ArticleJournal of cellular and molecular medicine2020
Toll-like receptor involvement in adolescent scoliotic facet joint degeneration.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Technical insights and implications of thoracolumbar spine and neural tissue harvesting in recently deceased organ donors: a direct anterior approach integrated into multi-organ procurement protocols.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Article
- Lumbar muscle morphology and composition in adolescent idiopathic scoliosis: a magnetic resonance study.Spine deformity · 2026Article
- Exosome-mediated cholesterol flow drives scoliosis progression via promoting the spinal cartilage-bone positive feedback.Communications biology · 2026Article
- Emerging pathogenetic mechanisms in adolescent idiopathic scoliosis: the role of inflammation and gut microbiota.Journal of orthopaedic surgery and research · 2026Review
- The Toll-like Receptor-2/4 Antagonist, Sparstolonin B, and Inflammatory Diseases: A Literature Mining and Network Analysis.Cardiovascular drugs and therapy · 2025Article
- The TLR-M-CSF axis is implicated in increased bone turnover and curve progression in adolescent idiopathic scoliosis.Arthritis research & therapy · 2025Article
- Scoliosis as a Paradigm of Pathological Spinal Curvature: Molecular Mechanisms and Imaging Innovations : Molecular and Imaging Insights in Scoliosis.Galen medical journal · 2025Review
- Investigating the causal links between inflammatory cytokines and scoliosis through bidirectional Mendelian randomization analysis.JOR spine · 2024Article
- The experimental study of mir-99a-5p negative regulation of TLR8 receptor mediated-mediated innate immune response in rabbit knee cartilage injury.Immunity, inflammation and disease · 2024Article
- Article
- Zhuifeng tougu capsules inhibit the TLR4/MyD88/NF-κB signaling pathway and alleviate knee osteoarthritis:Frontiers in pharmacology · 2022Article
- Toll-like receptor involvement in adolescent scoliotic facet joint degeneration.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Facet joint osteoarthritis is prevalent in young patients with adolescent idiopathic scoliosis (AIS) and might contribute to back pain. Toll-like receptors (TLR) have been linked to cartilaginous tissue degeneration but their involvement in facet joint osteoarthritis in AIS patients is still unknown. We compared baseline gene expression levels of TLRs -1, -2, -4, and -6 in scoliotic and non-scoliotic chondrocytes and found higher expression levels in scoliotic chondrocytes with significantly higher TLR2 levels. Furthermore, TLR expression correlated strongly and significantly with inflammatory and catabolic markers in scoliotic but not in non-scoliotic chondrocytes. TLR activation with a synthetic TLR2/6 agonist resulted in a robust induction and release of pro-inflammatory and catabolic factors which exacerbated proteoglycan loss in scoliotic but not in non-scoliotic cartilage. We also detected a higher abundance of alarmins including S100A8/9 and biglycan in scoliotic cartilage. Finally, the small-molecule antagonists Sparstolonin B and o-Vanillin reduced catabolism following induction with naturally occurring alarmins and the synthetic TLR2/6 agonist. The high baseline expression, robust responsiveness and strong and significant correlation with proteases and pro-inflammatory cytokines suggest that TLRs are key regulators of facet joint degeneration in AIS. Blocking their activity could therefore potentially modify disease progression.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.