Instability Of Lumbar Spine Research Articles

The Effect of L5 Morphology on Prevention of L5-S1 Degeneration Following Floating Fusion for Degenerative Spine Disorders.

Retrospective Study. The selection of floating fusion or lumbosacral fusion arises when treating patients with instability or stenosis of the lower lumbar spine concomitantly radiographic degeneration of L5-S1. This study aimed to investigate the preoperative anatomical or morphological factors affecting the survivorship of the L5-S1 after floating fusion. This study included 77 patients who had undergone floating fusion surgery through the TLIF approach. Preoperative radiographic parameters were evaluated using anteroposterior and lateral lumbar spine radiographs. The patients were divided into two groups according to the Modified Pfirrmann Grading and total endplate score. Multivariable regression analysis was performed to explore the relationships between the anatomical or morphological characteristics of L5 and the degeneration of L5-S1. The disc degeneration group exhibited a smaller height ratio of the iliac crest (Hi) and a less L5 deep position. Furthermore, the right/left height of L4 (Hr/Hl) and the right/left width of transverse process of L5 (CRt/CLt) were significantly higher in the disc and endplate degeneration groups. Multiple logistic regression analysis revealed that Hi and CRt were independently associated with L5-S1 disc degeneration, whereas Hr was a significant risk factor for L5-S1 endplate degeneration. Anatomical and morphological characteristics of L5, such as smaller Hi, higher CRt and Hr, were associated with an increased risk of L5-S1 degeneration in patients after floating fusion. These findings may indicate the fusion level when addressing lower lumbar degenerative diseases and the concurrent radiographic degeneration of L5-S1.

Inactivation of Tnf-α/Tnfr signaling attenuates progression of intervertebral disc degeneration in mice.

Intervertebral disc degeneration (IVDD) is a major cause of low back pain (LBP), worsened by chronic inflammatory processes associated with aging. Tumor necrosis factor alpha (Tnf-α) and its receptors, Tnf receptor type 1 (Tnfr1) and Tnf receptor type 2 (Tnfr2), are upregulated in IVDD. However, its pathologic mechanisms remain poorly defined. To investigate the role of Tnfr in IVDD, we generated global Tnfr1/2 double knockout (KO) mice and age-matched control C57BL/6 male mice, and analyzed intervertebral disc (IVD)-related phenotypes of both genotypes under physiological conditions, aging, and lumbar spine instability (LSI) model through histological and immunofluorescence analyses and μCT imaging. Expression levels of key extracellular matrix (ECM) proteins in aged and LSI mice, especially markers of cell proliferation and apoptosis, were evaluated in aged (21-month-old) mice. At 4 months, KO and control mice showed no marked differences of IVDD-related parameters. However, at 21 months of age, the loss of Tnfr expression significantly alleviated IVDD-like phenotypes, including a significant increase in height of the nucleus pulposus (NPs) and reductions of endplates (EPs) porosity and histopathological scores, when compared to controls. Tnfr deficiency promoted anabolic metabolism of the ECM proteins and suppressed ECM catabolism. Tnfr loss largely inhibited hypertrophic differentiation, and, in the meantime, suppressed cell apoptosis and cellular senescence in the annulus fibrosis, NP, and EP tissues without affecting cell proliferation. Similar results were observed in the LSI model, where Tnfr deficiency significantly alleviated IVDD and enhanced ECM anabolic metabolism while suppressing catabolism. The deletion of Tnfr mitigates age-related and LSI-induced IVDD, as evidenced by preserved IVD structure, and improved ECM integrity. These findings suggest a crucial role of Tnf-α/Tnfr signaling in IVDD pathogenesis in mice. Targeting this pathway may be a novel strategy for IVDD prevention and treatment.

“Functional Outcome Following Pedicle Screw Instrumentation and Fusion for Low-Grade Lumbar Spinal Instability in Tertiary Care Hospital in South India”

“Functional Outcome Following Pedicle Screw Instrumentation and Fusion for Low-Grade Lumbar Spinal Instability in Tertiary Care Hospital in South India”

Osteopontin deficiency promotes cartilaginous endplate degeneration by enhancing the NF-κB signaling to recruit macrophages and activate the NLRP3 inflammasome

Intervertebral disc degeneration (IDD) is a major cause of discogenic pain, and is attributed to the dysfunction of nucleus pulposus, annulus fibrosus, and cartilaginous endplate (CEP). Osteopontin (OPN), a glycoprotein, is highly expressed in the CEP. However, little is known on how OPN regulates CEP homeostasis and degeneration, contributing to the pathogenesis of IDD. Here, we investigate the roles of OPN in CEP degeneration in a mouse IDD model induced by lumbar spine instability and its impact on the degeneration of endplate chondrocytes (EPCs) under pathological conditions. OPN is mainly expressed in the CEP and decreases with degeneration in mice and human patients with severe IDD. Conditional Spp1 knockout in EPCs of adult mice enhances age-related CEP degeneration and accelerates CEP remodeling during IDD. Mechanistically, OPN deficiency increases CCL2 and CCL5 production in EPCs to recruit macrophages and enhances the activation of NLRP3 inflammasome and NF-κB signaling by facilitating assembly of IRAK1-TRAF6 complex, deteriorating CEP degeneration in a spatiotemporal pattern. More importantly, pharmacological inhibition of the NF-κB/NLRP3 axis attenuates CEP degeneration in OPN-deficient IDD mice. Overall, this study highlights the importance of OPN in maintaining CEP and disc homeostasis, and proposes a promising therapeutic strategy for IDD by targeting the NF-κB/NLRP3 axis.

Slit3 by PTH-Induced Osteoblast Secretion Repels Sensory Innervation in Spine Porous Endplates to Relieve Low Back Pain.

During aging, the spine undergoes degenerative changes, particularly with vertebral endplate bone expansion and sclerosis, that is associated with nonspecific low back pain (LBP). We reported that parathyroid hormone (PTH) treatment could reduce vertebral endplate sclerosis and improve pain behaviors in aging, SM/J and young lumbar spine instability (LSI) mice. Aberrant innervation noted in the vertebral body and endplate during spinal degeneration was reduced with PTH treatment in aging and LSI mice as quantified by PGP9.5 + and CGRP + nerve fibers, as well as CGRP expression in dorsal root ganglia (DRG). The neuronal repulsion factor Slit3 significantly increased in response to PTH treatment mediated by transcriptional factor FoxA2. PTH type1 receptor (PPR) and Slit3 deletion in osteoblasts prevented PTH-reduction of endplate porosity and improvement in behavior tests, whereas PPR deletion in chondrocytes continued to respond to PTH. Altogether, PTH stimulates Slit3 to repel sensory nerve innervation and provides symptomatic relief of LBP associated with spinal degeneration.

Network pharmacology and experimental validation to reveal the pharmacological mechanisms of Astragaloside Ⅳ in treating intervertebral disc degeneration

This study aims to identify potential targets and regulatory mechanisms of Astragaloside Ⅳ (AS-Ⅳ) in treating intervertebral disc degeneration (IDD) through network pharmacology analysis with experimental validation. Lumbar spine instability (LSI) mouse models were first established and treated with AS-Ⅳ. Micro-CT, safranin O-fast green staining, IDD score, RT-PCR and immunohistochemistry staining were employed to demonstrate the effect of AS-Ⅳ. Network pharmacology was used to predict the signaling pathways and potential targets of AS-Ⅳ in treating IDD. RT-PCR and immunohistochemistry staining were used to elucidate and validate the mechanism of AS-Ⅳ in vivo. Animal experiments showed that AS-Ⅳ maintained disc height and volume, improved matrix metabolism in LSI mice, and restored Col2α1, ADAMTS-5, Aggrecan, and MMP-13 expression in degenerated discs. Network pharmacology analysis identified 32 cross-targets between AS-Ⅳ and IDD, and PPI network analysis filtered out 11 core genes, including ALB, MAPK1, MAPK14 (p38 MAPK), EGFR, TGFBR1, MAPK8, MMP3, ANXA5, ESR1, CASP3, and IGF1. Enrichment analysis revealed that 7 of the 11 core target genes enriched in the MAPK signaling pathway, and AS-Ⅳ exhibited stable binding to them according to molecular docking results. Experimental validation indicated that AS-Ⅳ reversed mRNA levels of 7 core targets in degenerated disc tissues in LSI mice. Immunohistochemistry staining further revealed that AS-Ⅳ treatment mainly depressed IDD-elevated protein levels of EGFR, p38 MAPK and CASP3 in the annulus fibrosus. This study elucidates that AS-Ⅳ alleviates lumbar spine instability-induced IDD in mice, suggesting the mechanism may involve inhibition of the EGFR/MAPK signaling pathway.

Orthopedic robot-assisted endoscopic transforaminal lumbar interbody fusion for lumbar disc herniation with lumbar instability

To explore the safety and effectiveness of the robot-assisted system for transforaminal percutaneous endoscopic in the treatment of lumbar disc herniation with lumbar instability. From October 2021 to March 2023, 26 patients with single-segment lumbar disc herniation and lumbar spinal instability were treated with robot-assisted system for transforaminal percutaneous endoscopic. The operation time, intraoperative blood loss, incision length, postoperative drainage volume, postoperative ambulation activity time, postoperative hospitalization time were record. The intervertebral space height and the lumbar lordosis angle before and after surgery were observed and compared. Pain level was evaluated using the visual analogue scale(VAS). The clinical efficacy was evaluated by Oswestry disability index(ODI). The interbody fusion was evaluated by Brantigan Steffee criteria. All patients successfully completed the operation, the operation time ranged form 105 to 109 min with an average of (150.8±24.1) min. Intraoperative blood loss ranged form 35 to 88 ml with an average of (55.5±16.4) ml. Incision length ranged form 1.4 to 3.5 cm with an average of (2.3±0.8) cm. Postoperative drainage volume ranged form 15 to 40 ml with an average of (28.5±7.8) ml. Postoperative ambulation time ranged form 15 to 30 h with an average of (22.8±4.5) h. Postoperative hospitalization time was 3 to 7 d with an average of (4.2±1.3) d. Total of 26 patients were followed up, the duration ranged from 12 to 16 months with an average of (14.0±1.3) months. The VAS and ODI at 1 week [(2.96±0.72) points, (41.63±4.79)%] and 12 months[(1.27±0.60) points, (13.11±2.45)%] were significantly different from those before surgery[(6.69±0.93) points, (59.12±5.92)%], P<0.01. The height of the intervertebral space (11.95±1.47) mm and lumbar lordosis (57.46±7.59)° at 12 months were significantly different from those before surgery [(6.67±1.20) mm, (44.08±7.79)°], P<0.01. At 12 months after surgery, all patients had no pedicle screw rupture or dislocation of the fusion cage, and the intervertebral fusion was successful. According to Brantigan-Steffee classification, 17 cases were grade D and 9 cases were grade E. Robot-assisted system for transforaminal percutaneous endoscopic for the treatment of single-segment lumbar disc herniation with lumbar instability improved the accuracy and safety of the operation, and the clinical effect of early follow-up is accurate.

Efficacy and safety of conservative treatment in patients with neurologically intact thoracolumbar burst fractures: a meta-analysis

Objective. To conduct a meta-analysis of studies focused on the conservative treatment of thoracolumbar burst fractures, and to determine the efficacy and safety of this method in the observed group of patients.Material and Methods. The study was performed following PRISMA guidelines. Inclusion criteria for meta-analysis were as follows: availability of full-text version of the article in English or Russian; A3 or A4 type fractures according to the AOSpine classification, or burst fractures of types IIA, IIB or IIC according to the Denis classification, or a direct indication of the presence of a burst fracture without its classification; absence of neurological deficit; age over 18 years; detailed description of treatment outcomes or complications; and a follow-up for at least one year.Results. The meta-analysis included 29 articles describing the results of treatment of 1107 patients. At the time of admission, the following radiographic parameters were calculated for patients: mean kyphotic angle, 13.6 (95 % CI, 10.8–16.5), degree of vertebral body compression, 39.9 % (95 % CI, 27.7–52.0), and the degree of compression of the spinal canal lumen, 41.7 % (95 % CI, 29.2–54.2). A follow-up examination revealed a significant increase in segmental kyphosis by 3%, in vertebral body compression by 3.7 %, and lysis of bone fragments with a decrease in the degree of spinal canal stenosis by 2 times. The incidence of neurological deficit and progression of thoracic and lumbar spine instability was 5.8 % (95 % CI, 4.1–8.1) and 6.5 % (95 % CI, 4.5–9.3), respectively. Recovery of work ability according to Denis scale was as follows: W1 and W2 – 74.7 % (95 % CI, 63.9–83.1); W3 – 14.1 % (95 % CI, 10.2–19.3); and W4 and W5 – 14.8 % (95 % CI, 8.8–23.9).Conclusion. Conservative treatment of neurologically intact thoracolumbar burst fractures can be an effective and safe option if the angular deformity does not exceed 16 degrees and the anterior vertebral body compression rate is up to 52 %. With conservative therapy, a twofold reduction in spinal canal stenosis was observed due to the lysis of bone fragments. The pooled prevalence of radiculopathy or myelopathy with conservative therapy was 5.8 %. Orthopedic intervention due to the progression of instability of the damaged segment may be required in 6.5 % of patients. More than 90 % of patients returned to full-time work following conservative therapy. Comparative studieson the effectiveness of conservative therapy versus surgical treatment should be continued to form clear recommendations for the choice of treatment tactics for patients with uncomplicated fractures of the thoracic and lumbar spine.

Senescence of endplate osteoclasts induces sensory innervation and spinal pain.

Spinal pain affects individuals of all ages and is the most common musculoskeletal problem globally. Its clinical management remains a challenge as the underlying mechanisms leading to it are still unclear. Here, we report that significantly increased numbers of senescent osteoclasts (SnOCs) are observed in mouse models of spinal hypersensitivity, like lumbar spine instability (LSI) or aging, compared to controls. The larger population of SnOCs is associated with induced sensory nerve innervation, as well as the growth of H-type vessels, in the porous endplate. We show that deletion of senescent cells by administration of the senolytic drug Navitoclax (ABT263) results in significantly less spinal hypersensitivity, spinal degeneration, porosity of the endplate, sensory nerve innervation and H-type vessel growth in the endplate. We also show that there is significantly increased SnOC-mediated secretion of Netrin-1 and NGF, two well-established sensory nerve growth factors, compared to non-senescent OCs. These findings suggest that pharmacological elimination of SnOCs may be a potent therapy to treat spinal pain.

Senescence of endplate osteoclasts induces sensory innervation and spinal pain.

Spinal pain affects individuals of all ages and is the most common musculoskeletal problem globally. Its clinical management remains a challenge as the underlying mechanisms leading to it are still unclear. Here, we report that significantly increased numbers of senescent osteoclasts (SnOCs) are observed in mouse models of spinal hypersensitivity, like lumbar spine instability (LSI) or aging, compared to controls. The larger population of SnOCs is associated with induced sensory nerve innervation, as well as the growth of H-type vessels, in the porous endplate. We show that deletion of senescent cells by administration of the senolytic drug Navitoclax (ABT263) results in significantly less spinal hypersensitivity, spinal degeneration, porosity of the endplate, sensory nerve innervation, and H-type vessel growth in the endplate. We also show that there is significantly increased SnOC-mediated secretion of Netrin-1 and NGF, two well-established sensory nerve growth factors, compared to non-senescent OCs. These findings suggest that pharmacological elimination of SnOCs may be a potent therapy to treat spinal pain.

Senescence of endplate osteoclasts induces sensory innervation and spinal pain

Spinal pain affects individuals of all ages and is the most common musculoskeletal problem globally. Its clinical management remains a challenge as the underlying mechanisms leading to it are still unclear. Here, we report that significantly increased numbers of senescent osteoclasts (SnOCs) are observed in mouse models of spinal hypersensitivity, like lumbar spine instability (LSI) or aging, compared to controls. The larger population of SnOCs is associated with induced sensory nerve innervation, as well as the growth of H-type vessels, in the porous endplate. We show that deletion of senescent cells by administration of the senolytic drug Navitoclax (ABT263) results in significantly less spinal hypersensitivity, spinal degeneration, porosity of the endplate, sensory nerve innervation, and H-type vessel growth in the endplate. We also show that there is significantly increased SnOC-mediated secretion of Netrin-1 and NGF, two well-established sensory nerve growth factors, compared to non-senescent OCs. These findings suggest that pharmacological elimination of SnOCs may be a potent therapy to treat spinal pain.

Pip5k1γ promotes anabolism of nucleus pulposus cells and intervertebral disc homeostasis by activating CaMKII-Ampk pathway in aged mice.

Degenerative disc disease (DDD) represents a significant global health challenge, yet its underlying molecular mechanisms remain elusive. This study aimed to investigate the role of type 1 phosphatidylinositol 4-phosphate 5-kinase (Pip5k1) in intervertebral disc (IVD) homeostasis and disease. All three Pip5k1 isoforms, namely Pip5k1α, Pip5k1β, and Pip5k1γ, were detectable in mouse and human IVD tissues, with Pip5k1γ displaying a highest expression in nucleus pulposus (NP) cells. The expression of Pip5k1γ was significantly down-regulated in the NP cells of aged mice and patients with severe DDD. To determine whether Pip5k1γ expression is required for disc homeostasis, we generated a Pip5k1γfl/fl; AggrecanCreERT2 mouse model for the conditional knockout of the Pip5k1γ gene in aggrecan-expressing IVD cells. Our findings revealed that the conditional deletion of Pip5k1γ did not affect the disc structure or cellular composition in 5-month-old adult mice. However, in aged (15-month-old) mice, this deletion led to several severe degenerative disc defects, including decreased NP cellularity, spontaneous fibrosis and cleft formation, and a loss of the boundary between NP and annulus fibrosus. At the molecular level, the absence of Pip5k1γ reduced the anabolism of NP cells without markedly affecting their catabolic or anti-catabolic activities. Moreover, the loss of Pip5k1γ significantly dampened the activation of the protective Ampk pathway in NP cells, thereby accelerating NP cell senescence. Notably, Pip5k1γ deficiency blunted the effectiveness of metformin, a potent Ampk activator, in activating the Ampk pathway and mitigating lumbar spine instability (LSI)-induced disc lesions in mice. Overall, our study unveils a novel role for Pip5k1γ in promoting anabolism and maintaining disc homeostasis, suggesting it as a potential therapeutic target for DDD.

Lumbar instability remodels cartilage endplate to induce intervertebral disc degeneration by recruiting osteoclasts via Hippo-CCL3 signaling

Degenerated endplate appears with cheese-like morphology and sensory innervation, contributing to low back pain and subsequently inducing intervertebral disc degeneration in the aged population.1 However, the origin and development mechanism of the cheese-like morphology remain unclear. Here in this study, we report lumbar instability induced cartilage endplate remodeling is responsible for this pathological change. Transcriptome sequencing of the endplate chondrocytes under abnormal stress revealed that the Hippo signaling was key for this process. Activation of Hippo signaling or knockout of the key gene Yap1 in the cartilage endplate severed the cheese-like morphological change and disc degeneration after lumbar spine instability (LSI) surgery, while blocking the Hippo signaling reversed this process. Meanwhile, transcriptome sequencing data also showed osteoclast differentiation related gene set expression was up regulated in the endplate chondrocytes under abnormal mechanical stress, which was activated after the Hippo signaling. Among the discovered osteoclast differentiation gene set, CCL3 was found to be largely released from the chondrocytes under abnormal stress, which functioned to recruit and promote osteoclasts formation for cartilage endplate remodeling. Over-expression of Yap1 inhibited CCL3 transcription by blocking its promoter, which then reversed the endplate from remodeling to the cheese-like morphology. Finally, LSI-induced cartilage endplate remodeling was successfully rescued by local injection of an AAV5 wrapped Yap1 over-expression plasmid at the site. These findings suggest that the Hippo signaling induced osteoclast gene set activation in the cartilage endplate is a potential new target for the management of instability induced low back pain and lumbar degeneration.

MINK1 deficiency stimulates nucleus pulposus cell pyroptosis and exacerbates intervertebral disc degeneration

Intervertebral disc (IVD) degeneration, induced by aging and irregular mechanical strain, is highly prevalent in the elderly population, serving as a leading cause of chronic low back pain and disability. Evolving evidence has revealed the involvement of nucleus pulposus (NP) pyroptosis in the pathogenesis of IVD degeneration, while the precise regulatory mechanisms of NP pyroptosis remain obscure. Misshapen/Nck-interacting kinase (NIK)-related kinase 1 (MINK1), a serine-threonine protein kinase, has the potential to modulate the activation of NLRP3 inflammasome, indicating its pivotal role in governing pyroptosis. In this study, to assess the significance of MINK1 in NP pyroptosis and IVD degeneration, NP tissues from patients with varying degrees of IVD degeneration, and IVD tissues from both aging-induced and lumbar spine instability (LSI) surgery-induced IVD degeneration mouse models, with or without MINK1 ablation, were meticulously evaluated. Our findings indicated a notable decline in MINK1 expression in NP tissues of patients with IVD degeneration and both mouse models as degeneration progresses, accompanied by heightened matrix degradation and increased NP pyroptosis. Moreover, MINK1 ablation led to substantial activation of NP pyroptosis in both mouse models, and accelerating ECM degradation and intensifying the degeneration phenotype in mechanically stress-induced mice. Mechanistically, MINK1 deficiency triggered NF-κB signaling in NP tissues. Overall, our data illustrate an inverse correlation between MINK1 expression and severity of IVD degeneration, and the absence of MINK1 stimulates NP pyroptosis, exacerbating IVD degeneration by activating NF-κB signaling, highlighting a potential innovative therapeutic target in treating IVD degeneration.

Senescent-like macrophages mediate angiogenesis for endplate sclerosis via IL-10 secretion in male mice

Endplate sclerosis is a notable aspect of spine degeneration or aging, but the mechanisms remain unclear. Here, we report that senescent macrophages accumulate in the sclerotic endplates of lumbar spine instability (LSI) or aging male mouse model. Specifically, knockout of cdkn2a (p16) in macrophages abrogates LSI or aging-induced angiogenesis and sclerosis in the endplates. Furthermore, both in vivo and in vitro studies indicate that IL-10 is the primary elevated cytokine of senescence-related secretory phenotype (SASP). Mechanistically, IL-10 increases pSTAT3 in endothelial cells, leading to pSTAT3 directly binding to the promoters of Vegfa, Mmp2, and Pdgfb to encourage their production, resulting in angiogenesis. This study provides information on understanding the link between immune senescence and endplate sclerosis, which might be useful for therapeutic approaches.

Unprecedented journey to 650 transpedicular screws using freehand technique and intraoperative C-arm imaging with technical nuances.

Pedicle screw placement plays a crucial role in treating various cases such as fractures, scoliosis, degenerative spine issues, and kyphosis, reinforcing all three spinal columns simultaneously. While three-dimensional navigation-assisted pedicle screw placement is considered superior, the freehand technique relies on anatomical landmarks and tactile feedback, with observed low complication rates. This was a prospective single-center study conducted over a period of 3 years. It included all patients of dorsal, lumbar, and sacral spinal instability of myriad etiology. Previously operated patients and sick obtunded patients were excluded from the study. In our study, we included 102 patients including 62 (60.7%) males and 40 (39.2%) females. More than half of patients were young in the age group of 20-50 years. Our study population had a varied etiology with 43.1% of patients having vertebral column instability due to trauma. The other etiologies were spondylolisthesis and lumbar canal stenosis (39.2%), Pott's spine (11.7%), tumors (2.9%), and osteoporotic fractures (2.9%). Majority of patients (44.1%) presented with lower backache with radiculopathy. All the transpedicular screws inserted were evaluated by C-arm to assess for screw fixation. In the first year of our study, an average of 4 anteroposterior (AP) and 4 lateral C-arm X-ray shots were taken per screw placement. In the next year, an average of 3 AP and 3 lateral shots and finally in the last year of our study only 2 AP and 2 lateral C-arm X-ray shots were taken per screw placement. Out of 650 screws placed, 4 screws were identified to cause breach with maximum breaches in the lumbar spine fixation. In dorsal spine fixation, there was 1 lateral breach at D10. In lumbar spine fixation, there were 3 breaches: two medial one each at L4 and L5 and one anterior at L2 level. The various complications include wound infection, temporary and permanent neurological deficit, screw breakage, screw misplacement, cerebrospinal fluid leaks, nonunion, and spinal epidural hematoma. Our study has provided strong encouragement to persist with the freehand technique in transpedicular fixation surgeries after a certain number of cases given the minimal breaches and complications observed. There are subtle technical nuances as we increase the number of cases with less exposure of anatomical landmarks and X-rays. Success hinges on experience, adherence to technique, and thorough preoperative planning. Further research and extended follow-up periods are necessary to firmly establish this technique as the gold standard.

Traction Spurs in the Lumbar Spine: A Historical Overview and Future Perspectives.

Numerous studies have explored the connection between lumbar osteophytes, their pathophysiology, and instability since Macnab's 1971 report on traction spurs as an indicator of lumbar instability. This study provides a narrative historical overview of traction spurs, a classic finding that suggests lumbar instability. It summarizes the causes of anterior lumbar vertebral osteophytes, the relationship between traction spurs and lumbar spinal instability, and the clinical significance of traction spurs. Vertebral osteophytes are grouped into two categories, namely, traction spurs or claw spurs, which represent different stages of the same pathological process. Traction spurs are indicative of instability and occur in the early stage of disc degeneration, characterized by temporary dysfunction or instability. Traction spur formation following fusion surgery can predict union or nonunion, and it serves as an indicator of preoperative and postoperative segmental instability. The relationship between traction spurs and radiographic instability, as well as their association with imaging findings such as CT and MRI, has been clarified. Additionally, finite element analysis and mechanical testing have been used to investigate the significance of traction spurs. However, further research is needed to verify that traction spurs are an accurate indicator of pre- and postoperative lumbar instability.

Evaluation of Percutaneous Transpedicular Fixation in thoracic and lumbar spine instability

Evaluation of Percutaneous Transpedicular Fixation in thoracic and lumbar spine instability

REHABILITATION OF PATIENTS WITH CERVICAL AND LUMBAR SPINE INSTABILITY USING TYMO ROBOTIC STABILOMETRICAL PLATFORM.

Introduction. The musculoskeletal system plays a vital role in maintaining posture and facilitating human movement, with the muscles often subjected to significant stress. Stabilometry can be used for evaluating postural balance and aiding in rehabilitation. This study aimed to assess the efficacy of the TYMO robotic stabilometric platform for the rehabilitation of patients with cervical and lumbar spine instability.Participants and methods. The study was conducted on the stable platform TYMO (Tyromotion). The study included 30 healthy students (group 1), 28 patients with instability of the cervical vertebra, who underwent standard rehabilitation treatment (group 2), 28 patients with instability of the cervical vertebra, who additionally used with a stabiloplatform (group 3), 29 patients with with instability of the lumbar spine, who received standard rehabilitation treatment (group 4), 29 patients with instability of the lumbar spine, who were additionally treated with a stabiloplatform (group 5). Groups 3 and 5, alongside with standard rehabilitation treatment, received a 10-day course involving stabiloplatform training. The parameters of the Center of Force (COF) section and load distribution were analyzed. Results and Discussion. When analyzing the respective indices across all groups in various functional positions prior to the treatment, the values were significantly increased. The use of the stabiloplatform proved to be effective in the treatment of patients, leading to the normalization of these indices. Notably, its application yielded a lasting therapeutic effect, whereas conventional physiotherapeutic methods fell short in achieving a lasting impact. Conclusions: Patients with cervical or lumbar spine instability demonstrate impaired balance test indicators. Following a 10-day treatment regimen with traditional rehabilitation methods, improvements are observed across all indicators, but they do not fully restore to the control levels in all functional positions. Furthermore, after one month, indicators deteriorate in nearly all functional positions. Training using a stabiloplatform is an effective approach in the treatment of patients with cervical or lumbar spine instability, and its use demonstrates a sustained therapeutic benefit.

Rasch analysis, reliability, and validity of the Turkish version of the Lumbar Spine Instability Questionnaire.

Lumbar instability is an important condition that can be seen frequently in people with low back pain, affecting both the progression and the choice of appropriate exercise. The Lumbar Spine Instability Questionnaire (LSIQ) is a simple and low-cost tool for evaluating disturbed back stability in people with low back pain. The aim of this study is to develop the Turkish version of the LSIQ (LSIQ-T) and to evaluate its psychometric properties using the Rasch model. One hundred participants with chronic low back pain completed the LSIQ-T. The LSIQ-T was repeated for 30 participants after 1 week to establish its test-retest reliability. While internal and external construct validity were investigated using Rasch analysis and the Spearman correlation coefficient, respectively, reliability was evaluated in terms of internal consistency by Cronbach's alpha and the Person Separation Index (PSI). All items of the LSIQ-T were found to fit the Rasch model (chi-square: 34.07 (df = 15), p = 0.0033). The internal construct validity was good, the overall mean item fit residual was 0 (SD: 0.765), and the mean person fit residual was 0.322 (SD: 1.123). Internal consistency reliability was low with a PSI of 0.63 although Cronbach's alpha was acceptable (0.68). When the test-retest reliability was examined via differential item functioning (DIF) by time, none of the items showed DIF. The LSIQ-T is a valid unidimensional scale for the Turkish population. Although the LSIQ-T had low internal consistency, it demonstrated unidimensionality and is appropriate for use. Therefore, the LSIQ-T can be used in clinical practice and scientific research.