Incidence and temporal changes in lumbar degeneration and low back pain in child and adolescent weightlifters: A prospective 5-year cohort study.
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ABSTRACT:
SUBMITTER: Yoshimizu R
PROVIDER: S-EPMC9242517 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Back pain is common and costly. Although lumbar disc degeneration has long been regarded as a major contributor to back pain, how disc degeneration leads to back pain remains unclear. Recent studies observed microglia activation in the spinal cord after disc degeneration, suggesting activated microglia may be involved in discogenic back pain. To determine whether microglia activation participates in disc degeneration-induced back pain, we used a modified disc puncture-induced degeneration-related back pain mouse model to examine the changes in spinal microglia and investigate the potential link between microglia activation and discogenic back pain. In this study, 46 CX3CR1GFP/+ male mice were used in experimental and sham groups. A modified posterolateral retroperitoneal approach was used to expose the L3/L4 disc to induce the needle puncture in the experimental group. Behavioral tests, including grip force and physical function, were used to measure back pain at pre- and postsurgery. The L3 dorsal root ganglions and lumbar spinal cord were obtained at postoperative weeks 1 to 4 followed by immunofluorescence with different antibodies. Micrographs were obtained by confocal microscopy, and morphometric measurements of microglia were analyzed using Imaris. The punctured disc underwent progressive degeneration and mice with disc degeneration showed impaired grip force and physical function. Compared to the control mice, the number of microglia in the lumbar spinal cord was significantly increased in the disc-punctured animals. Moreover, accumulated microglia exhibited larger soma size and lesser ramification in the disc-injured mice. Immunofluorescence demonstrated colony-stimulating factor 1, a cytokine that promotes microglia repopulation, was significantly increased in L3 dorsal root ganglions, whereas its receptor colony-stimulating factor 1 receptor was upregulated on microglia in the disc-injured mice. In summary, lumbar disc puncture caused progressive disc degeneration which induced microglia activation and back pain in mice. Increased colony-stimulating factor 1/colony-stimulating factor 1 receptor signaling is involved in the disc degeneration-induced microglia activation and back pain.
| S-EPMC6243401 | biostudies-literature
Project description:BackgroundLow back pain (LBP) is a common chief complaint from athletes. Lumbar spondylolysis (LS) is a common sport injury. Severe LS is likely to cause spinal instability, resulting in lumbar spondylolisthesis or lumbar disc herniation, and even damage to the spinal nerve roots. The incidence of LS is approximately 5% in the adult population, and nearly half of young athletes with LBP are diagnosed with LS. This meta-analysis analyzed the incidence of LS in athletes with LBP.MethodsPubMed, Embase, Cochrane (Cochrane Central Register of Controlled Trials), and Web of Science databases were systematically searched for published case report and retrospective analyses related to the topic from the date of database creation to January 1,2023. Relevant literature was screened and information extracted, and risk of bias was assessed for included studies using the methodological index for non-randomized-studies scale. Single-arm Meta-analysis was performed using R4.04 software. Heterogeneity was quantified by Cochran Q test and Higgins I2. Funnel plots were used to visualize publication bias, and Egger test and Begg test were used to statistical tests.ResultsA total of 9 studies (835 patients) were included in this study. Meta-analysis revealed that the prevalence of LS in athletes with LBP was estimated at 41.7%, [95% CI = (0.28-0.55)], but this prevalence varied considerably with the gender and age of the athletes.ConclusionThe estimated prevalence of LS in athletes with LBP is 41.7%, and future correlations between the prevalence of LS in adolescent athletes worldwide need to be assessed from different perspectives, including biomechanical, hormonal, anatomical, behavioral, and gender differences.
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Project description:BackgroundFew studies have quantified clinical improvement following minimally invasive lumbar decompression based on predominant back pain or leg pain.PurposeTo quantify improvement in patient-reported outcomes following minimally invasive lumbar decompression and determine the degree of improvement in back pain, leg pain, and disability in patients who present with predominant back pain or predominant leg pain.MethodsPatients who underwent primary, one-level minimally invasive lumbar decompression for degenerative pathology were retrospectively reviewed. Comparisons of visual analog scale (VAS) back and leg pain scores, Oswestry Disability Index (ODI) scores, and Short Form-12 (SF-12) mental and physical component scores from pre-operative to 6-week, 12-week, 6-month, and 1-year follow-up. Subgroup analyses were performed for patients with predominant back pain or predominant leg pain.ResultsA total of 102 patients were identified. Scores on VAS back and leg pain, ODI, and SF-12 physical component improved from pre-operative to all post-operative time points. After 1 year, patients reported a 2.8-point (47%) reduction in back pain and a 4-point (61.1%) reduction in leg pain scores; 52 patients with predominant back pain and 50 patients with predominant leg pain reported reductions in pain throughout the year following surgery. In both the back and leg pain cohorts, patients experienced reductions in ODI during the first 6 months and throughout 1-year follow-up, respectively. The majority of patients achieved minimum clinically important difference, regardless of predominant symptom.ConclusionsPatients reported improvements in back and leg pain following minimally invasive lumbar decompression regardless of predominant presenting symptom; however, patients with predominant leg pain may experience greater improvement than those with predominant back pain.
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Project description:Study designRetrospective observational study.ObjectivesThere is no consensus to predict improvement of lower back pain (LBP) in lumbar spinal stenosis after decompression surgery. The aim of this study was to evaluate the improvement of LBP and analyze the preoperative predicting factors for residual LBP.MethodsWe retrospectively reviewed 119 patients who underwent lumbar decompression surgery without fusion and had a minimum follow-up of 1 year. LBP was evaluated using the numerical rating scale (NRS), Japanese Orthopaedic Association Back Pain Evaluation Questionnaire (JOABPEQ) LBP score, and Roland-Morris Disability Questionnaire (RMDQ). All patients were divided into LBP improved group (group I) and LBP residual group (group R) according to the NRS score. Radiographic images were examined preoperatively and at the final follow-up. We evaluated spinopelvic radiological parameters and analyzed the differences between group I and group R.ResultsLBP was significantly improved after decompression surgery (LBP NRS, 5.7 vs 2.6, P < .001; JOABPEQ LBP score, 41.3 vs 79.6, P < .001; RMDQ, 10.3 vs 3.6, P < .001). Of 119 patients, 94 patients were allocated to group I and 25 was allocated to group R. There was significant difference in preoperative thoracolumbar kyphosis between group I and group R.ConclusionsMost cases of LBP in lumbar spinal stenosis were improved after decompression surgery without fusion. Preoperative thoracolumbar kyphosis predicted residual LBP after decompression surgery.
| S-EPMC7882817 | biostudies-literature
Project description:Low back pain is a prevalent global musculoskeletal issue, with a lifetime prevalence ranging from 49% to 70% in adults. Traditionally associated with adults, recent field surveys indicate comparable prevalence rates in children and adolescents, challenging earlier assumptions. Non-specific low back pain, where the source cannot be identified through diagnostic imaging, accounts for about 80%-90% of cases. Studies have shown that over 80% of adolescents with low back pain exhibit no underlying pathology. The prevalence of low back pain in younger populations varies widely, influenced by study methodology, age, and pain types. Research suggests that back pain prevalence in adolescents increases with age, with a shift in attitudes considering it is not necessarily indicative of specific issues. Level of evidence: level V.
| S-EPMC10693836 | biostudies-literature
Project description:BackgroundChronic low back pain (cLBP) affects millions of Americans and costs billions. Studies suggest a link between cLBP and joint hypermobility.MethodsWe conducted cross-sectional primary analyses of joint hypermobility and cLBP, lumbar spine osteoarthritis (OA), and lumbar facet joint OA (FOA) in 3 large studies-the Generalized Osteoarthritis Study, Genetics of Generalized Osteoarthritis Study, and Johnston County Osteoarthritis Project (total n = 5072). Associations of joint hypermobility and Beighton trunk flexion with cLBP and lumbar OA were estimated using separate adjusted logistic regression models. Adjusted pooled odds ratios (pORs) and 95% confidence intervals (CIs) were then summarized-using random effect univariate, multivariate crude, and adjusted models-and heterogeneity was determined (I2 statistic).ResultsIn univariate models, hypermobility was associated with symptomatic FOA (pOR = 0.64 [95% CI 0.44, 0.93]) but this result was not found in the multivariate models. In multivariate adjusted models, hypermobility was not significantly associated with cLBP and lumbar OA, but trunk flexion was inversely associated with cLBP (pOR = 0.40 [95% 0.26, 0.62]), spine OA (pOR = 0.66 [95% CI 0.50, 0.87]), symptomatic spine OA (pOR = 0.39 [95% CI 0.28, 0.53]), and symptomatic FOA (pOR = 0.53 [95% CI 0.37, 0.77]). Generally, between-study heterogeneity was moderate-high.ConclusionsHypermobility was not associated with cLBP or lumbar OA. The inverse association of trunk flexion with cLBP and lumbar OA may indicate a role for a flexible spine in avoiding or managing these conditions.
| S-EPMC6456963 | biostudies-literature
Project description:Low back pain (LBP) is the world's most debilitating condition. Disk degeneration has been regarded as a strong determinant associated with LBP. Overweight and obesity are public health concerns that affect every population worldwide and whose prevalence continues to rise. Studies have indicated strong associations between overweight/obesity and disk degeneration as well as with LBP. This broad narrative review article addresses the various mechanisms that may be involved leading to disk degeneration and/or LBP in the setting of overweight/obesity. In particular, our goal is to raise awareness of the role of fat cells and their involvement via altered metabolism or the release of adipokines as well as other pathways that may lead to the development of disk degeneration and LBP. Understanding the role of fat in this process may aid in the development of novel biological therapies and technologies to halt the progression or regenerate the disk. Moreover, with genetic advancements and the appreciation of genetic epidemiology, a more personalized approach to spine care may have to consider the role of fat in any preventative, therapeutic, and/or prognosis modalities toward the disk and LBP.
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Project description:Cellular senescence is a contributor to intervertebral disc (IVD) degeneration and low back pain. Here, we found that RG-7112, a potent mouse double-minute two protein inhibitor, selectively kills senescent IVD cells through apoptosis. Gene expression pathway analysis was used to compare the functional networks of genes affected by RG-7112, a pure synthetic senolytic with o-Vanillin a natural and anti-inflammatory senolytic. Both affected a functional gene network related to cell death and survival. O-Vanillin also affected networks related to cell cycle progression as well as connective tissue development and function. Both senolytics effectively decreased the senescence-associated secretory phenotype (SASP) of IVD cells. Furthermore, bioavailability and efficacy were verified ex vivo in the physiological environment of degenerating intact human discs where a single dose improved disc matrix homeostasis. Matrix improvement correlated with a reduction in senescent cells and SASP, supporting a translational potential of targeting senescent cells as a therapeutic intervention.
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Project description:BACKGROUND:A well-known supportive treatment for acute nonspecific back pain, elastic back support belts, are valued for their ability to accelerate natural self-healing, but there are concerns of a deconditioning effect due to their reliance on passive stabilization. METHODS:To evaluate the systematic effects of elastic abdominal belts on the trunk musculature, a total of 36 persons with acute lumbar back pain (no longer than one week) were divided into two groups: an abdominal belt wearing group (B) and a non-abdominal belt wearing control group (C). All were examined over a period of three weeks at three time points: T1 just after assignment, T2 one week later, and T3 further two weeks later. Surface EMG (sEMG) was used to record trunk muscle activation when walking on a treadmill at walking speeds of 2, 3, 4, 5, and 6 km/h. Similarly, pain intensity (VAS) and functional impairment (ODI) over time were recorded in both groups. RESULTS:Over the observation period, a slight advantage for decreased pain intensity (C: p<0.05 T2 vs. T1; B: p<0.01 T2 vs. T1, p<0.05 T3 vs. T1) and decreased functional impairment (Cohen's d vs. T1, C: T2 0.45, T3 0.86; B: T2 1.1, T3 1.0) was observed for the belt group. For the belt group both oblique abdominal muscles exhibited significantly lower sEMG throughout the observation period (external abdominal oblique muscle: (T1), T2, (T3), internal abdominal oblique muscle: T1, (T2), (T3)) and the sEMG for the back muscles ranged from unchanged to slightly elevated for this group, but never reached statistical significance. DISCUSSION:The reduced abdominal amplitude levels in the belt group likely result from the permanent elastic stabilization provided by the belt: the required elevated intra-abdominal pressure to enhance spinal stability is then provided by lessened abdominal muscle activity complemented by the belt's elastic support. With regard to the back muscles, the belt, due to its movement-restricting effect, tends to activate the paravertebral musculature. In this respect, the effect of elastic abdominal belts on the trunk muscles is not uniform. Therefore, the present results suggest that the effect of elastic abdominal belts appears to be more of a temporary neutral alteration of trunk muscle coordination, with some trunk muscles becoming more active and others less, and not a case of uniform deconditioning as is suspected.
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Project description:OBJECTIVE:Earlier studies documenting the effect of candidate genes on recovery have seldom taken into consideration the impact of emotional distress. Thus, we aimed to assess the modifying effect of emotional distress on genetic variability as a predictor for pain recovery in lumbar radicular (LRP) and low back pain (LBP). RESULTS:The study population comprised 201 patients and mean age was 41.7 years. The significant association between MMP9 rs17576 (B?=?0.71, 95% CI 0.18 to 1.24, p?=?0.009) and pain recovery remained statistically significant after adjusting for pain intensity at baseline, age, gender, smoking, body mass index, pain localization and emotional distress (B?=?0.68, 95% CI 0.18 to 1.18, p?=?0.008). In contrast, the association between OPRM1 (B?=?-?0.85, 95% CI -?1.66 to -?0.05, p?=?0.038) and pain recovery was abolished in the multivariate analysis (B?=?-?0.72, 95% CI -?1.46 to 0.02, p?=?0.058). Hence, MMP9 rs17576 and emotional distress independently seem to predict persistent back pain. The predictive effect of OPRM1 rs179971 with regard to the same outcome is probably dependent on other factors including emotional processing. Trial registration The Regional Committee for Medical Research and Ethics reference number 2014/1754.
| S-EPMC6712656 | biostudies-literature