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BackgroundIntervertebral disc degeneration (IDD) progression involves multiple factors, including loss of nucleus pulposus cells and extracellular matrix as the basic pathological mechanism of degeneration, and is closely related to cellular senescence and immune cell infiltration. The aim of study was to identify critical cellular senescence-related genes and immune cell infiltration characteristics in IDD.MethodsFour datasets, including GSE70362, GSE112216, GSE114169, and GSE150408, were downloaded from the Gene Expression Omnibus database. The senescence-related genes were acquired from the CellAge Database and intersected with differentially expressed genes (DEGs) between IDD and control samples for senescence-related DEGs (SRDEGs). Protein-protein interaction (PPI) network analysis was performed to obtain ten hub SRDEGs. A consensus cluster analysis based on these hub genes was performed to divide the patients into clusters. The functional enrichment, and immune infiltration statuses of the clusters were compared. Weighted gene co-expression network analysis was used to identified key gene modules. The overlapping genes from key modules, DEGs of clusters and hub SRDEGs were intersected to obtain potential biomarkers. To verify the expression of potential biomarkers, quantitative polymerase chain reaction (qPCR) and immunohistochemistry were performed by using human intervertebral disc tissues.ResultsIn the GSE70362 dataset, a total of 364 DEGs were identified, of which 150 were upregulated and 214 were downregulated, and 35 genes were selected as SRDEGs. PPI analysis revealed ten hub SRDEGs and consensus cluster analysis divided the patients into two clusters. Compared to Cluster 2, Cluster 1 was highly enriched in extracellular matrix organization and various metabolic process. The level of Follicular T helper cells in the Cluster 1 was significantly higher than that in the Cluster 2. IGFBP3 and NQO1 were identified as potential biomarkers. The remaining 3 datasets, and the result of qPCR and immunohistochemistry showed that the expression levels of NQO1 and IGFBP3 in the degenerated group were higher than those in the control or treatment groups.ConclusionSenescence-related genes play a key role in the development and occurrence of IDD. IGFBP3 and NQO1 are strongly correlated with immune infiltration in the IDD and could become novel therapeutic targets that prevent the progression of IDD.

Abstract Background Recent studies demonstrated that restoring sagittal alignment to the original Roussouly type can remarkably reduce complication rates after adult spinal deformity surgery. However, there is still no data proving the benefit of maintaining ideal Roussouly shape in the lumbar degenerative diseases and its association with the development of adjacent segment disease (ASD). Thus, this study was performed to validate the usefulness of Roussouly classification to predict the occurrence of ASD after lumbar fusion surgery. Materials and Methods This study retrospectively reviewed 234 consecutive patients with lumbar degenerative diseases who underwent 1- or 2-level fusion surgery. Demographic and radiographic data were compared between ASD and non-ASD groups. The patients were classified by both “theoretical” [based on pelvic incidence (PI)] and “current” (based on sacral slope) Roussouly types. The patients were defined as “matched” if their “current” shapes matched the “theoretical” types and otherwise as “mismatched”. The logistic regression analysis was performed to identify the factors associated with ASD. Finally, clinical data and spinopelvic parameters of “theoretical” and “current” types were compared. Results With a mean follow-up duration of 70.6 months, evidence of ASD was found in the 68 cases. Postoperatively, ASD group had more “current” shapes classified as type 1 or 2 and fewer as type 3 than the non-ASD group (p

Abstract Study design A retrospective case series. Objective To investigate whether unmatched rod contouring at the proximal end predisposed to the occurrence of proximal junctional kyphosis (PJK) in early-onset scoliosis (EOS) patients after traditional growing rods (TGR) treatment. Summary of background data TGR treatment has become a mainstay of treatment for EOS patients. PJK is one of the most common alignment-related complications. Methods A consecutive series of EOS patients who had undergone TGR treatment were retrospectively reviewed. They were divided into PJK and non-PJK groups according to the occurrence of PJK or not. Demographic data, surgical strategies, and radiographic parameters were recorded and compared between groups. Proximal junctional angle (PJA) was defined as the angle between the caudal endplate of the UIV and the cephalad endplate of the second supradjacent vertebra above the UIV, while proximal rod contouring angle (PRCA) was defined as the angle of proximal rod contouring, which was represented by the angle between the cephalad endplate of the UIV and the caudal endplate of the second vertebra caudal to the UIV. Unmatched proximal rod contouring was regarded if the postoperative PRCA-PJA difference was greater than 5°. Results This study finally included 73 patients. The mean age at the index surgery was 6.5 ± 2.2 years (range, 2–10 years). Mean follow-up lasted 5.0 ± 1.7 years (range, 2–9 years). They received mean 4.6 ± 1.6 lengthening procedures. There were 13 patients who were observed with PJK (18%). In comparison with the non-PJK group, the PJK group showed a larger preoperative major curve (82 ± 21° vs 70 ± 17°, P = 0.041) and global kyphosis (57 ± 6° vs. 44 ± 15°, P = 0.044). In addition, the PJK group had significantly larger postoperative PJA (10 ± 3 vs. 5 ± 3, P50°, postoperative PJA>10 and postoperative unmatched proximal rod contouring were the risk factors in predicting PJK after TGR treatment. Conclusion Approximately 18% EOS patients experienced PJK after TGR treatment. Unmatched proximal rod contouring may be an independent risk factor of PJK occurrence, in addition to greater preoperative GK and larger postoperative PJA. Level of evidence 3.

Study Design. Retrospective study. Objective: To investigate whether lumbar apex position had an impact on the development of adjacent segment disease (ASD) following transforaminal lumbar interbody fusion (TLIF). Summary of Background Data. Previous studies have demonstrated that solely concentrating on lumbar lordosis value is not suitable, and neglecting the significance of lumbar apex can lead to mechanical complications. However, the relationship between lumbar apex and ASD is still not well understood. Methods. In this retrospective study, 234 consecutive patients who underwent L3-5 or L4-5 TLIF for degenerative diseases were reviewed. The study evaluated the associations between sagittal parameters and pelvic incidence (PI). Patients were labeled "matched" when lumbar apex position aligned with the theoretical target, and "mismatched" when it did not. Multivariate analysis was applied to find the independent risk factors of ASD. In addition, a focused subanalysis was performed based on the lumbar apex position (ideal match, cranial from ideal, and caudal from ideal). Results. After an average follow-up period of 70.6 months, 68 cases were identified as having ASD. Postoperatively, 64.7% (44 of 68) of the patients with ASD exhibited a mismatched lumbar apex, compared with 41%(68 of 166) of those without ASD(P < 0.001). PI correlated significantly with proximal lordosis (PL) and lordosis distribution index (LDI) but not with distal lordosis (DL). Multivariate analysis identified age, L3--5 fusion, postoperative DL, and postoperative mismatched lumbar apex as independent risk factors of ASD. Upon the subanalysis, it was discovered that there were unique compensatory strategies in the cranial and caudal groups, with notable variations in postoperative DL, PL, and LDI among three groups (all P value of <0.05). Conclusion. Lumbar apex position significantly influenced the risk of ASD. To restore the lumbar apex to its ideal position, a proper value and distribution of DL should be attained. [ABSTRACT FROM AUTHOR]