ArticleAnatomical record (Hoboken, N.J. : 2007)2016
Elevated CD14 (Cluster of Differentiation 14) and Toll-Like Receptor (TLR) 4 Signaling Deteriorate Periapical Inflammation in TLR2 Deficient Mice.
Article in Anatomical record (Hoboken, N.J. : 2007), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Potential Association Between Apical Periodontitis and Cardiovascular Disease: A Narrative Review of Evidence and Clinical Implications.Anatolian journal of cardiology · 2026Review
- Exploring Persistent Apical Periodontitis in Humans: Integrative Genetic, Histological and Microbiological Perspectives for Translational Research.International endodontic journal · 2026Article
- Article
- Review
- Expression of Toll-like receptor 2, Dectin-1, and Osteopontin in murine model of pulpitis.Clinical oral investigations · 2023Article
- Screening of periodontitis-related genes and immune cells based on an integrated bioinformatics analysis.Annals of translational medicine · 2022Article
- Inhibition of the CXCL9-CXCR3 axis suppresses the progression of experimental apical periodontitis by blocking macrophage migration and activation.Scientific reports · 2021Article
- C1 Silencing Attenuates Inflammation and Alveolar Bone Resorption in Endodontic Disease.Journal of endodontics · 2019Article
- Endodontic Infection-induced Inflammation Resembling Osteomyelitis of the Jaws in Toll-like Receptor 2/Interleukin 10 Double-knockout Mice.Journal of endodontics · 2019Article
- Serum Amyloid A Contributes to Chronic Apical Periodontitis via TLR2 and TLR4.Journal of dental research · 2019Article
- Immunohistochemical and mRNA expression of RANK, RANKL, OPG, TLR2 and MyD88 during apical periodontitis progression in mice.Journal of applied oral science : revista FOB · 2018Article
- TLR4 expression and its immunopathogenic role in inflammatory radicular cysts: a clinicopathological study.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 4 countries.
Funding
Abstract
Apical periodontitis (periapical lesions) is an infection-induced chronic inflammation in the jaw, ultimately resulting in the destruction of apical periodontal tissue. Toll-like receptors (TLRs) are prominent in the initial recognition of pathogens. Our previous study showed that TLR4 signaling is proinflammatory in periapical lesions induced by a polymicrobial endodontic infection. In contrast, the functional role of TLR2 in regulation of periapical tissue destruction is still not fully understood. Using TLR2 deficient (KO), TLR2/TLR4 double deficient (dKO), and wild-type (WT) mice, we demonstrate that TLR2 KO mice are highly responsive to polymicrobial infection-induced periapical lesion caused by over activation of TLR4 signal transduction pathway that resulted in elevation of NF-kB (nuclear factor kappa B) and proinflammatory cytokine production. The altered TLR4 signaling is caused by TLR2 deficiency-dependent elevation of CD14 (cluster of differentiation 14), which is a co-receptor of TLR4. Indeed, neutralization of CD14 strikingly suppresses TLR2 deficiency-dependent inflammation and tissue destruction in vitro and in vivo. Our findings suggest that a network of TLR2, TLR4, and CD14 is a key factor in regulation of polymicrobial dentoalveolar infection and subsequent tissue destruction. Anat Rec, 299:1281-1292, 2016. © 2016 Wiley Periodicals, Inc.
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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.