Development Of Lumbar Disc Degeneration Research Articles

Persistent expression of NLRP3 in spinal microglia promotes development of lumbar disc degeneration.

Activated microglia play a critical role in the development of lumbar disc degeneration (LDD), which is a severe disease that causes neuropathic pain in affected people. Interleukin 1β (IL-1β) is a proinflammatory cytokine produced and secreted by activated microglia to induce the inflammation and the subsequent degradation of the disease discs. Recent findings suggest that activation of IL-1β in cells usually requires the involvement of NACHT, LRR and PYD domains-containing protein 3 (NLRP3)-induced formation of inflammasome. However, the importance of NLRP3 in spinal microglia in LDD is not known and thus addressed in the current study. NLRP3 expression was examined in the spinal discs. Correlation of NLRP3 levels in microglia with the pain score of the LDD patients or Thompson classification of the degeneration level of the patients was determined. The effects of persistent expression or depletion of NLRP3 on phagocytosis potential and production of proinflammatory cytokines in microglia were tested in vitro, while their effects on the severity of LDD and LDD-associated neuropathic pain were assessed in a mouse model for LDD. NLRP3 was exclusively expressed in microglia in the spinal discs. NLRP3 levels in microglia strongly correlated with the pain score of the LDD patients, and modestly correlated with the Thompson classification of the degeneration level of the patients. Persistent NLRP3 expression in microglia increased both their phagocytosis potential and production of proinflammatory cytokines, while NLRP3-depleted microglia decreased both their phagocytosis potential and production of proinflammatory cytokines. In a mouse model for LDD, persistent NLRP3 activation in microglia significantly increased the severity of LDD and LDD-associated neuropathic pain, while specific depletion of NLRP3 in microglia significantly attenuated the severity of LDD and reduced the LDD-associated neuropathic pain. Persistent activation of NLRP3 in spinal microglia promotes development of LDD, while suppression of NLRP3 in microglia could be a promising strategy for LDD therapy.

Diabetes Mellitus-A Risk Factor for the Development of Lumbar Disc Degeneration: A Retrospective Study of an Indian Population.

Study Design:A retrospective study.Objectives:To determine the association between type-2 diabetes mellitus (T2DM) and the severity of lumbar disc degeneration disease (LDDD).Methods:We included 199 patients with low back pain (LBP) who visited our hospital from 2016 to 2018. All patients were divided into 3 groups as per inclusion criteria. Group A, patients without DM (n = 75); group B, patients with controlled DM (n = 72); and group C, patients with uncontrolled DM (n = 52). The patients were further subdivided into group B1, DM duration ≤10 years (n = 38); group B2, DM duration >10 years (n = 34); group C1 DM duration ≤10 years (n = 28); and group C2, DM duration >10 years (n = 24). Sex, age, body mass index, occupation, smoking history, alcohol use, and duration of T2DM were recorded. The severity of LDDD was evaluated using the 5-level Pfirrmann grading system. Operated patients’ disc materials were sent for histological examination.Results:Demographic data showed no difference among groups (P > 0.5), except age. Patients with DM showed more severe disc degeneration compared with patients without DM. The average Pfirrmann scores between groups A and B1 had no difference; groups B2, C1, and C2 showed higher average Pfirrmann scores than group A (P < 0.05). Groups B2 and C2 showed higher average Pfirrmann scores than groups B1 and C1 (P < 0.05). Groups C1 and C2 showed higher average Pfirrmann scores than groups B1 and B2 (P < 0.05). The severity of LDDD was significantly related to DM duration in both groups B and C (P < 0.05). DM groups showed increased disc apoptosis and matrix aggrecan fragmentation, disc glycosaminoglycan content and histological analysis were significantly different; the results are similar to Pfirrmann score results.Conclusions:DM duration >10 years and uncontrolled DM were risk factors for LDDD.

The impact and distinction of \u2018lipid healthy but obese\u2019 and \u2018lipid abnormal but not obese\u2019 phenotypes on lumbar disc degeneration in Chinese

BackgroundLipid abnormality and obesity have been proposed to be associated with lumbar disc degeneration, but little is known about the effect of ‘lipid healthy but obese’ (LH-O) and ‘lipid abnormal but not obese’ (LA-NO) phenotypes on lumbar disc degeneration in Chinese. The study aims to determine the impact and distinction of LH-O and LA-NO phenotypes on lumbar disc degeneration in Chinese, and to identify the association of related factors with risk of lumbar disc degeneration.MethodsA total of 678 individuals were included with lumbar magnetic resonance imaging, serum lipid levels and anthropometric measurements. Obesity was defined on the basis of body mass index or waist to hip ratio (WHR). Pfirrmann score and Weishaupt’s scale were utilized to assess the degree of disc degeneration and facet joint degeneration.ResultsThe incidence of the LH-O and LA-NO phenotypes were 11.4% and 18.1%, respectively. LA-NO phenotype demonstrates a high incidence for disc degeneration (P < 0.05), while LH-O phenotype confers a severe disc degeneration grade (P < 0.05). No statistical difference in the percentage of severe facet joint degeneration grade in each group (P > 0.05). Elevated triglycerides and greater WHR may be the risk factors for lumbar disc degeneration in Chinese.ConclusionLH-O and LA-NO phenotypes are common with different status of disc degeneration in Chinese. Elevated triglycerides and abdominal obesity appear to play crucial roles in the development of lumbar disc degeneration.

Epigenetic modulation of macrophage polarization prevents lumbar disc degeneration.

Inflammation plays an essential role in the development of lumbar disc degeneration (LDD), although the exact effects of macrophage subtypes on LDD remain unclear. Based on previous studies, we hypothesized that M2-polarization of local macrophages and simultaneous suppression of their production of fibrotic transforming growth factor beta 1 (TGFβ1) could inhibit progression of LDD. Thus, we applied an orthotopic injection of adeno-associated virus (AAV) carrying shRNA for DNA Methyltransferase 1 (DNMT1) and/or shRNA for TGFβ1 under a macrophage-specific CD68 promoter to specifically target local macrophages in a mouse model for LDD. We found that shDNMT1 significantly reduced levels of the pro-inflammatory cytokines TNFα, IL-1β and IL-6, significantly increased levels of the anti-inflammatory cytokines IL-4 and IL-10, significantly increased M2 macrophage polarization, significantly reduced cell apoptosis in the disc degeneration zone and significantly reduced LDD-associated pain. The anti-apoptotic and anti-pain effects were further strengthened by co-application of shTGFβ1. Together, these data suggest that M2 polarization of macrophages induced by both epigenetic modulation and suppressed production and release of TGFβ1 from polarized M2 macrophages, may have a demonstrable therapeutic effect on LDD.

Serum CXCL12/SDF-1 level is positively related with lumbar intervertebral disc degeneration and clinical severity.

This study aimed to examine whether stromal cell-derived factor-1 (SDF-1) or C-X-C chemokine ligand 12 (CXCL12) participates in the development of lumbar disc degeneration, as implicated earlier by the level of CXCL12 correlating with this disease. It enrolled 145 patients with symptomatic lumbar intervertebral disc degeneration (IDD) and 130 asymptomatic healthy controls with no indication of IDD. Radiological assessment of the IDD patients was targeted at the lumbar vertebra region, based on Pfirrmann grade. Degeneration of the multifidus and psoas major muscles was evaluated using Goutallier classification. Visual Analogue Scale (VAS) and Oswestry Disability Index (ODI) scores were obtained for assessing the severity of manifestation. The levels of serum CXCL12, IL-6 and TNF-α were determined by ROC curve analysis, resulting in their prognostic value for Pfirrmann grading. Higher levels of serum CXCL12 were found in patients with IDD than in asymptomatic individuals, and were positively related to the Pfirrmann grade as well as multifidus muscle degeneration. Furthermore, serum CXCL12 concentration showed a significant correlation with the VAS and ODI scores. In addition, elevated serum CXCL12 levels were related to serum levels of TNF-α and IL-6. The ROC curve analysis implicated that CXCL12 could function as a biomarker of the early-mediate phase of IDD development. In summary, the serum CXCL12/SDF-1 level is positively related with lumbar IDD and its clinical severity.

Vitamin D Receptor gene polymorphisms and plasma levels are associated with lumbar disc degeneration

The purpose of this study was to investigate the association of Vitamin D Receptor (VDR) gene polymorphisms and VDR levels with lumbar disc degeneration (LDD). TaqMan SNP Genotyping Assay was utilized to probe VDR gene polymorphisms including the FokI (rs2228570), ApaI (rs7975232) and TaqI (rs731236) in 454 patients with LDD and 485 controls. Enzyme-Linked Immunosorbent Assay (ELISA) was used to detect plasma VDR levels. The patients with LDD were divided into three subgroups (subgroup 1: lumbar disc herniation; subgroup 2: lumbar spinal stenosis; subgroup 3: lumbar spondylolisthesis) to further probe the association of plasma VDR levels and VDR gene polymorphisms and LDD. Moreover, immunohistochemistry (IHC) was implemented to evaluate VDR expression in lumbar degenerated disc and normal disc. Allele and genotype frequency of TaqI (rs731236) were significantly different in patients with LDD and controls (all P < 0.05). For TaqI polymorphism, the frequencies of T allele were significantly higher in the LDD patients compared with controls (OR = 1.319; 95%CI 1.091 to 1.595; P = 0.004, adjusted (OR = 1.319; 95%CI 1.091 to 1.595; P = 0.004, adjusted OR = 1.383; 95%CI 1.135 to 1.684; P = 0.016). Furthermore, the allele distribution showed a higher frequency of the T allele in the patients with lumbar disc herniation in subgroup 1 (OR = 1.384; 95% CI 1.105 to 1.732; P = 0.004, adjusted OR = 1.319; 95%CI 1.091 to 1.595; P = 0.016). Plasma VDR levels and VDR expression were significantly lower in patients with LDD compared with controls (all P < 0.05). Moreover, the TT genotype of TaqI polymorphism was significantly associated with lower plasma VDR levels in patients with LDD (P = 0.002). TaqI (rs731236) polymorphism was associated with a predisposition to LDD. Plasma VDR and VDR expression levels may be the marker for the occurrence and development of LDD.

The Effects of Spinopelvic Parameters Such As Lumbar Lordosis and Sacral Slope Angles in the Development of Lumbar Disc Degeneration

The Effects of Spinopelvic Parameters Such As Lumbar Lordosis and Sacral Slope Angles in the Development of Lumbar Disc Degeneration

Five-year development of lumbar disc degeneration-a prospective study.

To examine the impact of demographic, clinical, and genetic factors as well as herniated discs on 5-year development of disc degeneration in the lumbar spine, and to investigate associations between changes in lumbar degenerative findings and pain. In 144 patients with lumbar radicular pain or low back pain, we scored disc degeneration, herniated discs, and high-intensity zones in the posterior annulus fibrosus on lumbar magnetic resonance imaging (MRI) at baseline and 5-year follow-up. Genotyping (TaqMan assay) was performed for genes encoding vitamin D receptor (VDR), collagen XIα (COL11A), matrix metalloproteinase 1/9 (MMP1/MMP9), and interleukin 1α/1RN (IL-1α/IL-1RN). Associations were analyzed using multivariate linear regression adjusted for age, sex, smoking, body mass index, and baseline scores for degenerated discs and herniated discs (when analyzing impact of baseline factors) or for pain (when analyzing associations with pain). Progression of disc degeneration over 5years was significantly (p < 0.001) related to higher age and less disc degeneration at baseline, but not to sex, smoking, body mass index, herniated discs, or variants in the studied genes. No associations were identified between changes in disc degeneration or high-intensity zones and pain at 5-year follow-up. However, increased number of herniated discs over 5years was associated with pain at rest (p = 0.019). Age and disc degeneration at baseline, rather than genetic factors, influenced the 5-year development of disc degeneration in patients with lumbar radicular pain or low back pain. Development of herniated discs was related to pain at rest.

The Effects of Spinopelvic Parameters such as Lumbar Lordosis and Sacral Slope Angles in The Development of Lumbar Disc Degeneration

The Effects of Spinopelvic Parameters such as Lumbar Lordosis and Sacral Slope Angles in The Development of Lumbar Disc Degeneration

Asymmetry between the superior and inferior endplates is a risk factor for lumbar disc degeneration.

Endplate pathology plays an important role in the development of lumbar disc degeneration. Previous research paid little attention to differences between the superior and inferior endplates as a possible risk factor for disc degeneration. The purpose of this study was to test the hypothesis that asymmetry between the superior and inferior endplates is a risk factor for the development of lumbar disc degeneration. A total of 134 patients with lumbar disc herniation (LDH) and 100 healthy adults ("Controls") underwent magnetic resonance imaging scans. Each disc was categorized as non-degenerated (Pfirrmann grades I-II) or degenerated (Pfirrmann grades III-V) and get the following three groups: "Degenerated LDH" discs (n = 145), "Non-degenerated LDH" discs (n = 525) and "Non-degenerated Control" discs (n = 500). On mid-sagittal image, the lumbar endplate morphology could be categorized into three types: Flat, concave, and irregular. Superior and inferior endplates of a given disc were "symmetric" if both were of the same type, and "asymmetric" if they were of different types. The proportion of asymmetric endplates at L4-5 was higher in the "Degenerated LDH" discs group (47%) than in the "Non-degenerated LDH" discs group (21%) or "Non-degenerated Control" discs group (7%) (p < 0.05). At L5-S1 the proportions were 73%, 55%, and 38% (p < 0.05). Asymmetry of superior and inferior endplates in the mid-sagittal plane is a risk factor for lumbar disc degeneration. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:2469-2475, 2018.

Association of collagen I, IX and vitamin D receptor gene polymorphisms with radiological severity of intervertebral disc degeneration in Southern European Ancestor.

Several genomic loci have been previously found to be associated with intervertebral disc degeneration, so far. Data are mostly derived from northern European countries whereas data derived from Southern European Ancestor are limited. This study aimed to evaluate the association between radiological disease severity of lumbar disc degeneration and certain genetic loci in a sample of participants from Southern Europe. Seventy-five patients with mild to severe lumbar disc degeneration and 25 healthy controls were enrolled into the study. In each subject, each lumbar intervertebral disc was separately examined to obtain a total radiological score for disease severity. In addition, single-nucleotide polymorphisms of predefined genetic samples were analyzed in all participants: COL1A1 Sp1, COL9a2 Trp2, COL9a3 Trp3, and VDR TaqI. Degeneration scores were significantly worse in cases with COL1A1 Sp1, COL9a3 Trp3, and VDR TaqI mutations; however, COL9a2 Trp2 mutation was not associated with a difference in the severity of disc degeneration. In addition, subjects with mutation in more than one gene sample (n = 20) had significantly worse degeneration scores than the remaining study participants (n = 80) (17.70 ± 2.72 vs. 21.81 ± 1.81, p < 0.001). Single-nucleotide polymorphisms occurring in COL1A1, COL9a3 and VDR genes seem to be associated with the development of lumbar disc degeneration in this cohort, possibly with even more pronounced association when multiple mutations are present in the same individual. By further prospective twin studies in associated genes and analyses of their relationship with environmental factors in an internationally sampled large cohort will make a more clear-minded conclusion about their association with disc degeneration, which would yield better appreciation and clinical planning of some predisposed people for these pathologies.

Association of the Polymorphism of TRAIL with the Risk and Severity of Lumbar Disc Degeneration in Chinese Han Population

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induces apoptosis of various normal and tumor cells. Apoptosis plays an important role in the development of lumbar disc degeneration (LDD). The aim of this study was to determine whether the 1595C/T polymorphism of the TRAIL gene is associated with the increased risk and severity of LDD in the Chinese Han population. This study consisted of 312 patients with LDD and 196 healthy controls. The grade of disc degeneration was determined according to Schneiderman's classification for magnetic resonance imaging (MRI). The genotype frequency of the 1595C/T polymorphism was in agreement with the Hardy-Weinberg equilibrium (p=0.278). Patients with LDD had significantly lower frequencies of CT and TT genotypes compared with normal controls (p<0.001). In addition, a lower frequency of the T allele was found in patients with LDD than normal controls (p<0.001). Unconditional logistic regression analysis revealed that CT and TT genotypes were both significantly associated with a reduced risk of LDD compared with the CC genotype (p<0.001; odds ratio [OR] 0.327; 95% confidence interval [95% CI] 0.217-0.493 and p<0.001; OR 0.393; 95% CI 0.234-0.661, respectively). Furthermore, the T allele was significantly associated with a decreased risk of LDD compared with the C allele (p<0.001; OR 0.483; 95% CI 0.369-0.633). In addition, the CT and TT genotypes, as well as the T allele, were associated with lower degenerative grades of LDD compared with the CC genotype and the C allele, respectively (p=0.008 and p=0.001, respectively). The 1595C/T polymorphism of TRAIL may be adversely associated with the risk and severity of LDD in the Chinese Han population.

Role of vitamin D3 in treatment of lumbar disc herniation--pain and sensory aspects: study protocol for a randomized controlled trial.

BackgroundVitamin D receptors have been identified in the spinal cord, nerve roots, dorsal root ganglia and glial cells, and its genetic polymorphism association with the development of lumbar disc degeneration and herniation has been documented. Metabolic effects of active vitamin D metabolites in the nucleus pulposus and annulus fibrosus cells have been studied. Lumbar disc herniation is a process that involves immune and inflammatory cells and processes that are targets for immune regulatory actions of vitamin D as a neurosteroid hormone. In addition to vitamin D’s immune modulatory properties, its receptors have been identified in skeletal muscles. It also affects sensory neurons to modulate pain. In this study, we aim to study the role of vitamin D3 in discogenic pain and related sensory deficits. Additionally, we will address how post-treatment 25-hydroxy vitamin D3 level influences pain and sensory deficits severity. The cut-off value for serum 25-hydroxy vitamin D3 that would be efficacious in improving pain and sensory deficits in lumbar disc herniation will also be studied.Methods/DesignWe will conduct a randomized, placebo-controlled, double-blind clinical trial. Our study population will include 380 cases with one-level and unilateral lumbar disc herniation with duration of discogenic pain less than 8 weeks. Individuals who do not have any contraindications, will be divided into three groups based on serum 25-hydroxy vitamin D3 level, and each group will be randomized to receive either a single-dose 300,000-IU intramuscular injection of vitamin D3 or placebo. All patients will be under conservative treatment. Pre-treatment and post-treatment assessments will be performed with the McGill Pain Questionnaire and a visual analogue scale. For the 15-day duration of this study, questionnaires will be filled out during telephone interviews every 3 days (a total of five times). The initial and final interviews will be scheduled at our clinic. After 15 days, serum 25-hydroxy vitamin D3 levels will be measured for those who have received vitamin D3 (190 individuals).Trial registrationIranian Registry for Clinical Trials ID: IRCT2014050317534N1 (trial registration: 5 June 2014)

Polymorphism in the Hypoxia-Inducible Factor 1alpha Gene May Confer Susceptibility to LDD in Chinese Cohort

ObjectiveThis study aimed to investigate whether or not hypoxia-inducible factor-1α (HIF-1α) gene variants are associated with the susceptibility and clinical characteristics of lumbar disc degeneration (LDD).MethodsWe examined 320 patients with LDD and 447 gender- and age-matched control subjects. We also determined the HIF-1α gene variants, including C1772T (P582S) and G1790A (A588T) polymorphisms.ResultsSignificant differences were observed in allelic and genotypic distributions of 1790 A > G polymorphisms between LDD cases and control subjects. Logistic regression revealed that 1790 AA genotypes indicated a protective effect against the development of LDD. The HIF-1α 1790 A > G polymorphisms also affected the severity of LDD as evaluated based on the modified Japanese Orthopedic Association (mJOA) scores. The 1790 AA genotype carriers exhibited significantly lower mJOA scores than AG and GG carriers. C1772T did not show any association with the risk and severity of LDD.ConclusionOur study suggested that HIF-1α 1790 A > G polymorphisms may be used as a molecular marker to determine the susceptibility and severity of LDD.

Incidence and Risk Factors for Lumbar Degenerative Disc Disease in the United States Military 1999–2008

The epidemiology of lumbar degenerative disc disease (DDD) is poorly understood, and the incidence of this disorder has not previously been characterized for a young, physically active population. This study sought to evaluate the incidence of lumbar DDD, and identify risk factors for its development, among individuals serving in the U.S. military over a 10-year period. The Defense Medical Epidemiology Database was queried for the years 1999-2008 using the International Classification of Diseases, Ninth Revision, Clinical Modification code for lumbar disc degeneration (722.52). Overall incidence was determined and multivariate Poisson regression analysis was performed to identify risk factors among demographic characteristics such as age, sex, race, military rank, and branch of service. White race, female sex, Army, Air Force, or Marine service, enlisted positions within the ranks, and age were found to be significant risk factors for the development of lumbar disc degeneration. Increased age appeared to be one of the most important risk factors, with adjusted incidence rates successively increasing for each age group under study. The incidence of lumbar DDD in this young, racially diverse, and physically active population is higher than most other degenerative conditions.

Risk factors for lumbar disc degeneration: a 5-year prospective MRI study in asymptomatic individuals.

A longitudinal magnetic resonance imaging investigation of lumbar disc degeneration in asymptomatic individuals was conducted. To investigate risk factors for the development or deterioration of lumbar disc degeneration. Numerous studies have explored the significance of certain risk factors for the development or progression of disc degeneration, but no comprehensive longitudinal magnetic resonance imaging-based study has been reported that simultaneously considers clinical, morphologic, physical, psychosocial, and occupational risk factors. In the 5-year follow-up evaluation of 41 asymptomatic individuals, the risk factors for the development of lumbar disc degeneration and its progression were investigated. All 41 individuals had a magnetic resonance imaging scan at baseline and at the minimum 5-year follow-up assessment using the same scanner and protocol. The magnetic resonance images were analyzed independently by two radiologists with regard to disc degeneration. Various predictor variables were assessed both at baseline and follow-up, with special emphasis on physical job characteristics, sports activities, and magnetic resonance image-based morphologic findings. Of the 41 individuals, 17 (41%) exhibited a deterioration of the disc status. In 10 individuals, the progression of disc degeneration was one grade or more. Only a weak correlation existed between progressive disc degeneration and low back pain development during a 5-year follow-up period. Multiple logistic regression analysis demonstrated that the extent of disc herniation (odds ratio [OR], 12.63; confidence interval [CI], 1.24-128.49), the lack of sports activities (OR, 2.71; CI, 1.04-7.07), and night shift work (OR, 23.01; CI, 1.26-421.31) were significant predictors for disc degeneration during follow-up evaluation when control was used for the number of degenerated discs at baseline, gender, age, and body mass index. The results indicate that the extent of disc herniation, the lack of sports activities, and night shift work are significant risk factors for the development of lumbar disc degeneration and its progression.

Familial predisposition for lumbar degenerative disc disease. A case-control study.

A case-control study using magnetic resonance imaging and plain radiography to evaluate whether a family history of lumbar disc herniation is a risk factor for disc degeneration. To evaluate the significance of a family history of operated lumbar disc herniation in the development of lumbar disc degeneration and lumbar disc herniation. There are only a few epidemiologic studies indicating that a family history of intervertebral disc herniation is a risk factor for juvenile disc herniation. Recently, similarities in degenerative findings of the lumbar spine between identical twins have been reported. In the case group, 24 patients who were the immediate relatives of patients who had undergone surgery for disc herniation and who presented or had a history of low back pain and/or unilateral leg pain were included. Control individuals included 72 age- and gender-matched outpatients who reported low back pain and/or leg pain without a family history of operated disc herniation. The incidence, level, and topographic location of disc herniation/diffuse bulge; the incidence and grade of disc degeneration observed on magnetic resonance images; and degenerative changes suggesting disc degeneration observed on plain radiographs were compared between the relatives of patients with disc herniation (cases) and the controls. The incidence of disc degeneration at L4-L5 and L5-S1 in cases (L4-L5, 18/24; L5-S1, 18/24) and controls (L4-L5, 45/72; L5-S1, 43/72) was similarly high. However, the grade of disc degeneration according to magnetic resonance imaging signal intensity on the T2-weighted sagittal image using Schneiderman's four-grade classification was significantly more severe in cases (L4-L5: Grade 1, 6/24; Grade 2, 4/24; Grade 3, 13/ 24; Grade 4, 1/24; L5-S1: Grade 1, 6/24; Grade 2: 3/24, Grade 3: 12/24, Grade 4: 3/24) than in controls (L4-L5: Grade 1, 27/72; Grade 2, 24/72; Grade 3, 20/72; Grade 4, 1/72; P = 0.034; L5-S1: Grade 1, 29/72; Grade 2, 23/72; Grade 3, 13/72; Grade 4, 7/72; P = 0.023; Mann-Whitney U test). The incidence of disc herniation/diffuse bulge at L4-L5 (16/24) and L5-S1 (11/24) in cases was higher than that in controls (L4-L5, 33/72; P = 0.07; L5-S1, 17/ 72; P = 0.04; chi-square test). The current study provided evidence that a family history of operated lumbar disc herniation has a significant implication in lumbar degenerative disc disease. There may be a genetic factor in the development of lumbar disc herniation as an expression of disc degeneration.