ArticleInternational journal of molecular sciences2022
NLRP3 Inflammasome Negatively Regulates RANKL-Induced Osteoclastogenesis of Mouse Bone Marrow Macrophages but Positively Regulates It in the Presence of Lipopolysaccharides.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- Intelligent responsive alloy scaffold temporally regulates the immune-osteogenic axis for the treatment of infectious bone defects.Bioactive materials · 2026Article
- Ultrasensitive multiplex salivary cytokine profiling reveals distinct immune signatures in dental caries.BDJ open · 2026Article
- From sugar to flames: the detrimental role of pyroptosis in diabetes-associated bone loss.Molecular biology reports · 2026Review
- Mechanical Stimulation Drives Multicellular Synergy and Signaling Pathways in Developing Skeletal Tissues.Sports medicine (Auckland, N.Z.) · 2026Review
- LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism.Cell death & disease · 2026Article
- The risk of osteoporosis in COPD: An analysis of sex differences and mediating effects based on NHANES.NPJ primary care respiratory medicine · 2026Article
- Emerging Role of the NLRP3 Inflammasome in the Onset of Oral Diseases and Its Potential as a Therapeutic Target.International journal of molecular sciences · 2026Review
- Context-dependent roles of the NLRP3 inflammasome in osteomyelitis and strategies for precision modulation.Frontiers in immunology · 2026Review
- The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target.Immunity, inflammation and disease · 2025Review
- The circadian regulator PER1 inhibits osteoclastogenesis by activating inflammatory genes.bioRxiv : the preprint server for biology · 2025Article
- Porphyromonas gingivalis induces Zbp1-mediated macrophages PANoptosis in periodonitis pathophysiology.Experimental & molecular medicine · 2025Article
- Deciphering B Cell Heterogeneity and Pathogenic Mechanisms in Osteoporosis Through Single-Cell RNA Sequencing.BioMed research international · 2025Article
- Article
- Pyroptosis in Skeleton Diseases: A Potential Therapeutic Target Based on Inflammatory Cell Death.International journal of molecular sciences · 2024Review
- BML-111 inhibit HBMC oral health · 2024Article
- Pyroptosis mediates osteoporosis via the inflammation immune microenvironment.Frontiers in immunology · 2024Review
- Dental Pulp Stem Cell-Derived Exosomes Regulate Anti-Inflammatory and Osteogenesis in Periodontal Ligament Stem Cells and Promote the Repair of Experimental Periodontitis in Rats.International journal of nanomedicine · 2023Article
- Screening of crosstalk and pyroptosis-related genes linking periodontitis and osteoporosis based on bioinformatics and machine learning.Frontiers in immunology · 2022Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
In inflammatory bone diseases such as periodontitis, the nucleotide-binding oligomerization domain, leucine-rich repeat, and pyrin domain-containing 3 (NLRP3) inflammasome accelerates bone resorption by promoting proinflammatory cytokine IL-1β production. However, the role of the NLRP3 inflammasome in physiological bone remodeling remains unclear. Here, we investigated its role in osteoclastogenesis in the presence and absence of lipopolysaccharide (LPS), a Gram-negative bacterial component. When bone marrow macrophages (BMMs) were treated with receptor activator of nuclear factor-κB ligand (RANKL) in the presence of NLRP3 inflammasome inhibitors, osteoclast formation was promoted in the absence of LPS but attenuated in its presence. BMMs treated with RANKL and LPS produced IL-1β, and IL-1 receptor antagonist inhibited osteoclastogenesis, indicating IL-1β involvement. BMMs treated with RANKL alone produced no IL-1β but increased reactive oxygen species (ROS) production. A ROS inhibitor suppressed apoptosis-associated speck-like protein containing a caspase-1 recruitment domain (ASC) speck formation and NLRP3 inflammasome inhibitors abrogated cytotoxicity in BMMs treated with RANKL, indicating that RANKL induces pyroptotic cell death in BMMs by activating the NLRP3 inflammasome via ROS. This suggests that the NLRP3 inflammasome promotes osteoclastogenesis via IL-1β production under infectious conditions, but suppresses osteoclastogenesis by inducing pyroptosis in osteoclast precursors under physiological conditions.
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