ArticleWorld journal of orthopedics2025
Fundamentals of intervertebral disc degeneration and related discogenic pain.
Article in World journal of orthopedics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- The Sinuvertebral Nerve and Basivertebral Nerve: Analyzing the Central Role of the Vertebral-Disc Unit in Chronic Low Back Pain.Current pain and headache reports · 2026Review
- Organ-on-a-Chip Technology: Advances in Modeling Inflammation, Neurovascularization and Nociception in Human Intervertebral Disc Degeneration.Smart medicine · 2026Review
- Spondylolysis and spondylolisthesis is associated with disc degeneration in pediatric patients.Spine deformity · 2026Article
- Coronal curvature angle and asymmetrical blood vessel distribution in intervertebral discs from aged cadavers: a pilot study.Spine deformity · 2026Article
- TRPC6-Mediated CaCells · 2026Article
- Kallikrein-kinin system as a potential target for the treatment of intervertebral disc degeneration.European journal of medical research · 2025Review
- Chronic low back pain and exercise: a molecular perspective on aerobic and anaerobic core training.Molecular biology reports · 2025Review
Corrections and comments
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Authors and funding
1 author.
Funding
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Abstract
Lumbar intervertebral disc degeneration is thought to be the main cause of low back pain, although the mechanisms by which it occurs and leads to pain remain unclear. In healthy adult discs, vessels and nerves are present only in the outer layer of the annulus fibrosus and in the bony endplate. Animal models, and histological and biomechanical studies have shown that annulus tear or endplate injury is the initiating factor for painful disc degeneration. Injury to the disc triggers a local inflammatory repair response that activates nociceptors and promotes the synthesis of neuropeptides such as substance P and calcitonin gene-related peptide, by dorsal root ganglion neurons. These neuropeptides are transported to injured discs and act as pro-inflammatory molecules, promoting the production of an "inflammatory soup" by inducing vasodilatation and plasma extravasation as well as by promoting the release of chemical mediators from disc cells and infiltrating immune cells, causing neurogenic inflammation that leads to progressive disc degeneration and discogenic pain.
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