ReviewArthritis research & therapy2006
Osteoclasts; culprits in inflammatory osteolysis.
Review in Arthritis research & therapy, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 137 citations in OpenAlex.
- An RBP-J-heparan sulfate-dependent gatekeeper directs macrophage fate between inflammatory regulation and osteoclastogenesis.bioRxiv : the preprint server for biology · 2026Article
- Developmental Pathways of Immature CD11cInternational journal of molecular sciences · 2026Review
- Bone Marrow Adipoq-lineage Progenitors: an Emerging Osteoclast Niche Cell Population.Current osteoporosis reports · 2025Review
- Divergent Requirements for Glutathione Biosynthesis During Osteoclast Differentiation In Vitro and In Vivo.Antioxidants (Basel, Switzerland) · 2025Article
- Immune cells: the key mediator between the gut microbiota and osteoporosis.Frontiers in immunology · 2025Review
- Glutaminolysis provides nucleotides and amino acids to regulate osteoclast differentiation in mice.EMBO reports · 2024Article
- Prevotella histicola Prevented Particle-Induced Osteolysis via Gut Microbiota-Dependent Modulation of Inflammation in Ti-Treated Mice.Probiotics and antimicrobial proteins · 2024Article
- Jagged1 Acts as an RBP-J Target and Feedback Suppresses TNF-Mediated Inflammatory Osteoclastogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Review
- TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis.Nature communications · 2022Article
- Is the Use of Bisphosphonates Putting Horses at Risk? An Osteoclast Perspective.Animals : an open access journal from MDPI · 2022Review
- Micro-Osteoperforations Induce TNF-α Expression and Accelerate Orthodontic Tooth Movement via TNF-α-Responsive Stromal Cells.International journal of molecular sciences · 2022Article
- Review
- Collagen VIα2 chain deficiency causes trabecular bone loss by potentially promoting osteoclast differentiation through enhanced TNFα signaling.Scientific reports · 2020Article
- Uncovering a Shared Epitope-Activated Protein Citrullination Pathway.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Niclosamide and its derivative DK-520 inhibit RANKL-induced osteoclastogenesis.FEBS open bio · 2020Article
- Rac1 Inhibition Via Srgap2 Restrains Inflammatory Osteoclastogenesis and Limits the Clastokine, SLIT3.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- IL-33 Inhibits TNF-α-Induced Osteoclastogenesis and Bone Resorption.International journal of molecular sciences · 2020Article
- Regulatory network mediated by RBP-J/NFATc1-miR182 controls inflammatory bone resorption.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Intrinsic Restriction of TNF-Mediated Inflammatory Osteoclastogenesis and Bone Resorption.Frontiers in endocrinology · 2020Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periarticular osteolysis, a crippling complication of rheumatoid arthritis, is the product of enhanced osteoclast recruitment and activation. The osteoclast, which is a member of the monocyte/macrophage family, is the exclusive bone resorptive cell, and its differentiation and activation are under the aegis of a variety of cytokines. Receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor are the essential osteoclastogenic cytokines and are increased in inflammatory joint disease. Tumor necrosis factor-alpha, which perpetrates arthritic bone loss, exerts its osteoclastogenic effect in the context of RANKL with which it synergizes. Achieving an understanding of the mechanisms by which the three cytokines affect the osteoclast has resulted in a number of active and candidate therapeutic targets.
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.