Expression of PAR2 and NF-κB in human primary dental pulp odontoblasts during the progression of caries

Author:

Alisa Wichaidit,Namthip Patinotham,Kullanun Nukaeow,Aunwaya Kaewpitak

Abstract

Increased proteinase-activated receptor-2 (PAR2) expression is observed in various diseases related to inflammation. However, the expression of PAR2 in odontoblasts in response to dental caries has not been investigated. Therefore, to explore the functions of odontoblasts during the progression of carious infection, we measured PAR2 and NF-κB expression using immunofluorescence techniques in the odontoblast layer and pulpocytes in the sub-odontoblast region of 44 teeth extracted from children undergoing dental treatment (eight sound samples, 13 early carious samples, 16 advanced carious samples, and eight exposed pulp samples). PAR2 and NF-κB were expressed at moderate levels in sound teeth with non-carious pulp, and the expression levels changed as caries progressed. PAR2 was significantly upregulated in the odontoblast layer during early-stage and advanced-stage caries, and reduced below healthy levels in teeth with exposed pulp. NF-κB was significantly upregulated in early-stage caries and significantly downregulated in advanced-stage and late-stage caries. Moreover, in the sub-odontoblast region, NF-κB expression increased with the progression of caries. Overall, this study suggests PAR2 may represent a crucial cell signalling receptor in the dentine-pulp complex during dental inflammation, and that NF-κB may be one of the key pathways that regulate inflammatory immune responses in the dental pulp.

Publisher

Peertechz Publications Private Limited

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3