ReviewCurrent osteoporosis reports2024
Neutrophils in Inflammatory Bone Diseases.
Review in Current osteoporosis reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 15 citations in OpenAlex.
- Neutrophil-derived apoptotic bodies function as decoy signals to preserve bone integrity during infectious osteomyelitis.Bone research · 2026Article
- The NLRP12 Osteoimmune Checkpoint: Coordinating Inflammatory Signaling and Bone Remodeling.Biomedicines · 2026Review
- From Bone Marrow Reserve to Metastatic Niche: How Neutrophil-Lineage Cells Shape Skeletal Colonization.International journal of molecular sciences · 2026Review
- Neutrophil extracellular traps in osteoporosis: mechanistic links to bone remodeling imbalance and therapeutic perspectives.Molecular biology reports · 2026Review
- Turmeric-derived nanovesicles reprogram pathological NETosis to mitigate inflammatory bone loss.Journal of nanobiotechnology · 2026Article
- Article
- Lutein Attenuates Synovial Hyperplasia, Cartilage Loss, and Bone Erosion by Suppressing Inflammatory Pathways in Rheumatoid Arthritis.International journal of medical sciences · 2026Article
- Immune cell senescence and chronic bone diseases: osteoimmune mechanisms and therapeutic perspectives.Frontiers in immunology · 2026Review
- Periodontitis Leads to Systemic Bone Loss through Neutrophil Reprogramming.Journal of dental research · 2026Article
- Combination of single-cell and bulk RNA-seq reveals changes in the immune landscape in osteomyelitis.Frontiers in immunology · 2026Article
- Oxidative stress mediated oleanolic acid therapeutic potential in rheumatoid arthritis: focus on the mechanisms.Frontiers in pharmacology · 2026Review
- Neutrophils: a Central Point of Interaction Between Immune Cells and Nonimmune Cells in Rheumatoid Arthritis.Clinical reviews in allergy & immunology · 2025Review
- Correlation between REDOX enzymes and NET markers expression during the development of periapical lesions in mice.Clinical oral investigations · 2025Article
- Causal Associations of the Alterations in Peripheral Blood Immune Cell Characteristics on the Incidence of Osteoporosis: A Bidirectional Mendelian Randomization Study.Therapeutics and clinical risk management · 2025Article
- From "immune silence" to "immune dialogue": modification strategies for bone substitutes based on bone immunomodulatory characteristics.Frontiers in cell and developmental biology · 2025Review
- Critical signaling pathways in osteoclast differentiation and bone resorption: mechanisms and therapeutic implications for periprosthetic osteolysis.Frontiers in cell and developmental biology · 2025Review
- From macrophage polarization to clinical translation: immunomodulatory hydrogels for infection-associated bone regeneration.Frontiers in cell and developmental biology · 2025Review
- IL33-induced neutrophil extracellular traps (NETs) mediate a positive feedback loop for synovial inflammation and NET amplification in rheumatoid arthritis.Experimental & molecular medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
purpose of reviewIn this review, we summarize the current evidence that suggests that neutrophils play a key role in facilitating damage to local bone structures. RECENT
findingsNeutrophil infiltration is a hallmark of inflammatory bone diseases such as rheumatoid arthritis (RA) and periodontitis disease (PD). Both of these human diseases are marked by an imbalance in bone homeostasis, favoring the degradation of local bone which ultimately leads to erosions. Osteoclasts, a multinucleated resident bone cell, are responsible for facilitating the turnover of bone and the bone damage observed in these diseases. The involvement of neutrophils and neutrophil extracellular trap formation have recently been implicated in exacerbating osteoclast function through direct and indirect mechanisms. We highlight a recent finding that NET proteins such as histones and elastase can generate non-canonical, inflammatory osteoclasts, and this process is mediated by post-translational modifications such as citrullination and carbamylation, both of which act as autoantigens in RA. It appears that NETs, autoantibodies, modified proteins, cytokines, and osteoclasts all ultimately contribute to local and permanent bone damage in RA and PD. However, more studies are needed to fully understand the role of neutrophils in inflammatory bone diseases.
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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.