ArticleBone & joint research2022
Septic arthritis in an in vivo murine model induced by
Article in Bone & joint research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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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.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Regulated Cell Death Pathways in Chondrocytes During Septic Arthritis: Current Evidence and Future Perspectives.Journal of inflammation research · 2026Review
- Characterization of a mouse model of osteoarticular infection using clinical isolates ofJBMR plus · 2025Article
- Diagnosis and surgical treatment of chronic destructive septic hip arthritis.Arthroplasty (London, England) · 2025Review
- Dual neutralization of TGF-β and IL-21 regulates Th17/Treg balance by suppressing inflammatory signalling in the splenic lymphocytes of Staphylococcus aureus infection-induced septic arthritic mice.Immunologic research · 2025Article
- Trained immunity of synovial macrophages is associated with exacerbated joint inflammation and damage after Staphylococcus aureus infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Single-cell RNA sequencing reveals the differentiation and regulation of endplate cells in human intervertebral disc degeneration.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims
methodsAdult male C57Bl/6 mice (n = 75) were randomized into three groups to receive 1.0 to 1.4 × 10
resultsChondrocyte death was greater with 8325-4 (96.2% (SD 5.5%); p < 0.001) than DU1090 (28.9% (SD 16.0%); p = 0.009) and both were higher than controls (3.8% (SD 1.2%)). Histology revealed cartilage/bone damage with 8325-4 or DU1090 compared to controls (p = 0.010). Both infected groups lost weight (p = 0.006 for both) and experienced limb swelling (p = 0.043 and p = 0.018, respectively). Joints inoculated with bacteria showed significant alterations in gait cycle with a decreased stance phase, increased swing phase, and a corresponding decrease in swing speed.
conclusionMurine joints inoculated with Hla-producing 8325-4 experienced significantly more chondrocyte death than those with DU1090, which lack the toxin. This was despite similar immune responses, indicating that Hla was the major cause of chondrocyte death. Hla-deficient DU1090 also elevated chondrocyte death compared to controls, suggesting a smaller additional deleterious role of the immune system on cartilage.Cite this article:
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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.