ArticlePloS one2016
Interleukin-33 and RANK-L Interplay in the Alveolar Bone Loss Associated to Periodontitis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- The Role of Regulatory T Cells in Periodontitis With or Without Systemic Diseases: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- IL-36γ is a pivotal inflammatory player in periodontitis-associated bone loss.Scientific reports · 2019Trial
- Mechanisms of the IL-33/ST2 Signaling Axis in Regulating Bone Metabolism.Biomolecules · 2026Review
- Periodontal Disease and Its Association withMicroorganisms · 2026Review
- Impact of LiveMicroorganisms · 2025Article
- Serum cytokines in periodontal diseases.Periodontology 2000 · 2025Review
- The Influence of Genetic Polymorphisms ofInternational journal of dentistry · 2025Article
- The IL-33/ST2 axis is protective against acute inflammation during the course of periodontitis.Nature communications · 2024Article
- Evaluation of Serum Interleukin-33 Level in Iraqi Patients with and without Periodontal Disease.Clinical, cosmetic and investigational dentistry · 2024Article
- Involvement of the Notch signaling system in alveolar bone resorption.The Japanese dental science review · 2023Review
- New insights into inflammatory osteoclast precursors as therapeutic targets for rheumatoid arthritis and periodontitis.Bone research · 2023Review
- Biomarkers for the severity of periodontal disease in patients with obstructive sleep apnea:IL-1 β, IL-6, IL-17A, and IL-33.Heliyon · 2023Article
- Molecular Basis beyond Interrelated Bone Resorption/Regeneration in Periodontal Diseases: A Concise Review.International journal of molecular sciences · 2023Review
- DAMPs and alarmin gene expression patterns in aging healthy and diseased mucosal tissues.Frontiers in oral health · 2023Article
- Article
- Mapping of DNA methylation-sensitive cellular processes in gingival and periodontal ligament fibroblasts in the context of periodontal tissue homeostasis.Frontiers in immunology · 2023Article
- Mast Cell Cytokines in Acute and Chronic Gingival Tissue Inflammation: Role of IL-33 and IL-37.International journal of molecular sciences · 2022Review
- Update on B Cell Response in Periodontitis.Advances in experimental medicine and biology · 2022Article
- Application of Ligature-Induced Periodontitis in Mice to Explore the Molecular Mechanism of Periodontal Disease.International journal of molecular sciences · 2021Review
- CGF Membrane Promotes Periodontal Tissue Regeneration Mediated by hUCMSCs through Upregulating TAZ and Osteogenic Differentiation Genes.Stem cells international · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionChronic Periodontitis (CP) is an inflammatory disease of bacterial origin that results in alveolar bone destruction. Porphyromonas gingivalis (Pg), one of the main periopathogens, initiates an inflammatory cascade by host immune cells thereby increasing recruitment and activity of osteoclasts, the bone resorbing cells, through enhanced production of the crucial osteoclastogenic factor, RANK-L. Antibodies directed against some cytokines (IL-1β, IL-6 and TNF-α) failed to exhibit convincing therapeutic effect in CP. It has been suggested that IL-33, could be of interest in CP.
objectivethe present study aims to analyze whether and how IL-33 and RANK-L and/or their interplay are involved in the bone destruction associated to CP. MATERIAL AND
methodsmRNAs and protein expressions of IL-33 and RANK-L were analyzed in healthy and CP human gingival samples by immunohistochemistry (IHC) and RT-qPCR. Murine experimental periodontitis (EP) was induced using Pg infected ligature and Pg free ligature around the first maxillary molar. Alveolar bone loss was recorded by μCT. Mouse gingival explants were stimulated for 24 hours with IL-33 and RANK-L mRNA expression investigated by RT-qPCR. Human oral epithelial cells were infected by Pg for 6, 12; 24 hours and IL-33 and RANK-L mRNA expressions were analyzed by RT-qPCR.
resultsIL-33 is overexpressed in gingival epithelial cells in human affected by CP as in the murine EP. In human as in murine gingival cells, RANK-L was independently induced by Pg and IL-33. We also showed that the Pg-dependent RANK-L expression in gingival epithelial cells occured earlier than that of IL-33.
conclusionOur results evidence that IL-33 overexpression in gingival epithelial cells is associated with CP and may trigger RANK-L expression in addition to a direct effect of Pg. Finally, IL-33 may act as an extracellular alarmin (danger signal) showing proinflammatory properties in CP perpetuating bone resorption induced by Pg infection.
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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.