Trial reportScientific reports2019
IL-36γ is a pivotal inflammatory player in periodontitis-associated bone loss.
Trial report in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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
17 citing papers in PubMed, 25 citations in OpenAlex.
- The Outcome of Intracellular Selenomonas sputigena and its Impact on Gingival Keratinocytes.Molecular oral microbiology · 2026Article
- Periodontal Disease and Its Association withMicroorganisms · 2026Review
- Oral microbiome, periodontal disease and systemic bone-related diseases in the era of homeostatic medicine.Journal of advanced research · 2025Review
- Serum cytokines in periodontal diseases.Periodontology 2000 · 2025Review
- Transcriptome Analysis of Porphyromonas gingivalis Lipopolysaccharide-Induced Early Gene Expression in Human Gingival Keratinocytes.Journal of periodontal research · 2025Article
- Peripheral blood immune cell levels differ with the stage and grade of periodontitis in systemically healthy individuals.Clinical oral investigations · 2025Article
- Multi-organ frailty is enhanced by periodontitis-induced inflammaging.Inflammation and regeneration · 2025Article
- FloxedCells · 2024Article
- Illuminating the oral microbiome: cellular microbiology.FEMS microbiology reviews · 2023Article
- New insights into inflammatory osteoclast precursors as therapeutic targets for rheumatoid arthritis and periodontitis.Bone research · 2023Review
- Molecular Basis beyond Interrelated Bone Resorption/Regeneration in Periodontal Diseases: A Concise Review.International journal of molecular sciences · 2023Review
- Mechanism and application ofFrontiers in public health · 2023Review
- Treponema denticola Induces Interleukin-36γ Expression in Human Oral Gingival Keratinocytes via the Parallel Activation of NF-κB and Mitogen-Activated Protein Kinase Pathways.Infection and immunity · 2022Article
- The mechanism on Prevotella melaninogenica promoting the inflammatory progression of oral lichen planus.Clinical and experimental immunology · 2022Article
- Down-regulated IL36RN expression based on peripheral blood mononuclear cells and plasma of periodontitis patients and its clinical significance.Journal of clinical laboratory analysis · 2021Article
- Akkermansia muciniphila and Its Pili-Like Protein Amuc_1100 Modulate Macrophage Polarization in Experimental Periodontitis.Infection and immunity · 2020Article
- IL-1 Superfamily Members and Periodontal Diseases.Journal of dental research · 2020Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Periodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis. The newer members of the IL-1 family, IL-36s (IL-36α/IL-36β/IL-36γ/IL-36Ra/IL-38) are known to be involved in host defense against P. gingivalis in oral epithelial cells (OECs) and are considered as key inflammatory mediators in chronic diseases. The aim of this study was to investigate the potential role of IL-36s in periodontitis. We showed here that IL-36γ mRNA gingival expression is higher in periodontitis patients, whereas IL-36β and IL-36Ra mRNA expression are lower compared to healthy controls. Interestingly, the elevated IL-36γ expression in patients is positively correlated with the RANKL/OPG ratio, an index of bone resorption. In vitro, IL-36γ expression was induced through TLR2 activation in primary OECs infected with P. gingivalis but not in gingival fibroblasts, the most widespread cell type in gingival connective tissue. In OECs, recombinant IL-36γ enhanced the expression of inflammatory cytokines (IL-1β, IL-6, TNF-α and IL-36γ), of TLR2 and importantly, the RANKL/OPG ratio. These findings suggest that IL-36γ could be a pivotal inflammatory player in periodontitis by perpetuating gingival inflammation and its associated alveolar bone resorption and could be a relevant therapeutic target.
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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.