ReviewSeminars in immunology2016
Immune and regulatory functions of neutrophils in inflammatory bone loss.
Review in Seminars in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
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
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- Assessment of the role of Trichomonas tenax in the etiopathogenesis of human periodontitis: A systematic review.PloS one · 2019Pooled it
- A dysbiotic microbiome triggers TScience translational medicine · 2018Trial
- From Bone Marrow Reserve to Metastatic Niche: How Neutrophil-Lineage Cells Shape Skeletal Colonization.International journal of molecular sciences · 2026Review
- Periodontitis as a Model for Inflammatory Uncoupling of Bone Remodeling.Journal of periodontal research · 2026Review
- The Nox2 NADPH oxidase regulates neutrophilic inflammation in the oral cavity.Mucosal immunology · 2026Article
- Mucosal Inflammation Shapes Human Neutrophil States in Tissue and Circulation.bioRxiv : the preprint server for biology · 2026Article
- Spinosin Suppresses RANKL-induced Osteoclastogenesis and Alleviates LPS-induced Cranial Osteolysis: A Study based on Network Pharmacology and Experimental Validation.Current medicinal chemistry · 2026Article
- Immunomodulatory Biomaterials for Bone and Soft Tissue Chronic Inflammation Diseases.Small science · 2025Review
- [Role of Trained Immunity in the Association Between Periodontitis and Rheumatoid Arthritis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2025Review
- Neutrophils at the Crossroads of Oral Microbiome Dysbiosis and Periodontal Disease.Microorganisms · 2025Review
- Topography-based implants for bone regeneration: Design, biological mechanism, and therapeutics.Materials today. Bio · 2025Review
- Immunoporosis: The hidden link between aging immune cells and bone fragility.Journal of orthopaedic translation · 2025Review
- Grem1 inhibits osteogenic differentiation of MBMSCs in OVX rats through BMP/Smad1/5 signaling pathway.Regenerative therapy · 2025Article
- Limited proteolysis of neutrophil granule proteins by the bacterial protease RgpB depletes neutrophil antimicrobial capacity.Journal of leukocyte biology · 2025Article
- Microbiological and molecular aspects of periodontitis pathogenesis: an infection-induced inflammatory condition.Frontiers in cellular and infection microbiology · 2025Review
- Multi-dimensional role of AGEs in periodontitis: from matrix remodeling to neuro-immune crosstalk.Frontiers in immunology · 2025Review
- DNA methylation and immune regulation in osteoporosis: emerging epigenetic targets for drug discovery.Frontiers in pharmacology · 2025Review
- Immune cells: the key mediator between the gut microbiota and osteoporosis.Frontiers in immunology · 2025Review
- 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
- Selective modulation of the bone remodeling regulatory system through orthodontic tooth movement-a review.Frontiers in oral health · 2025Review
22 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Although historically viewed as merely anti-microbial effectors in acute infection or injury, neutrophils are now appreciated to be functionally versatile with critical roles also in chronic inflammation. Periodontitis, a chronic inflammatory disease that destroys the tooth-supporting gums and bone, is particularly affected by alterations in neutrophil numbers or function, as revealed by observations in monogenic disorders and relevant mouse models. Besides being a significant debilitating disease and health burden in its own right, periodontitis is thus an attractive model to dissect uncharted neutrophil-associated (patho)physiological pathways. Here, we summarize recent evidence that neutrophils can contribute to inflammatory bone loss not only through the typical bystander injury dogma but intriguingly also through their absence from the affected tissue, where they normally perform important immunomodulatory functions. Moreover, we discuss recent advances in the interactions of neutrophils with the vascular endothelium and - upon extravasation - with bacteria, and how the dysregulation of these interactions leads to inflammatory tissue damage. Overall, neutrophils have both protective and destructive roles in periodontitis, as they are involved in both the maintenance of periodontal tissue homeostasis and the induction of inflammatory bone loss. This highlights the importance of developing approaches that promote or sustain a fine balance between homeostatic immunity and inflammatory pathology.
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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.