ReviewJournal of orthopaedic translation2026
Mechanistic insights into cartilage-sensory nerve crosstalk in osteoarthritis progression.
Review in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- From cartilage-sensory nerve crosstalk to clinically actionable pain phenotyping in osteoarthritis.Journal of orthopaedic translation · 2026Article
- Integrating mechanistic research and emerging technologies to advance clinical translation in orthopaedics.Journal of orthopaedic translation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) pain arises from dynamic crosstalk between degraded cartilage and sensitized sensory nerves. Cartilage-derived signals, including nerve growth factor (NGF), pro-inflammatory cytokines, and matrix-degrading enzymes, promote nerve sprouting and hyperexcitability. While sensory afferents release neuropeptides that further amplify inflammation and cartilage degeneration. Altered joint mechanics additionally activate mechanosensitive ion channels, linking biomechanical stress to nociceptive signaling. This review summarizes current knowledge on cartilage-sensory nerve interactions in OA and their contribution to pain progression. We discuss key molecular mediators, biomarkers, and therapeutic targets, and provide an overview of Core Take-Home Messages and Clinical Significance: •Cartilage actively contributes to OA pain by engaging in bidirectional crosstalk with sensory nerves.•Inflammatory mediators, neuropeptides, and mechanosensitive ion channels form an integrated network driving OA pain.•Predictive The Translational Potential of this Article: This review highlights cartilage-sensory nerve crosstalk as a key mechanism underlying osteoarthritis pain, moving beyond a structure-centric view of disease progression. Mechanistic insights into neuroinflammatory and mechanosensitive pathways support the development of biomarkers for pain phenotyping and patient stratification. These insights have direct implications for clinical trial design and interpretation, particularly in addressing discordance between structural and symptomatic outcomes.
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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.