ReviewSchmerz (Berlin, Germany)2019
[Inflammation and osteoarthritis-related pain].
Review in Schmerz (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
30 citing papers in PubMed, 53 citations in OpenAlex.
- miR-584-5p alleviates osteoarthritis by targeting HIF1A to regulate chondrocyte function and extracellular matrix metabolism.Journal of orthopaedic surgery and research · 2026Article
- Evidence for acetylcholinesterase as an early mediator in knee osteoarthritis: insights from synovial fluid analyses.Clinical rheumatology · 2026Article
- Cuproptosis: Biomarkers, Mechanisms and Treatments in Diseases.Molecules (Basel, Switzerland) · 2026Review
- Pain mechanism and management strategy of rheumatoid arthritis.Frontiers in pain research (Lausanne, Switzerland) · 2025Review
- Recent advances in injectable hydrogels for osteoarthritis treatments.Frontiers in bioengineering and biotechnology · 2025Review
- Monosodium Iodoacetate Induces Knee Osteoarthritis in Rats in a Dose- and Time-Dependent Manner.Journal of pain research · 2025Article
- Heat-KilledNutrients · 2024Article
- Quercetin Modulates Ferroptosis via the SIRT1/Nrf-2/HO-1 Pathway and Attenuates Cartilage Destruction in an Osteoarthritis Rat Model.International journal of molecular sciences · 2024Article
- Relationship between systemic immune-inflammation index and osteoarthritis: a cross-sectional study from the NHANES 2005-2018.Frontiers in medicine · 2024Article
- [Concept for integrative pain treatment of osteoarthritis of the knee based on the evidence for conservative and complementary therapies].Schmerz (Berlin, Germany) · 2023Review
- The Effect of the Mixed Extract ofCurrent issues in molecular biology · 2023Article
- Article
- Protective effects of Pudilan Tablets against osteoarthritis in mice induced by monosodium iodoacetate.Scientific reports · 2023Article
- PPAR-PPAR research · 2023Article
- From Low-Grade Inflammation in Osteoarthritis to Neuropsychiatric Sequelae: A Narrative Review.International journal of molecular sciences · 2022Review
- The release of osteoclast-stimulating factors on supraphysiological loading by osteoprogenitors coincides with expression of genes associated with inflammation and cytoskeletal arrangement.Scientific reports · 2022Article
- Circular RNA circ_0020014 contributes to osteoarthritis progression via miR-613/ADAMTS5 axis.Bosnian journal of basic medical sciences · 2022Article
- Infiltration Profile of Regulatory T Cells in Osteoarthritis-Related Pain and Disability.Biomedicines · 2022Article
- The Epigenetic Mechanisms Involved in Chronic Pain in Rodents: A Mini- Review.Current neuropharmacology · 2022Review
- [Pain prevention in the primary care setting : Facts for resident physicians].Schmerz (Berlin, Germany) · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is one of the major causes of chronic pain. Although OA has long been considered a non-inflammatory "wear and tear" disease leading to loss of articular cartilage, recent findings provide convincing evidence that inflammatory mechanisms play a pivotal role in the pathophysiology of OA. In OA mononuclear cells (e. g. T‑cells and macrophages) infiltrate the synovial membrane and the levels of pro-inflammatory cytokines in peripheral blood and synovial fluid samples are elevated. Increased release of inflammatory mediators including interleukin (IL) IL-1β, IL-6, IL-8, IL-15 und tumor necrosis factor alpha (TNF‑α) induces the expression of proteolytic enzymes such as matrix metalloproteinases resulting in cartilage breakdown. Molecular and cellular interactions between the immune and nervous system are also involved in the development of OA-related pain. Inflammatory mediators including IL-6 und TNF‑α lead to peripheral sensitization of joint nociceptors and growth factors (e. g. NGF) trigger the expression of TRPV1 channels in primary afferents. Moreover, neuropeptides reduce the threshold of nociceptors of OA joints. The current review highlights the role of inflammatory mechanisms in OA-induced joint pain considering clinical signs of inflammation and major inflammatory pathways.
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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.