ReviewCritical reviews in immunology2018
Does TNF Promote or Restrain Osteoclastogenesis and Inflammatory Bone Resorption?
Review in Critical reviews in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 22 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
- Vascular-lymphatic dual circulation in bone health and disease: Mechanistic coupling and translational therapeutics.Journal of orthopaedic translation · 2026Review
- Biologic immunomodulators and spinal fusion: evidence, mechanisms, and perioperative considerations.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- CX3CR1 and CCR2: dynamic myeloid cell states across inflammatory diseases with implications for oral health and disease.Frontiers in immunology · 2026Review
- Senescent immune cells, inflammaging, and bone loss: therapeutic potential and translational challenges of senolytics in osteoporosis.Frontiers in endocrinology · 2026Review
- Osteoporosis and Fracture Risk in Ovarian Cancer: Beyond the Oncologic Burden.Diagnostics (Basel, Switzerland) · 2025Review
- Article
- GPR40/GPR120 Agonist GW9508 Improves Metabolic Syndrome-Exacerbated Periodontitis in Mice.International journal of molecular sciences · 2024Article
- Roles of inflammatory cell infiltrate in periprosthetic osteolysis.Frontiers in immunology · 2023Review
- The Roles of TRAF3 in Immune Responses.Disease markers · 2023Review
- Altered IGF-I activity and accelerated bone elongation in growth plates precede excess weight gain in a mouse model of juvenile obesity.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Association of Antibiotic Alterations in Gut Microbiota With Decreased Osseointegration of an Intramedullary Nail in Mice With and Without Osteomyelitis.Frontiers in endocrinology · 2021Article
- miR-346-3p promotes osteoclastogenesis via inhibiting TRAF3 gene.In vitro cellular & developmental biology. Animal · 2020Article
- The Bones of Children With Obesity.Frontiers in endocrinology · 2020Review
- Periprosthetic Osteolysis: Mechanisms, Prevention and Treatment.Journal of clinical medicine · 2019Review
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
Abstract
Chronic inflammation is one of the most evident and common pathological conditions leading to deregulated osteoclastogenesis and bone remodeling. Tumor necrosis factor (TNF) as a pleiotropic cytokine plays a key role, not only in inflammation, but also in bone erosion in diseases associated with bone loss. TNF can stimulate the proliferation of osteoclast precursors and, in most conditions, act together with other cytokines and growth factors such as receptor activator of nuclear factor (NF)-[kappa]B ligand (RANKL), interleukin-6, and transforming growth factor beta to synergistically promote osteoclast formation and bone resorption in vivo. A longstanding enigma in the field is why TNF alone is not able to induce osteoclast differentiation as effectively as the same superfamily member RANKL, a physiological master osteoclastogenic cytokine. Recent studies have highlighted several lines of evidence showing the intrinsic mechanisms through RBP-J, NF-[kappa]B p100/TNF receptor-associated factor 3, or interferon regulatory factor-8 that restrain TNF-induced osteoclast differentiation and bone resorption. These feedback inhibitory mechanisms driven by TNF shed light into the current paradigm of osteoclastogenesis and would provide novel therapeutic implications on controlling inflammatory bone resorption.
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.