ArticleInternational endodontic journal2023
Regulation of caries-induced pulp inflammation by NLRP3 inflammasome: A laboratory-based investigation.
Article in International endodontic journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Spatial Transcriptomics-Inspired Targeted Hydrogel for Dental Pulp Therapy via Strengthen Macrophage Communication.Advanced healthcare materials · 2026Article
- Ultrasensitive multiplex salivary cytokine profiling reveals distinct immune signatures in dental caries.BDJ open · 2026Article
- Lipoteichoic Acid Stimulation of Macrophages Causes Mitochondrial Dysfunction.International dental journal · 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
- Objectively Diagnosing Pulpitis: Opportunities and Methodological Challenges in the Development of Point-of-Care Assays.International journal of molecular sciences · 2025Review
- The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review.Dentistry journal · 2025Review
- Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.Journal of inflammation research · 2025Review
- Pyroptosis in Pulpitis.Journal of inflammation research · 2025Review
- Guanylate-binding protein 5-mediated autophagy can promote the clearance of intracellular F. nucleatum in dental pulp cells during pulpitis.BMC oral health · 2024Article
- LPS-Induced Neuron Cell Apoptosis through TNF-α and Cytochrome c Expression in Dental Pulp.European journal of dentistry · 2024Article
- The effects of NLRP3 inflammasome inhibition or knockout in experimental apical periodontitis induced in mice.Clinical oral investigations · 2024Article
- Regulation of caries-induced pulp inflammation by NLRP3 inflammasome: A laboratory-based investigation.International endodontic journal · 2023Article
- GCF NLRP3 as a Biomarker for Assessing Endodontic Treatment Outcomes in Symptomatic Irreversible Pulpitis: A Comparative Nonrandomized, Observational Cross-Sectional Study.Journal of International Society of Preventive & Community DentistryArticle
- Spatiotemporal quantification of gingival crevicular fluid NLRP3 expression during non-surgical endodontic management of pulp necrosis with symptomatic apical periodontitis: A prospective case-control analysis.Journal of oral biology and craniofacial researchArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 3 countries.
Funding
Abstract
aimTo evaluate the expression and function of the nod-like receptor pyrin domain containing 3 (NLRP3) inflammasome in caries induced pulpitis. METHODOLOGY: NLRP3 expression was determined with immunohistochemistry in the dental pulp and qPCR in dental pulp cells (DPCs). THP-1 macrophages expressing the apoptosis-related speck-like protein (ASC) and green fluorescent protein (GFP) fusion protein were used to assess NLRP3 inflammasome activation by live cell imaging, following treatment with lipopolysaccharide (LPS) and lipoteichoic acid (LTA). Caspase I inhibitor was used to confirm inflammasome activation. An ex-vivo pulpitis model in which the DPCs were co-cultured with THP-1 macrophages was used to study the effect of the NLRP3 inflammasome inhibitor (MCC950), and cytokines were measured using ELISA and multiplex array. Data were analysed using the t-test or anova followed by a Bonferroni post hoc test with the level of significance set at p ≤ .05.
resultsNLRP3 inflammasome was differentially expressed in dental pulp of sound and carious teeth. Treatment of DPCs with LTA significantly upregulates NLRP3 and IL-1 β-expression (p < .05) and in induces more ASC specks formation compared to LPS. IL-β release in response to LTA treatment is significantly reduced with Caspase I inhibitor suggesting inflammasome dependent mechanism (p < .01). NLRP3-specific inhibitor, MCC950, significantly reduced IL-1β and IL-6 in an ex-vivo pulpitis model (p < .01) but had no effect on IL-8 or matrix metalloproteinase-9 (MMP-9).
conclusionsExpression and upregulation of NLRP3 inflammasome with caries and LTA treatment suggest a role in caries-induced pulpitis. NLRP3 inhibitor attenuated the release of selective inflammatory cytokines and could be a potential treatment target that merit further investigation.
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