ReviewCurrent rheumatology reports2002
Mechanisms of bone resorption and new bone formation in spondyloarthropathies.
Review in Current rheumatology reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Monocytes and Macrophages in Spondyloarthritis: Functional Roles and Effects of Current Therapies.Cells · 2022Review
- Association Between Dentin Matrix Protein 1 (rs10019009) Polymorphism and Ankylosing Spondylitis in a Chinese Han Population from Shandong Province.Chinese medical journal · 2016Article
- The roles of testicular orphan nuclear receptor 4 (TR4) in cerebellar development.Cerebellum (London, England) · 2008Article
- Proteinases in the joint: clinical relevance of proteinases in joint destruction.Arthritis research & therapy · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spondyloarthropathies (SpA) share clinical features such as sacroiliitis, axial immobility, and peripheral arthropathies. They also share a strong association with human leukocyte antigen-B27, implicating T cells and antigen-presenting cells in the disease process. Inflammation seems to underlie the pathogenesis of SpA, particularly in the axial skeleton and entheses. Pathologic bone loss and formation occur simultaneously in inflamed regions, suggesting an inflammation-induced dysregulation of osteoclast and osteoblast activity. Pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNFa) appear to be central to the disease, because TNFa blockade has been shown to effectively improve clinical outcome. Other cytokines such as transforming growth factor-beta, interferon-gamma (IFNg), and interleukin-18 are also likely to be important in SpA. Activated T cells have been shown to produce cytokines such as IFNg and receptor activator of nuclear-factor- kappaB ligand, with direct effects on osteoclastogenesis. The dual role of T cells in immunobiology and skeletal biology provides a possible link between human leukocyte antigen-B27, pro-inflammatory cytokines, and bone cells in SpA.
Indexed as
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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.