Search

Background Circular RNAs (circRNAs) play an important role in the progression of intervertebral disc (IVD) degeneration (IVDD). Using bioinformatics analysis, we have found that the expression of circRNA hsa_circ_0059955 was significantly downregulated in IVDD tissues. However, the relevant mechanism of hsa_circ_0059955 in the progression of IVDD remains unclear. Methods CCK-8 and flow cytometry assays were used to evaluate cell proliferation and apoptosis. In addition, Western blot assay was used to detect the expressions of ITCH, p73, CDK2 in nucleus pulposus (NP) cells. Moreover, a puncture-induced IVDD rat model was established to explore the role of hsa_circ_0059955 in IVDD. Results The level of hsa_circ_0059955 was significantly decreased in IVDD tissues from IVDD patients. Itchy E3 ubiquitin protein ligase (ITCH) is the host gene of hsa_circ_0059955, and downregulation of hsa_circ_0059955 significantly decreased the expression of ITCH in NP cells. In addition, downregulation of hsa_circ_0059955 markedly inhibited proliferation and induced apoptosis and cell cycle arrest in NP cells. Moreover, in vivo study illustrated that overexpression of hsa_circ_0059955 ameliorated IVDD in rats. Conclusion Downregulation of hsa_circ_0059955 could induce apoptosis and cell cycle arrest in NP cells in vitro, while overexpression of hsa_circ_0059955 attenuated the IVDD in a puncture-induced rat model in vivo. Therefore, hsa_circ_0059955 might serve as a therapeutic target for the treatment of IVDD.

Osteoporosis (OP) is a systemic bone metabolic disease with complicated pathogenesis and is difficult to cure clinically. The regulatory mechanisms of OP are needed to be further investigated. In the present study, we focused on the role of myocardial infarction-associated transcript (MIAT) in OP development and examined the underlying mechanism. The serum expression levels of MIAT in samples from patients with OP and healthy controls were compared using quantitative reverse transcription-PCR (qRT-PCR). The dual-luciferase reporter assay was used to confirm the relationship between MIAT and its potential target microRNA, i.e., miR-150-5p. Moreover, bone marrow-derived mesenchymal stem cells (BMSCs) were cultured and transfected with MIAT shRNA, with or without miR-150-5p inhibitor. EdU staining and colony formation analysis were performed to determine the proliferation ability of these cells. Furthermore, the TUNEL assay and flow cytometry were used to assess BMSC apoptosis. Finally, RT-PCR and Western blot assays were employed to assess the expression of osteogenic differentiation biomarkers. Compared with controls, the expression of MIAT was significantly increased, whereas that of miR-150-5p was markedly decreased in patients with OP. MIAT and miR-150-5p expression levels exhibited a strong negative correlation. Furthermore, osteogenic differentiation indicators were suppressed in serum of OP patients. MIAT was downregulated, and miR-150-5p was upregulated in induced to osteogenic differentiation BMSCs. Furthermore, downregulation of MIAT dramatically promoted osteogenic differentiation, increased proliferation, and inhibited apoptosis in BMSCs; miR-150-5p inhibitor abrogated the effects of MIAT. In conclusion, lncRNA MIAT can regulate the proliferation, apoptosis, and osteogenic differentiation of BMSCs.

Background: Accumulating evidence demonstrates that long non-coding RNAs (lncRNAs) are associated with the development of osteoporosis. This study aimed to investigate the effects of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on osteogenic differentiation and cell apoptosis in osteoporosis. Methods: hindlimb unloading (HU) was performed to establish osteoporosis model in vivo. MicroCT was applied for pathological analysis. Microgravity (MG) was used to construct osteoporosis in vitro. The mRNA and miRNA expression was determined using RT-qPCR. Protein expression was determined using western blot. The binding sites between miR-485-5p and MALAT1/Wnt family member 7B (WNT7B) was predicted by bioinformatics analysis and verified by luciferase and RNA pull-down assays. Cellular functions were determined by ALP staining, Alizarin red staining, and flow cytometry assays. Results: MALAT1 expression was downregulated in HU mice and MG treated MC3T3-E1 cells. However, overexpression of MALAT1 upregulated the expression of Bmp4, Col1a1, Spp1, and enhanced ALP activity. Additionally, overexpression of MALAT1 inhibited apoptosis, decreased Bax and caspase-3 levels, and increased Bcl-2 level. Moreover, MALAT1 overexpression improved bone phenotype in vivo. MALAT1 functioned as a ceRNA to upregulate WNT7B. Overexpression of miR-485-5p rescued the promotion of osteogenic differentiation and the inhibition of apoptosis induced by MALAT1. Knockdown of WNT7B abolished the facilitation of osteogenic differentiation and the suppression of apoptosis induced by downregulation of miR-485-5p. Conclusion: In conclusion, MALAT1 promoted osteogenic differentiation and inhibited cell apoptosis through miR-485-5p/WNT7B axis, which suggested that MALAT1 is a potential target to alleviate osteoporosis.

ASB16 antisense RNA 1 (ASB16-AS1) is a cancer-associated long non-coding RNA that contributes to tumorigenesis and tumor development. Nevertheless, to the best of our knowledge, whether and how ASB16-AS1 is implicated in osteosarcoma (OS) malignancy remains unclear and therefore warrants exploration. Our current study focused on making in-depth investigation of ASB16-AS1 in OS. In the present study, the expression pattern of ASB16-AS1 in OS tissues and cell lines was analyzed. In addition, we examined the clinical value of ASB16-AS1 for OS patients. Furthermore, we explored the impacts of ASB16-AS1 on the malignant phenotype of OS cells in vitro and in vivo as well as the underlying mechanism.ASB16-AS1, microRNA-760 (miR-760) and hepatoma-derived growth factor (HDGF) expressions were measured using reverse transcription-quantitative PCR. Cell proliferation and apoptosis were evaluated using CCK-8 and flow cytometry analyses, respectively, and cell migration and invasion were determined via cell migration and invasion assays.ASB16-AS1 expression was significantly elevated in OS tissues and cell lines, and increased ASB16-AS1 expression was related to patients' tumor size, TNM stage, and distant metastasis. The overall survival rate of OS patients presenting high ASB16-AS1 expression was shorter than that of patients presenting low ASB16-AS1 expression. Reduced ASB16-AS1 expression inhibited OS cell proliferation, migration, and invasion; promoted cell apoptosis; and impaired tumor growth in vivo. Mechanistically, ASB16-AS1 served as a sponge for miR-760 and positively modulated the expression of its target HDGF. Finally, inhibiting miR-760 and restoring HDGF expression abolished the impacts of ASB16-AS1 knockdown on the malignant characteristics of OS cells.ASB16-AS1 is a novel oncogenic lncRNA in OS cells. ASB16-AS1 increased HDGF expression by sponging miR-760, thereby conferring cancer-promoting roles in OS. ASB16-AS1 is a potential early diagnostic and therapeutic target in OS.

Background: To investigate the therapeutic effect of Hydroxy-safflower yellow A (HSYA) on rat’s osteoporosis and explore its potential mechanism of action.Methods: Bilateral ovariectomized female rats (OVX) were used to establish a postmenopausal rat model of osteoporosis. HSYA was given as an intervention, and estradiol was used as a positive control. The levels of serum alkaline phosphatase (ALP), calcium ion (Ca2+), and inorganic phosphorus (IP) were used to detect bone loss. Three months after modeling, the rats were sacrificed and the rat’s ovaries, kidneys, tibia, and femur were used to calculate the organ index. The bone marrow of the femur of the rats was stained with Giemsa staining. The femur strength of rats was measured by INSTRON. The degree of osteoporosis was detected by pathological staining after decalcification of bone tissue. Predicted the main targets of HSYA in combination with bioinformatics, and the proteins related to osteoclast differentiation were detected in combination with western blotting. The effect of HSYA on the differentiation of RAW264.7 cells into osteoclasts was observed.Results: The Giemsa staining and serum test results showed that the operation was successful and affected bone metabolism. In the bone strength test, HSYA significantly increased the maximum threshold of femoral load in rats. Pathological examination showed that tibial cartilage, trabecular bone, and cortex significantly increased after treatment with HYSA. The number of osteoblasts increased while the number of osteoclasts decreased—elevated levels of type I and III collagen. Autodock was used for molecular docking of potential targets of HSYA. qPCR and western blot were used to show that the expression levels of CA2 and osteoclast differentiation-related proteins were significantly decreased after HSYA treatment. Cell level results showed that HSYA could inhibit the activity of osteoclasts and the ability of RAW264.7 cells to differentiate into osteoclasts.Conclusion: HSYA can inhibit the differentiation and formation of osteoclasts by inhibiting the expression of CA2 and relieving osteoporosis symptoms in OVX rats.

Ruofeng Yin,1 Junzhi Liu,2 Dongxu Zhao,1 Fei Wang1 1Department of Orthopedics, China-Japan Union Hospital Jilin University, Changchun, Jilin 130033, People’s Republic of China; 2Department of Quality Control, China-Japan Union Hospital Jilin University, Changchun, Jilin 130033, People’s Republic of ChinaCorrespondence: Fei WangDepartment of Orthopedics, China-Japan Union Hospital Jilin University, No. 126, Xiantai Road, Changchun, Jilin 130033, People’s Republic of ChinaEmail wangfei_king@163.comPurpose: ASB16 antisense RNA 1 (ASB16-AS1) is a cancer-associated long non-coding RNA that contributes to tumorigenesis and tumor development. Nevertheless, to the best of our knowledge, whether and how ASB16-AS1 is implicated in osteosarcoma (OS) malignancy remains unclear and therefore warrants exploration. Our current study focused on making in-depth investigation of ASB16-AS1 in OS. In the present study, the expression pattern of ASB16-AS1 in OS tissues and cell lines was analyzed. In addition, we examined the clinical value of ASB16-AS1 for OS patients. Furthermore, we explored the impacts of ASB16-AS1 on the malignant phenotype of OS cells in vitro and in vivo as well as the underlying mechanism.Methods: ASB16-AS1, microRNA-760 (miR-760) and hepatoma-derived growth factor (HDGF) expressions were measured using reverse transcription-quantitative PCR. Cell proliferation and apoptosis were evaluated using CCK-8 and flow cytometry analyses, respectively, and cell migration and invasion were determined via cell migration and invasion assays.Results: ASB16-AS1 expression was significantly elevated in OS tissues and cell lines, and increased ASB16-AS1 expression was related to patients’ tumor size, TNM stage, and distant metastasis. The overall survival rate of OS patients presenting high ASB16-AS1 expression was shorter than that of patients presenting low ASB16-AS1 expression. Reduced ASB16-AS1 expression inhibited OS cell proliferation, migration, and invasion; promoted cell apoptosis; and impaired tumor growth in vivo. Mechanistically, ASB16-AS1 served as a sponge for miR-760 and positively modulated the expression of its target HDGF. Finally, inhibiting miR-760 and restoring HDGF expression abolished the impacts of ASB16-AS1 knockdown on the malignant characteristics of OS cells.Conclusion: ASB16-AS1 is a novel oncogenic lncRNA in OS cells. ASB16-AS1 increased HDGF expression by sponging miR-760, thereby conferring cancer-promoting roles in OS. ASB16-AS1 is a potential early diagnostic and therapeutic target in OS.Keywords: osteosarcoma therapy, ASB16-AS1, hepatoma-derived growth factor, microRNA-760

Rationale: Intraspinal anesthesia, the most common anesthesia type of orthopedic operation, is regarded as safe and simple. Despite of the rare incidence, puncture related complication of intraspinal anesthesia is catastrophic for spinal cord. Here we present an intradural hematoma case triggered by improper anesthesia puncture. The principal reason of this tragedy was rooted in the neglect of spine deformities diagnosis before anesthesia. To the best of our knowledge, there is no specific case report focusing on the intradural hematoma triggered by improper anesthesia puncture. Patient concerns: Hereby a case of thoracolumbar spinal massive hematoma triggered by intraspinal anesthesia puncture was reported. The presenting complaint of the patient was little neurologic function improvement after surgery at 6-month follow-up. Diagnoses: Emergency MRI demonstrated that massive spindle-like intradural T2-weighted image hypointense signal masses from T12 to S2 badly compressed the dural sac ventrally, and his conus medullaris was at L3/4 intervertebral level with absence of L5 vertebral lamina. Hereby, the diagnoses were congenital spinal bifida, tethered cord syndrome, spine intradural hematoma, and paraplegia. Interventions: Urgent surgical interventions including laminectomy, spinal canal exploration hematoma removal, and pedicle fixation were performed. The patient received both medication (mannitol, mecobalamin, and steroids) and rehabilitation (neuromuscular electric stimulation, hyperbaric oxygen). Outcomes: Postoperation, he had regained only hip and knee flexion at II grade strength. His neurologic function was unchanged until 3 weeks postoperation. Six-month follow-up showed just little neurologic function improvement, and the American Spinal Injury Association grade was C. Lessons: By presenting an intradural hematoma case triggered by improper anesthesia puncture, we shared the treatment experience and discussed the potential mechanism of neurologic compromise. The principal reason for this tragedy is preanesthesia examination deficiency. Necessary radiology examinations must be performed to prevent misdiagnosis for spinal malformation.

MicroRNAs (miRNAs) are small conserved RNAs regulating specific target genes in posttranscriptional levels. They have been involved in multiple processes of tumor progression, including cell proliferation. miR-214-5p (also miR-214*) is a newly identified miRNA, and its functions are largely unknown. In this study, we explore the role of miR-214-5p in the proliferation and invasion of human osteosarcoma (OS) cells. The results showed that miR-214-5p was sharply reduced in OS tissues and cell lines, compared with normal tissues and cell lines. In addition, the miR-214-5p mimic greatly increased the miR-214-5p level and significantly decreased the proliferation and invasion of HOS and G293 OS cells. In contrast, the miR-214-5p inhibitor had a completely opposite effect on the miR-214-5p level, cell proliferation, and cell invasion. Moreover, bioinformatics and luciferase reporter gene assays confirmed that miR-1908 targeted the mRNA 3-UTR region of ROCK1, a characterized tumor promoter in OS. In conclusion, miR-214-5p was identified as a new tumor suppressor, which directly targeted ROCK1 and suppressed proliferation of human OS cells.

RASSF4, a member of the RASSF family, is broadly expressed in normal tissues but often inactivated in human cancers. Despite various studies on RASSF4, its role in osteosarcoma remains unclear. Therefore, in this study, we investigated the effects of RASSF4 expression on osteosarcoma cells and explored the underlying mechanism. The results of our study showed that RASSF4 was lowly expressed in osteosarcoma tissues and cells. RASSF4 overexpression significantly inhibited proliferation, migration, and invasion as well as the EMT process in osteosarcoma cells. Meanwhile, we found that RASSF4 overexpression markedly decreased the protein expression of -catenin, cyclin D1, and c-Myc in osteosarcoma cells. In conclusion, our findings showed that RASSF4 overexpression inhibits proliferation, invasion, EMT, and Wnt signaling pathway in osteosarcoma cells. Thus, RASSF4 may be considered a novel target for osteosarcoma treatment.

Introduction Reports pertaining to ureteral injury sustained during lumbar disc surgery are rare; most ureteral injuries in this setting involve laceration or transection. Patient concerns We report a rare case of a 55-year-old man who presented with complete left ureteral necrosis 20 days after sustaining ureteral transection during lumbar disc surgery. Diagnosis The patient presented with seroperitoneum caused by left ureteral injury; post-operative histopathological examination of surgical specimen after discectomy had revealed ureter-like tissue. Exploratory laparoscopic surgery revealed necrosis of a long segment of ureter, which was not amenable to treatment with conventional methods. Intervention We used a spiral bladder muscle flap with vascular pedicles to repair the ureteral defect. Outcomes Post-operative period was uneventful and the patient showed good recovery. Conclusion Spiral bladder muscle flap with vascular pedicles may be used to repair extensive ureteric injury.

Rationale: Traumatic nucleus pulposus sequestration (TNPS) usually occurs concurrently with severe destruction of bone. TNPS combined with a slight thoracolumbar flexion- distraction fracture, triggering a disastrous nerve injury, has rarely been reported. Due to the atypical radiologic manifestations, such a patient can easily be overlooked. Patient concerns: Hereby, we present a TNPS patient as well as a slight thoracolumbar flexion-distraction fracture and serious neurologic symptoms. Diagnoses: T12 spinous process fracture, L1 flexion distraction fracture, thoracolumbar traumatic nucleus pulposuse sequestration and lower limbs incomplete paralysis Interventions: To avoid further neurologic compromise, an urgent laminectomy and exploration of the spinal canal was performed. Outcomes: After decompression OR and 4 months rehabilitation, the patient's neurologic function improved remarkably. Lessons: A slight flexion-distraction fracture following injury is liable to eclipse the concurrence of TPNS. For this patient, a high-resolution MRI was needed to make a definitive diagnosis and guide surgery. Once TPNS has been diagnosed, sufficient decompression and discectomy surgery should be performed without delay.

Studies have shown that miR-145-3p functions as a tumor suppressor and is associated with tumor growth and metastasis. This study intends to uncover the mechanism of a tumor suppressor of miR-145-3p. The expressions of miR-194 in osteosarcoma cell lines and tissues were monitored by real-time PCR. The proliferation ability was examined by MTT assay. The apoptosis and autophagy of cells were monitored by flow cytometry and microcopy, respectively. The regulation of miR-145-3p on HDAC4 was determined by luciferase assays and western blot assay. The results showed that miR-145-3p was significantly reduced in the osteosarcoma compared with the normal bone tissue. Overexpression of miR-145-3p significantly attenuated the proliferation and induced the apoptosis and autophagy of osteosarcoma cells. Furthermore, we demonstrated that miR-145-3p has inhibited the malignant behavior of osteosarcoma by down-regulating HDAC4 expression. These findings suggested that miR-145-3p may act as a tumor suppressor in osteosarcoma. MiR-145-3p/HDAC4 may be a novel therapeutic target in treatment of osteosarcoma.

Background This study aimed to investigate the bone morphogenetic protein-2 (BMP-2) levels in serum and synovial fluid (SF) of patients with primary knee osteoarthritis (OA) and to exam its correlation with radiographic and symptomatic severity of the disease. Material/methods A total of 37 knee OA patients and 20 healthy controls were enrolled in this study. Knee OA radiographic grading was performed according to the Kellgren-Lawrence (KL) grading system by evaluating X-ray changes observed in anteroposterior knee radiography. Symptomatic severity of the disease was evaluated according to the Western Ontario McMaster University Osteoarthritis Index (WOMAC) scores. BMP-2 levels in serum and SF were determined using enzyme-linked immunosorbent assay. Results Serum BMP-2 level in patients with knee OA was higher than that in healthy controls. Knee OA patients with KL grade 4 showed significantly elevated BMP-2 levels in the serum and SF compared with those with KL grade 2 and 3. Knee OA patients with KL grade 3 had significant higher SF levels of BMP-2 than those with KL grade 2. BMP-2 levels in the serum and SF of knee OA patients were both positively correlated with KL grades and WOMAC scores. Conclusions BMP2 levels in serum and SF were closely related to the radiographic and symptomatic severity of knee OA and may serve as an alternative biochemical parameter to determine disease severity of primary knee OA.

The operating room is an important place for the treatment of patients undergoing surgery, the quality level of clinical nursing has a direct influence in the therapeutic effect of patients. In the present study, four components instructional design mode (4C training mode) was applied in the training of professional nurses in the operating room, it involved the following aspects: regular skill knowledge analysis, goals setting, as well as the construction and implementation of the project. Targeted training methods and training content were formulated in accordance with the learning ability and knowledge reserve of different professional nurses, and different skills required to master, to fully mobilize the enthusiasm and initiative of nurses, thereby to improve the operation and comprehensive level of nurses in the operation room to achieve good results.

To explorec Histocompatibility of nano-hydroxyapatite/poly-co-glycolic acid tissue engineering bone modified by mesenchymal stem cells with vascular endothelial frowth factor transinfected.Rat bone marrow mesenchymal stem cells (BMSCs) was separated, using BMSCs as target cells, and then vascular endothelial growth factor (VEGF) gene was transfected. Composite bone marrow mesenchymal stem cells and cells transfected with nano-hydroxyapatite (HA)/polylactic-co-glycolic acid (PLGA). The composition of cell and scaffold was observed.The blank plasmid transfection was 39.1%, 40.1% in VEGF group. The cell adhesion and growth was found on the scaffold pore wall after 5 days, and the number of adherent cells in the nano-HA/PLGA composite scaffold material basically had no significant difference in both.Although the nano-HA/PLGA scaffold material is still not fully meet the requirements of the matrix material for bone tissue engineering, but good biocompatibility, structure is its rich microporous satisfaction in material mechanics, toughening, enhanced obviously. Composition scaffold with BMSCs transfected by VEGF plasmid, the ability of angiogenesis is promoted.

Normal 0 21 false false false ES-CL X-NONE X-NONE Background : Overexpression or mutated activation of Fibroblast growth factor receptor 3 (FGFR3) is involved in the pathogenesis of many tumors. More and more studies focus on the potential usage of therapeutic antibodies against FGFR3. Results : In this study, a novel single-chain Fv (ScFv) against FGFR3 was prepared and characterized. To achieve the soluble expression, ScFv was fused with Sumo (Small ubiquitin-related modifier) by polymerase chain reaction (PCR), and cloned into pET-20b. The recombinant bacteria were induced by 0.5 mM Isopropyl-β-D- thiogalactopyranoside (IPTG) for 16 h at 20oC, and the supernatant liquid of Sumo-ScFv was harvested and purified by Ni-NTA chromatography. After cleaved by the Sumo protease, the recombinant ScFv was released from the fusion protein, and further purified by Ni-NTA chromatography. The purity of ScFv was shown to be higher than 95% and their yield reached 4 mg per liter of bacterial culture. In vitro data showed ScFv can significantly attenuate FGF9-induced the phosphorylation of FGFR3. Conclusion: We provide a novel method to produce soluble expression and bioactive functions of ScFv in Escherichia coli . /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Tabla normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-parent:""; mso-padding-alt:0cm 5.4pt 0cm 5.4pt; mso-para-margin-top:0cm; mso-para-margin-right:0cm; mso-para-margin-bottom:10.0pt; mso-para-margin-left:0cm; line-height:115%; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-ansi-language:ES-CL; mso-fareast-language:EN-US;}

Rationale Tertiary syphilis can manifest as gummatous disease, but gumma of the spine has been extremely rarely reported. Patient concerns A 61-year-old male complained of worsening pain and numbness in both lower legs for four weeks. Diagnoses Syphilis of the Lumbar Spine. Interventions Pedicle screw fixation (L3-S1) and posterior decompression of the vertebral canal at L4-5 were performed. Outcomes The postoperative VAS score of both lower extremities decline to 2 from 7 at admission. Dorsal thumb extensor motor power (left/right) at day 7 postoperatively was 3/3 (versus admission: 1/1). Laboratory examinations showed normal white blood cell count (versus admission: 13.8 × 10/L; reference value: 4.00-10.00 × 10/L) and decline in C-reactive protein (20.35 mg/L versus admission: 77.43 mg/L; reference value: 0.00-10.00 mg/mL) and ESR (58 mm versus admission: 73 mm; reference value: 0-15 mm). Lessons Our case illustrates that although gummatous disease of the spine may be extremely rare, it should be considered in the differential diagnosis of tuberculosis or malignancy of the spine so as to avoid a wrong diagnosis and incorrect treatment.

To explore the distribution of Schmorl's nodes (SN) in normal adult lumbar spine and determine the association of lumbar disc degeneration and lumbar spine motion.A total of 1 179 individuals underwent magnetic resonance imaging (MRI) scans. They had an age range of 15-85 years and were grouped by 10 years. The distribution of SNs along lumbar spine and their relationship with age and gender were examined by single factor analysis of variance chi-square test. Spine specialists performed lumbar disc degeneration evaluations through the Pfirrmann's classification system. The relationship between SNs, age group, disc location and overall grades of lumbar disc degeneration were analyzed by multiple Logistic regression.The prevalence of SNs was 28.4%. And SNs were observed more frequently in males than females (34.6% vs 20.2%) (P0.01). No significant inter-group difference existed in the incidence of SNs (P = 0.18). SNs were more common at L2 and L3 vertebral bodies (14.3% vs 14.4%) while least common at S1 vertebral body (1.5%). The highest incidence of SNs was found in discs with degeneration grades III (41.9%) and IV (45.3%). The occurrence of SN, aging and disc location were positively correlated with lumbar disc degeneration grade.With a high incidence in healthy individuals, SNs occur in discs at all degrees of degeneration. And the occurrence of SNs is positively associated with lumbar disc degeneration.