期刊
JAPANESE DENTAL SCIENCE REVIEW
卷 47, 期 2, 页码 161-166出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.jdsr.2011.02.001
关键词
Toll-like receptor (TLR); Nucleotide-binding oligomerization domain (NOD); Dental pulp fibroblast; Cytokine; Pulpitis
资金
- Japan Society for the Promotion of Science [16591915, 20592228, 20592229]
- Grants-in-Aid for Scientific Research [16591915, 20592228, 25670821, 23390435, 20592229] Funding Source: KAKEN
As caries-related bacteria invade deeply into dentin and come into close proximity to the pulp, inflammatory cells (such as lymphocytes, macrophages and neutrophils) infiltrate into the bacterium-invaded area and consequently pulpitis develops. Many types of cytokines and adhesion molecules are responsible for the initiation and progression of pulpitis. Dental pulp fibroblasts, a major cell type in the dental pulp, also have capacity to produce pro-inflammatory cytokines and express adhesion molecules in response to pathogen-associated molecular patterns (PAMPs), including lipopolysaccharide. The innate immune system senses microbial infection using pattern recognition receptors, such as Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD), for PAMPs. In this review, we summarize the roles of dental pulp fibroblasts in the recognition of invaded bacterium-related factors via TLR and NOD pathways, and the subsequent pulpal immune responses, leading to progressive pulpitis. (C) 2011 Japanese Association for Dental Science. Published by Elsevier Ltd. All rights reserved.
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