Repeat Surgery after Percutaneous Endoscopic Lumbar Discectomy for Adolescent Lumbar Disc Herniation: A Multicenter Observational Study.

Objective: The reported date in the repeat surgical intervention for adolescent lumbar disc herniation (ALDH) after percutaneous endoscopic lumbar discectomy (PELD) was quite scarce. This study aims to introduce cases of repeat surgeries after PELD for ALDH and assess the incidence, chief causes, repeat surgery methods, and surgical outcomes of repeat surgeries after PELD for ALDH.

Methods: A retrospective multicenter observational study was conducted on patients undergoing repeat surgeries after PELD for ALDH at four tertiary referral hospitals from January 2014 through August 2022.

Interpretable Machine Learning Model to Predict Bone Cement Leakage in Percutaneous Vertebral Augmentation for Osteoporotic Vertebral Compression Fracture Based on SHapley Additive exPlanations.

Study Design: Retrospective study.

Objectives: Our objective is to create comprehensible machine learning (ML) models that can forecast bone cement leakage in percutaneous vertebral augmentation (PVA) for individuals with osteoporotic vertebral compression fracture (OVCF) while also identifying the associated risk factors.

Methods: We incorporated data from patients (n = 425) which underwent PVA.

Scientific Bibliometric and Visual Analysis of Studies on Autophagy in Intervertebral Disc Degeneration Based on Web of Science.

Objective: To analyze the current research trends and potential mechanisms related to the role of autophagy in intervertebral disc degeneration (IVDD) and to provide new ideas for future research in this field.

Methods: All articles on IVDD and autophagy were retrieved and extracted from the Web of Science (WoS) core collection database. The results were evaluated and visualized using the bibliometric Web site, CiteSpace, and VOSviewer software, including annual articles published, countries, institutions, authors, journals, research areas, funding agencies, citations, and keywords.

Endoplasmic reticulum stress-mediated autophagy alleviates lipopolysaccharide-induced nucleus pulposus cell pyroptosis by inhibiting CHOP signaling in vitro.

Pyroptosis, a newly discovered pro-inflammatory programmed necrosis of cells, serves as an initiating and promoting event that leads to intervertebral disc (IVD) degeneration (IDD). Endoplasmic reticulum stress (ERS) and autophagy are vital regulatory mechanisms of cellular homeostasis, which is also closely related to IDD. However, the role and relationship of ERS and autophagy in the pyroptosis of nucleus pulposus cell (NPC) are not well understood.

The Mini-Open Wiltse Approach with Pedicle Screw Fixation Versus Percutaneous Pedicle Screw Fixation for Treatment of Neurologically Intact Thoracolumbar Fractures: A Systematic Review and Meta-Analysis.

Objective: The purpose of the present study was to compare the clinical outcomes and complications between the mini-open Wiltse approach with pedicle screw fixation (MWPSF) and percutaneous pedicle screw fixation (PPSF) in treating neurologically intact thoracolumbar fractures.

Methods: We comprehensively searched PubMed, Web of Science, Embase, and the Cochrane Library and performed a systematic review and meta-analysis of all randomized controlled trials and retrospective comparative studies assessing these important indexes of the 2 methods using Review Manager, version 5.4.

GATA4 promotes the senescence of nucleus pulposus cells via NF-κB pathway.

Purpose: Cell senescence plays a vital role in intervertebral disc degeneration. The regulatory mechanism of the cellular senescence of nucleus pulposus cells has not been fully elucidated. A recent study identified GATA4 as an emerging regulator of IMR90 cellular senescence.

Unfolded protein response alleviates acid-induced premature senescence by promoting autophagy in nucleus pulposus cells.

Acid-induced cellular senescence is a critical underlying mechanism of intervertebral disc (IVD) degeneration (IDD). Acid stimulation activates a variety of biological changes including autophagy, endoplasmic reticulum stress, and related unfolded protein response (UPR), which are important regulators of cellular senescence. However, the precise mechanism of acid-mediated UPR and autophagy in nucleus pulposus cell (NPC) senescence has not been fully elucidated.

Current Applications of Machine Learning in Spine: From Clinical View.

Study Design: Narrative review.

Objectives: This review aims to present current applications of machine learning (ML) in spine domain to clinicians.

Methods: We conducted a comprehensive PubMed search of peer-reviewed articles that were published between 2006 and 2020 using terms (spine, spinal, lumbar, cervical, thoracic, machine learning) to examine ML in spine.

Which Criterion for Wound Drain Removal is Better Following Posterior 1-Level or 2-Level Lumbar Fusion With Instrumentation: Time Driven or Output Driven?

Study Design: Case-control study.

Objectives: To compare the outcomes of 2 different criteria (time driven and output driven) for wound drain removal and identify which one is better.

Methods: 743 patients who underwent posterior lumbar fusion with instrumentation involving 1 or 2 motion segments were enrolled in this study.

A20 of nucleus pulposus cells plays a self-protection role via the nuclear factor-kappa B pathway in the inflammatory microenvironment.

Aims: Inflammatory response plays a pivotal role in the pathophysiological process of intervertebral disc degeneration (IDD). A20 (also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3)) is a ubiquitin-editing enzyme that restricts nuclear factor-kappa B (NF-κB) signalling. A20 prevents the occurrence of multiple inflammatory diseases.

ASIC1a activation induces calcium-dependent apoptosis of BMSCs under conditions that mimic the acidic microenvironment of the degenerated intervertebral disc.

Purpose: In the degenerated intervertebral disc (IVD), matrix acidity challenges transplanted bone marrow mesenchymal stem cells (BMSCs). The Ca2+-permeable acid-sensing ion channel 1a (ASIC1a) is responsible for acidosis-mediated tissue injury. The aim of our study was to confirm whether ASIC1a activation induces BMSC apoptosis under conditions that mimic the acidic microenvironment of the degenerated IVD.

A histocytological and radiological overview of the natural history of intervertebral disk: from embryonic formation to age-related degeneration.

Purpose: To elucidate the natural history of intervertebral disk (IVD) and characterize its embryonic beginnings and age-related degeneration.

Methods: Coronal sections of embryonic (E13.5-neonatal) and postnatal (4-60-week-old) Sprague-Dawley rat IVD were stained by a series of histological stainings (hematoxylin and eosin, Alcian blue, Picrosirius red, Masson, Periodic acid-Schiff).

Comparison of percutaneous endoscopic lumbar discectomy versus microendoscopic discectomy for the treatment of lumbar disc herniation: a meta-analysis.

Purpose: We conducted a systematic review and meta-analysis to compare the clinical outcomes of percutaneous endoscopic lumbar discectomy (PELD) and microendoscopic discectomy (MED) for the treatment of lumbar disc herniation (LDH), and to clarify whether PELD is more superior to MED.

Methods: We performed a comprehensive search in the databases of MEDLINE, EMBASE, PubMed, Web of Science, Cochrane database, CNKI, and Wanfang Data to acquire all relevant studies up to July 2018. The searched literatures were then screened according to the strict inclusion and exclusion criteria.

Protein kinase RNA-like ER kinase/eukaryotic translation initiation factor 2α pathway attenuates tumor necrosis factor alpha-induced apoptosis in nucleus pulposus cells by activating autophagy.

Cellular loss induced by tumor necrosis factor alpha (TNF-α) contributes to the pathogenesis of intervertebral disc (IVD) degeneration. Cellular stress induced by TNF-α activates several processes to restore cell homeostasis. These processes include autophagy, endoplasmic reticulum stress, and related unfolded protein response (UPR).

Nuclear factor-kappa B-dependent X-box binding protein 1 signalling promotes the proliferation of nucleus pulposus cells under tumour necrosis factor alpha stimulation.

Objectives: Tumour necrosis factor alpha (TNF-α) expressed by nucleus pulposus cells (NPCs) plays a critical role in intervertebral disc (IVD) degeneration. A key unfolded protein response (UPR) component, X-box binding protein 1 (XBP1) and nuclear factor-kappa B (NF-κB) are essential for cell survival and proliferation. The aim of our study was to elucidate the roles of XBP1 and NF-κB in IVD degeneration (IDD).

Acid-Sensing Ion Channel 1a Regulates Fate of Rat Nucleus Pulposus Cells in Acid Stimulus Through Endoplasmic Reticulum Stress.

Acid-sensing ion channel 1a (ASIC1a) participates in human intervertebral disc degeneration (IVDD) and regulates the destiny of nucleus pulposus cells (NPCs) in acid stimulus. However, the mechanism of ASIC1a activation and its downstream pathway remain unclear. Endoplasmic reticulum (ER) stress also participates in the acid-induced apoptosis of NPCs.

Endoplasmic Reticulum Stress Facilitates the Survival and Proliferation of Nucleus Pulposus Cells in TNF-α Stimulus by Activating Unfolded Protein Response.

Intervertebral disc (IVD) degeneration is closely related to inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α). The endoplasmic reticulum (ER) serves several important cell functions, which are essential for normal cell metabolism and survival. This study aims to clarify the role of ER stress and unfolded protein response (UPR) in TNF-α-induced biological changes in rat nucleus pulposus cells (NPCs) and IVD degeneration.

Formation, function, and exhaustion of notochordal cytoplasmic vacuoles within intervertebral disc: current understanding and speculation.

Notochord nucleus pulposus cells are characteristic of containing abundant and giant cytoplasmic vacuoles. This review explores the embryonic formation, biological function, and postnatal exhaustion of notochord vacuoles, aiming to characterize the signal network transforming the vacuolated nucleus pulposus cells into the vacuole-less chondrocytic cells. Embryonically, the cytoplasmic vacuoles within vertebrate notochord originate from an evolutionarily conserved vacuolation process during neurulation, which may continue to provide mechanical and signal support in constructing a mammalian intervertebral disc.

Endoplasmic Reticulum Stress Is Involved in Nucleus Pulposus Degeneration and Attenuates Low pH-Induced Apoptosis of Rat Nucleus Pulposus Cells.

The microenvironment of degenerative intervertebral disk (IVD) is characteristic of a high concentration of lactic acid and low pH levels, whereas the underlying mechanism has not been clearly defined. Endoplasmic reticulum (ER) is the hub of interactions between environmental signals and cellular biological functions, the malfunction of which is closely involved in the pathogenesis of multiple disorders, including IVD degeneration (IVDD). This research mainly aims at exploring what role ER stress plays in the natural process of IVDD and pH-induced apoptosis of rat nucleus pulposus (NP) cells (NPCs).

Tumor necrosis factor α modulates sodium-activated potassium channel SLICK in rat dorsal horn neurons via p38 MAPK activation pathway.

The dorsal horn (DH) of the spinal cord is the integrative center that processes and transmits pain sensation. Abnormal changes in ion channel expression can enhance the excitability of pain-related DH neurons. Sodium-activated potassium (K) channels are highly expressed particularly in the central nervous system; however, information about whether rat DH neurons express the SLICK channel protein is lacking, and the direct effects on SLICK in response to inflammation and the potential signaling pathway mediating such effects are yet to be elucidated.

Acid-sensing ion channel 1a regulates the survival of nucleus pulposus cells in the acidic environment of degenerated intervertebral discs.

Objectives: Activation of acid-sensing ion channel 1a (ASIC1a) is responsible for tissue injury caused by acidosis in nervous systems. But its physiological and pathological roles in nucleus pulposus cells (NPCs) are unclear. The aim of this study is to investigate whether ASIC1a regulates the survival of NPCs in the acidic environment of degenerated discs.