ReviewBiology2024
Roles of Toll-like Receptor Signaling in Inflammatory Bone Resorption.
Review in Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed.
- LPS-Induced TNF-α and IL-1 Signaling in Periodontitis: Molecular Mechanisms and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Isoorientin attenuates aging-induced bone deterioration by suppressing M1-mediated TLR4-MAPK-NF-κB inflammatory signaling.Biogerontology · 2026Article
- Review
- Medicine-food homologous bioactives in metabolic dysregulation-associated osteoporosis: a review of preclinical evidence and potential liver-bone and gut-bone actions.Chinese medicine · 2026Review
- Liraglutide, a GLP-1 Receptor Agonist, Mitigates LPS-Induced Osteoclastogenesis and Bone Loss by Downregulating Macrophage TNF-α Expression.International journal of molecular sciences · 2026Article
- Traumatic Occlusion Exacerbates Bone Resorption by Modifying Gene Expression in the Bone Tissue of Ligature-Induced Periodontitis in Mice.Journal of clinical periodontology · 2026Article
- Review
- Microbial messengers: decoding the gut microbiota's role in bone health through immunomodulation and exosomal signaling.NPJ biofilms and microbiomes · 2026Review
- Article
- The TLR10-Vitamin D Axis Facilitates Osteogenic Differentiation of Mesenchymal Stem Cells In Vitro.Cells · 2026Article
- Lacticaseibacillus rhamnosus LGG Suppresses Osteoclastogenesis via TLR6/NF-κB Modulation and Attenuates Ovariectomy-Induced Bone Loss in Mice.Probiotics and antimicrobial proteins · 2026Article
- Bone and Infections: An Osteoimmunological Interplay.International journal of molecular sciences · 2026Review
- Population-Scale Plasma Proteomic Profiles Associated with Chronic Periodontitis in the UK Biobank.International journal of molecular sciences · 2026Article
- Osteomyelitis related lameness across animal species: pathophysiology, etiology, epidemiology and experimental model approaches.Frontiers in veterinary science · 2026Review
- Adaptive hydrogel platforms for infected bone defect repair: microenvironmental responsiveness, osteoimmunomodulation, and regenerative remodeling.Frontiers in bioengineering and biotechnology · 2026Review
- Beyond receptor activation: biased toll-like receptor signaling in periodontal inflammation and regeneration.Frontiers in immunology · 2026Review
- Review
- Profiling the Bacterial Microbiome Across Peri-Implant Conditions.Journal of clinical periodontology · 2025Article
- The lysosomal catabolism of nucleic acids-critical regulators of the innate immune system.Nucleic acids research · 2025Review
- Impact of Hematopoietic CD14 on Oxidative Stress during Salt-Sensitive Hypertension and Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are pattern recognition receptors expressed in immune cells, including neutrophils, macrophages, and dendritic cells. Microbe-associated molecular patterns, including bacterial components, membranes, nucleic acids, and flagella are recognized by TLRs in inflammatory immune responses. Periodontal disease is an inflammatory disease known to cause local infections associated with gingival inflammation, subsequently leading to alveolar bone resorption. Prostaglandin E2 (PGE2) is a key mediator of TLR-induced inflammatory bone resorption. We previously reported that membrane-bound PGE synthase (mPGES-1)-deficient mice failed to induce bone resorption by lipopolysaccharide (LPS), a major pathogenic factor involved in periodontal bone resorption. Further experiments exploring specific pathogen-promoting osteoclast differentiation revealed that various TLR ligands induced osteoclast differentiation in a co-culture model. The ligands for TLR2/1, TLR2/6, TLR3, and TLR5, as well as TLR4, induce osteoclast differentiation associated with the production of PGE2 and the receptor activator of nuclear factor-kappa B ligand (RANKL), an inevitable inducer of osteoclast differentiation in osteoblasts. In vivo, local injection of TLR ligands, including TLR2/1, TLR2/6, and TLR3, resulted in severe alveolar bone resorption. This review summarizes the latest findings on TLR-mediated osteoclast differentiation and bone resorption in inflammatory diseases, such as periodontal diseases.
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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 Socratic graph.