ArticleThe Journal of biological chemistry2011
TLR2-dependent modulation of osteoclastogenesis by Porphyromonas gingivalis through differential induction of NFATc1 and NF-kappaB.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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
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Who cites it
58 citing papers in PubMed, 113 citations in OpenAlex.
- Trial
- The Innate Immune Memory That Bites Back: How Periodontitis May Train Neuroinflammation in Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Oxidized Low-Density Lipoprotein Enhances Toll-like Receptor-Mediated Osteoclastogenic Responses in the Absence of Exogenous RANKL: Implications for Inflammatory Osteoclastogenesis in Periodontitis.Medicina (Kaunas, Lithuania) · 2026Article
- Article
- Lactobacillus sakei CVL-001 Inhibits Osteoclast Differentiation Through TLR2 and GPCR-Dependent Pathways and Prevents Bone Loss in Ovariectomized Mice.Probiotics and antimicrobial proteins · 2026Article
- Article
- Periodontopathic bacteria in rheumatoid arthritis pathogenesis: bridging clinical associations to molecular mechanisms.Frontiers in immunology · 2025Review
- Napyradiomycin B4 Suppresses RANKL-Induced Osteoclastogenesis and Prevents Alveolar Bone Destruction in Experimental Periodontitis.ACS pharmacology & translational science · 2024Article
- MiRNA-23a-5p is the biomarkers for gouty arthritis and promotes inflammation in rats of gouty arthritis via MyD88/NF-κB pathway by induction TLR2.Archives of rheumatology · 2022Article
- Context-Dependent Roles for Toll-Like Receptors 2 and 9 in the Pathogenesis of Staphylococcus aureus Osteomyelitis.Infection and immunity · 2022Article
- Effects of salinity acclimation on histological characteristics and miRNA expression profiles of scales in juvenile rainbow trout (Oncorhynchus mykiss).BMC genomics · 2022Article
- Endosomal TLR3 signaling in stromal osteoblasts induces prostaglandin EThe Journal of biological chemistry · 2022Article
- Simvastatin intervention mitigates hypercholesterolemia-induced alveolar bone resorption in rats.Experimental and therapeutic medicine · 2021Article
- Sexual Dimorphism in Differentiating Osteoclast Precursors Demonstrates Enhanced Inflammatory Pathway Activation in Female Cells.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Biological Effects of β-Glucans on Osteoclastogenesis.Molecules (Basel, Switzerland) · 2021Review
- Lipopolysaccharide- TLR-4 Axis regulates Osteoclastogenesis independent of RANKL/RANK signaling.BMC immunology · 2021Article
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Inhibiting Monoacylglycerol Lipase Suppresses RANKL-Induced Osteoclastogenesis and Alleviates Ovariectomy-Induced Bone Loss.Frontiers in cell and developmental biology · 2021Article
- The Role of Toll-Like Receptors in Osteoclastogenesis.Journal of bone metabolism · 2020Article
- Ginsenoside Rb3 Inhibits Pro-Inflammatory Cytokines via MAPK/AKT/NF-κB Pathways and Attenuates Rat Alveolar Bone Resorption in Response toMolecules (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Osteolytic diseases, including rheumatoid arthritis, osteomyelitis, and periodontitis, are usually associated with bacterial infections. However, the precise mechanisms by which bacteria induce bone loss still remain unclear. Evidence exists that Toll-like receptor (TLR) signaling regulates both inflammation and bone metabolism and that the receptor activator of NF-κB ligand (RANKL) and its receptor RANK are the key regulators for bone remodeling and for the activation of osteoclasts. Here, we investigate the direct effects of the periodontal pathogen Porphyromonas gingivalis on osteoclast differentiation and show that P. gingivalis differentially modulates RANKL-induced osteoclast formation contingent on the state of differentiation of osteoclast precursors. In addition, although an optimal induction of cytokines by P. gingivalis is dependent on TLR2 and TLR4, as well as myeloid differentiation factor 88 and Toll/IL-1R domain-containing adaptor-inducing IFN-β, P. gingivalis utilizes TLR2/ myeloid differentiation factor 88 in modulating osteoclast differentiation. P. gingivalis modulates RANKL-induced osteoclast formation by differential induction of NFATc1 and c-Fos. More importantly, RANKL-mediated lineage commitment also has an impact on P. gingivalis-induced cytokine production. RANKL inhibits P. gingivalis-induced cytokine production by down-regulation of TLR/NF-κB and up-regulation of NFATc1. Our findings reveal novel aspects of the interactions between TLR and RANK signaling and provide a new model for understanding the mechanism underlying the pathogenesis of bacteria-mediated bone loss.
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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.