolisthesis without Modic changes group, and the bone mineral density was better in the lumbar spondylolisthesis with Modic changes group than that in the lumbar spondylolisthesis without Modic changes group, P < 0.05. The two groups statistically differed in intervertebral disc height (IDH) and disc angle on magnetic resonance imaging (MRI). In the classification of Modic changes, the incidence of type II was the highest. The incidence of Modic changes is higher in isthmic spondylolisthesis than in degenerative spondylolisthesis. With the aggravation of lumbar spondylolisthesis and intervertebral disc degeneration, the incidence of Modic changes gradually increased. Modic changes are most commonly seen in both the upper and lower endplates. Logistic regression analysis showed that the occurrence of Modic changes in lumbar spondylolisthesis was significantly correlated with IDH, disc angle on MRI, type of spondylolisthesis, degree of spondylolisthesis, and degree of intervertebral disc degeneration, P < 0.05. The occurrence of Modic changes is related to the type of spondylolisthesis, the degree of spondylolisthesis, the degree of disc degeneration, the decrease of intervertebral disc height, and local stress angulation.

Research Progress in Nucleus Pulposus Tissue Engineering in Lumbar Intervertebral Disc

Lumbar intervertebral disc degeneration is a common pathological process in the spine,with the main clinical symptoms of low back pain,numbness of lower limbs,and defecation dysfunction.The occurrence and development of lumbar intervertebral disc degeneration are determined by multiple factors,and the pathophysiological and cellular mechanisms remain to be fully understood.Nucleus pulposus tissue engineering is a new biotherapy that combines biological histology with material science to treat diseases including lumbar intervertebral disc degeneration.Clinicians should fully learn the complex relationship between nucleus pulposus tissue engineering and lumbar intervertebral disc degeneration,which will facilitate the clinical treatment of lumbar intervertebral disc degeneration,the rehabilitation of lumbar intervertebral disc after treatment,and the prevention of this disease in the population.

The Reciprocal Relationship Between Lumbar Intervertebral Disk Degeneration and the MRI-based Vertebral Bone Quality Score.

Retrospective longitudinal study. To investigate the association between lumbar intervertebral disk degeneration (DD) and the vertebral bone quality (VBQ) score. The VBQ score that is based on magnetic resonance imaging has been proposed as a measure of lumbar spine bone quality and is a significant predictor of healthy versus osteoporotic bone. However, the role of segmental contributing factors on VBQ is unknown. Nonsurgical patients who underwent repeated lumbar magnetic resonance imaging scans, at least three years apart primarily for low back pain were retrospectively included. VBQ was assessed as previously described. DD was assessed using the Pfirrmann grading (PFG) scale. PFG grades were summarized as PFG L1-4 for the upper three lumbar disk levels, as PFG L4-S1 for the lower two lumbar disc levels, and as PFG L1-S1 for all lumbar disc levels. Multivariable linear mixed models were used with adjustments for age, sex, race, body mass index, and the clustering of repeated measurements. A total of 350 patients (54.6% female, 85.4% White) were included in the final analysis, with a median age at baseline of 60.1 years and a body mass index of 25.8 kg/m 2 . VBQ significantly increased from 2.28 at baseline to 2.36 at follow-up ( P = 0.001). In the unadjusted analysis, a significant positive correlation was found between PFG L1-4 , PFG L1-S1 , and VBQ at baseline ( P < 0.05) that increased over time ( P < 0.005). In the adjusted multivariable analysis, PFG L1-4 ( β = -0.0195; P = 0.021), PFG L4-S1 ( β = -0.0310; P = 0.007), and PFG L1-S1 ( β = -0.0160; P = 0.012) were independently and negatively associated with VBQ. More advanced and long-lasting DD is associated with lower VBQ indicating less bone marrow fat content and potentially stronger bone. VBQ score as a marker of bone quality seems affected by DD.

Protective effects of Shensuitongzhi formula on intervertebral disc degeneration via downregulation of NF-κB signaling pathway and inflammatory response

Low back pain (LBP) is a common orthopedic disease over the world. Lumbar intervertebral disc degeneration (IDD) is regarded as an important cause of LBP. Shensuitongzhi formula (SSTZF) is a drug used in clinical treatment for orthopedic diseases. It has been found that SSTZF can have a good treatment for IDD. But the exact mechanism has not been clarified. The results showed that SSTZF protects against LSI-induced degeneration of cartilage endplates and intervertebral discs. Meanwhile, SSTZF treatment dramatically reduces the expression of inflammatory factor as well as the expression of catabolism protein and upregulates the expression of anabolism protein in LSI-induced mice. In addition, SSTZF delayed the progression of LSI-induced IDD via downregulation the level of NF-κB signaling key gene RELA and phosphorylation of key protein P65 in endplate chondrocytes. Our study has illustrated the treatment as well as the latent mechanism of SSTZF in IDD.

Artificial Intelligence Classification for Detecting and Grading Lumbar Intervertebral Disc Degeneration

Artificial Intelligence Classification for Detecting and Grading Lumbar Intervertebral Disc Degeneration

Sympathetic Neurotransmitter, VIP, Delays Intervertebral Disc Degeneration via FGF18/FGFR2-Mediated Activation of Akt Signaling Pathway.

Neuromodulation-related intervertebral disc degeneration (IVDD) is a novel IVDD pattern and are proposed recently. However, the mechanistic basis of neuromodulation and intervertebral disc (IVD) homeostasis remains unclear. Here, this study aimed to investigate the expression of postganglionic sympathetic nerve fiber-derived vasoactive intestinal peptide (VIP) system in human IVD tissue, and to assess the role of VIP-related neuromodulation in IVDD. Patient samples and in vitro cell experiments showed that the expression of receptors for VIP is negatively correlated with the severity of IVDD, and the administration of exogenous VIP can ameliorate interleukin 1β-induced nucleus pulposus (NP) cell apoptosis and inflammation. Further mRNA-seq analysis revealed that fibroblast growth factor 18- (FGF18)-mediated activation of V-akt murine thymoma viral oncogene homolog signaling pathway is involved in the protective effects of VIP on inflammation-induced NP cell degeneration. Further analysis identified VIP via its receptor vasoactive intestinal peptide receptor 2 can directly result in decreased expression of miR-15a-5p, which targeted FGF18. Finally, in vivo mice lumbar IVDD model confirmed that focally exogenous administration of VIP can effectively ameliorated the progression of IVDD, as shown by the radiological and histological analysis. In conclusion, these results indicated that sympathetic neurotransmitter, VIP, delayed IVDD via FGF18/FGFR2-mediated activation of V-akt murine thymoma viral oncogene homolog signaling pathway, which will broaden the horizon concerning how the neuromodulation correlates with IVDD and shed new light on novel therapeutical alternatives to IVDD.

Abdominal Fat is a Reliable Indicator of Lumbar Intervertebral Disc Degeneration than Body Mass Index

The objective of this study was to determine whether abdominal fat status correlates with low back pain (LBP) and lumbar intervertebral disc degeneration (IVDD) and to identify a new anthropometric index to predict the likelihood of developing LBP. Patients with chronic low back pain admitted to the Affiliated Hospital of Southwest Medical University from June 2022 to May 2023 were collected as the experimental group. Volunteers without LBP from June 2022 to May 2023 were also recruited as the control group. They underwent lumbar spine magnetic resonance imaging and had their body mass index (BMI) measured. Abdominal parameters were measured on T2-weighted median sagittal magnetic resonance imaging at the L3/4 level: abdominal diameter, sagittal abdominal diameter (SAD), and subcutaneous abdominal fat thickness (SAFT). Each lumbar IVDD was assessed using the Pfirrmann grading system. The differences in abdominal parameters and BMI between the experimental and control groups were compared, and the correlations between abdominal parameters, BMI, LBP, and IVDD were analyzed. Abdominal diameter, SAD, and SAFT had moderate-to-strong correlations with BMI. SAD was significantly associated with severe IVDD at L4-L5 and L5-S1 levels with odds ratio of 3.201 (95% confidence interval [CI]: 1.850-5.539, P<0.001) and 1.596 (95% CI: 1.072-2.378, P=0.021), respectively. BMI had no significant association with severe IVDD. In women, SAFT and BMI were significantly correlated with LBP; in men, only SAFT was significantly correlated with LBP. Appropriate cutoff values for men and women were 1.52cm (area under the curve=0.702, 95% CI: 0.615-0.789, P < 0.001) and 1.97cm (area under the curve=0.740, 95% CI: 0.662-0.818, P < 0.001), respectively. Men and women with SAFT of >1.52cm and >1.97cm, respectively, had significantly higher rates of LBP. SAD could predict severe IVDD better than BMI. SAFT is a better predictor of LBP than BMI, especially in men, and reliably distinguished patients with LBP from asymptomatic subjects with reliable cutoff values for men and women.

Macrophage migration inhibitory factor (MIF) promotes intervertebral disc degeneration through the NF-κB pathway, and the MIF inhibitor CPSI-1306 alleviates intervertebral disc degeneration in a mouse model.

Lumbar intervertebral disc degeneration(IDD) is a prevalent inflammatory disease caused by many proinflammatory factors, such as TNF and IL-1β. Migration inhibitory factor (MIF) is an upstream inflammatory factor widely expressed invivo that is associated with a variety of inflammatory diseases or malignant tumors and has potential therapeutic value in many diseases. We explored the role of MIF in intervertebral disc degeneration by regulating the content of exogenous MIF or the expression of MIF in cells. Upon inducing degeneration of nucleus pulposus (NP) cells with IL-1β, we found that the increase in intracellular and exogenous MIF promoted the catabolism induced by proinflammatory factors in NP cells, while silencing of the MIF gene alleviated the degeneration to some extent. In a mouse model, the intervertebral disc degeneration of MIF-KO mice was significantly less than that of wild-type mice. To explore the treatment of intervertebral disc degeneration, we selected the small-molecular MIF inhibitor CPSI-1306. CPSI-1306 had a therapeutic effect on intervertebral disc degeneration in the mouse model. In summary, we believe that MIF plays an important role in intervertebral disc degeneration and is a potential therapeutic target for the treatment of intervertebral disc degeneration.

Potential blood markers as screening tools for subjects with low back pain: an age- and gender-matched cross-sectional analysis

Background Mechanical and inflammatory factors were suggested as the causes of spine degeneration and low back pain (LBP). Previous studies partly reported the association of LBP with inflammation. However, none of them compared patients with LBP and asymptomatic subjects in terms of complete blood count and inflammatory markers in detail. We aimed to analyze the association of serum white blood cell (WBC) count, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) with chronic LBP by comparing the patients with chronic LBP and age- and gender-matched asymptomatic subjects. Methods Lumbar intervertebral disc degeneration and vertebral end-plates were evaluated using Pfirrmann grading and Modic classification on lumbar spine magnetic resonance images, respectively. Serum WBC counts, CRP levels, and ESRs were recorded from chart reviews. Results We included 147 patients with chronic LBP and 101 asymptomatic subjects. Patients with chronic LBP had significantly higher serum neutrophil, monocyte, and basophil counts, higher neutrophil-to-lymphocyte ratio, higher ESR, and lower serum CRP levels compared to the asymptomatic subjects. Serum monocyte and basophil cell counts and ESR were the most remarkable predictive factors for chronic LBP, severe IVDD, and Modic changes. Higher serum monocyte and basophil cell counts and higher serum ESR above cut-off values of 0.42 × 103/μL, 0.025 × 103/μL, and 3.5 mm/hour could be used as screening tools for subjects with persistent LBP in primary care. Discussion Higher serum monocyte and basophil counts and serum ESR above new cut-off values should highlight the need to obtain early spinal imaging to prevent chronicity in patients with LBP.