ArticleArthritis & rheumatology (Hoboken, N.J.)2016
Nociceptive Sensitizers Are Regulated in Damaged Joint Tissues, Including Articular Cartilage, When Osteoarthritic Mice Display Pain Behavior.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 100 citations in OpenAlex.
- Neural regulation of bone: from central neural circuits to peripheral innervation of the skeletal stem cell niche.Bone research · 2026Review
- TRPV4-Mast Cell Interactions in Neurogenic Inflammation and Chronic Diseases: A Narrative Review.International journal of molecular sciences · 2026Review
- A Review of Rodent Behavior, Mobility, and Pain Modifications in Response to Destabilization of the Medial Meniscus Injury.Biomedicines · 2025Review
- Pain mechanisms in osteoarthritis: recent discoveries and opportunities ahead.Connective tissue research · 2025Review
- Peripheral neuronal sensitization and neurovascular remodelling in osteoarthritis pain.Nature reviews. Rheumatology · 2025Review
- Pain mediator NGF improves chondrocyte extracellular matrix synthesis via PI3K/AKT pathway.Journal of orthopaedic surgery and research · 2025Article
- Combination of anti-inflammatory therapy and RNA interference by light-inducible hybrid nanomedicine for osteoarthritis treatment.Acta pharmaceutica Sinica. B · 2024Article
- SrHPOMaterials today. Bio · 2024Article
- Molecular pathogenesis of OA pain: Past, present, and future.Osteoarthritis and cartilage · 2024Review
- Description of Novel Molecular Factors in Lumbar DRGs and Spinal Cord Factors Underlying Development of Neuropathic Pain Component in the Animal Model of Osteoarthritis.Molecular neurobiology · 2024Article
- Pathological progress and remission strategies of osteoarthritic lesions caused by long-term joint immobilization.Arthritis research & therapy · 2023Article
- Pharmatherapeutic Treatment of Osteoarthrosis-Does the Pill against Already Exist? A Narrative Review.Journal of personalized medicine · 2023Review
- Human-specific duplicate CHRFAM7A gene is associated with more severe osteoarthritis and amplifies pain behaviours.Annals of the rheumatic diseases · 2023Article
- Piezo2 expressing nociceptors mediate mechanical sensitization in experimental osteoarthritis.Nature communications · 2023Article
- Role of Human Mesenchymal Stem Cells and Derived Extracellular Vesicles in Reducing Sensory Neuron Hyperexcitability and Pain Behaviors in Murine Osteoarthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- Transcriptomic analyses of joint tissues during osteoarthritis development in a rat model reveal dysregulated mechanotransduction and extracellular matrix pathways.Osteoarthritis and cartilage · 2023Article
- Interplay between cellular changes in the knee joint, circulating lipids and pain behaviours in a slowly progressing murine model of osteoarthritis.European journal of pain (London, England) · 2022Article
- Characterization of Non-Invasively Induced Post-Traumatic Osteoarthritis in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- The Genesis of Pain in Osteoarthritis: Inflammation as a Mediator of Osteoarthritis Pain.Clinics in geriatric medicine · 2022Review
- Localization of Nerve Growth Factor Expression to Structurally Damaged Cartilaginous Tissues in Human Lumbar Facet Joint Osteoarthritis.Frontiers in immunology · 2022Article
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
objectivePain is the most common symptom of osteoarthritis (OA), yet where it originates in the joint and how it is driven are unknown. The aim of this study was to identify pain-sensitizing molecules that are regulated in the joint when mice subjected to surgical joint destabilization develop OA-related pain behavior, the tissues in which these molecules are being regulated, and the factors that control their regulation.
methodsTen-week-old mice underwent sham surgery, partial meniscectomy, or surgical destabilization of the medial meniscus (DMM). Pain-related behavior as determined by a variety of methods (testing of responses to von Frey filaments, cold plate testing for cold sensitivity, analgesiometry, incapacitance testing, and forced flexion testing) was assessed weekly. Once pain-related behavior was established, RNA was extracted from either whole joints or microdissected tissue samples (articular cartilage, meniscus, and bone). Reverse transcription-polymerase chain reaction analysis was performed to analyze the expression of 54 genes known to regulate pain sensitization. Cartilage injury assays were performed using avulsed immature hips from wild-type or genetically modified mice or by explanting articular cartilage from porcine joints preinjected with pharmacologic inhibitors. Levels of nerve growth factor (NGF) protein were measured by enzyme-linked immunosorbent assay.
resultsMice developed pain-related behavior 8 weeks after undergoing partial meniscectomy or 12 weeks after undergoing DMM. NGF, bradykinin receptors B1 and B2, tachykinin, and tachykinin receptor 1 were significantly regulated in the joints of mice displaying pain-related behavior. Little regulation of inflammatory cytokines, leukocyte activation markers, or chemokines was observed. When tissue samples from articular cartilage, meniscus, and bone were analyzed separately, NGF was consistently regulated in the articular cartilage. The other pain sensitizers were also largely regulated in the articular cartilage, although there were some differences between the 2 models. NGF and tachykinin were strongly regulated by simple mechanical injury of cartilage in vitro in a transforming growth factor β-activated kinase 1-, fibroblast growth factor 2-, and Src kinase-dependent manner.
conclusionDamaged joint tissues produce proalgesic molecules, including NGF, in murine OA.
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