ArticlePain2008
TNF signaling contributes to the development of nociceptive sensitization in a tibia fracture model of complex regional pain syndrome type I.
Article in Pain, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 95 citations in OpenAlex.
- Article
- Identification of two biological subgroups of complex regional pain syndrome type 1 by transcriptomic profiling of skin and blood in women.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mechanisms of complex regional pain syndrome.Frontiers in pain research (Lausanne, Switzerland) · 2024Review
- Mechanisms of bone pain: Progress in research from bench to bedside.Bone research · 2022Review
- Preventive Supplementation of Omega-3 Reduces Pain and Pro-inflammatory Cytokines in a Mouse Model of Complex Regional Pain Syndrome Type I.Frontiers in integrative neuroscience · 2022Article
- Bradykinin Receptors Play a Critical Role in the Chronic Post-ischaemia Pain Model.Cellular and molecular neurobiology · 2021Article
- Chiropractic Care of a Patient With Complex Regional Pain Syndrome Type 1 (CRPS-1): A Case Report.Journal of chiropractic medicine · 2020Article
- Clindamycin inhibits nociceptive response by reducing tumor necrosis factor-α and CXCL-1 production and activating opioidergic mechanisms.Inflammopharmacology · 2020Article
- Article
- An Investigation of the Molecular Mechanisms Underlying the Analgesic Effect of Jakyak-Gamcho Decoction: A Network Pharmacology Study.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- Tibial post fracture pain is reduced in kinin receptors deficient mice and blunted by kinin receptor antagonists.Journal of translational medicine · 2019Article
- Article
- Microglial Modulation as a Target for Chronic Pain: From the Bench to the Bedside and Back.Anesthesia and analgesia · 2019Review
- Oxidative Stress Contributes to Fracture/Cast-Induced Inflammation and Pain in a Rat Model of Complex Regional Pain Syndrome.The journal of pain · 2018Article
- The Rodent Tibia Fracture Model: A Critical Review and Comparison With the Complex Regional Pain Syndrome Literature.The journal of pain · 2018Review
- Impact of the Autonomic Nervous System on the Skeleton.Physiological reviews · 2018Review
- A role for pericytes in chronic pain?Current opinion in supportive and palliative care · 2018Review
- Neuropeptide regulation of adaptive immunity in the tibia fracture model of complex regional pain syndrome.Journal of neuroinflammation · 2018Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Tibia fracture in rats initiates a cascade of nociceptive, vascular, and bone changes resembling complex regional pain syndrome type I (CRPS I). Previous studies suggest that the pathogenesis of these changes is attributable to an exaggerated regional inflammatory response to injury. We postulated that the pro-inflammatory cytokine tumor necrosis factor alpha (TNF) might mediate the development of CRPS-like changes after fracture. RT-PCR and EIA assays were used to evaluate changes in TNF expression and content in skin, nerve, and bone after fracture. Bilateral hindpaw thickness, temperature, and nociceptive thresholds were determined, and bone microarchitecture was measured using microcomputed tomography. Lumbar spinal cord Fos immunostaining was performed for quantification of Fos positive neurons. After baseline testing, the distal tibia was fractured and the hindlimb casted for 4 weeks. The rats were subcutaneously injected either with a soluble TNF receptor type 1 (sTNF-R1, 5mg/kg/d) or saline every 3 days over 28 days and then were retested at 4 weeks post-fracture. Tibia fracture chronically upregulated TNF expression and protein levels in the hindpaw skin and sciatic nerve. After fracture the rats developed hindpaw mechanical allodynia and unweighting, which were reversed by sTNF-R1 treatment. Consistent with the behavioral data, spinal Fos increased after fracture and this effect was inhibited by sTNF-R1 treatment. Collectively, these data suggest that facilitated TNF signaling in the hindlimb is an important mediator of chronic regional nociceptive sensitization after fracture, but does not contribute to the hindlimb warmth, edema, and bone loss observed in this CRPS I model.
Indexed as
Identifiers
What OpenQuestion holds
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.