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The role of NF-kappaB in the inflammatory processes related to dental caries, pulpitis, apical periodontitis, and periodontitis-a narrative review.

Authors :
Chen Z
Lang G
Xu X
Liang X
Han Y
Han Y
Source :
PeerJ [PeerJ] 2024 Aug 29; Vol. 12, pp. e17953. Date of Electronic Publication: 2024 Aug 29 (Print Publication: 2024).
Publication Year :
2024

Abstract

Tooth-related inflammatory disorders, including caries, pulpitis, apical periodontitis (AP), and periodontitis (PD), are primarily caused by resident oral microorganisms. Although these dental inflammatory conditions are typically not life-threatening, neglecting them can result in significant complications and greatly reduce an individual's quality of life. Nuclear factor κB (NF-κB), a family formed by various combinations of Rel proteins, is extensively involved in inflammatory diseases and even cancer. This study reviews recent data on NF-κB signaling and its role in dental pulp stem cells (DPSCs), dental pulp fibroblasts (DPFs), odontoblasts, human periodontal ligament cells (hPDLCs), and various experimental animal models. The findings indicate that NF-κB signaling is abnormally activated in caries, pulpitis, AP, and PD, leading to changes in related cellular differentiation. Under specific conditions, NF-κB signaling occasionally interacts with other signaling pathways, affecting inflammation, bone metabolism, and tissue regeneration processes. In summary, data collected over recent years confirm the central role of NF-κB in dental inflammatory diseases, potentially providing new insights for drug development targeting NF-κB signaling pathways in the treatment of these conditions. Keywords: NF-κB, dental caries, pulpitis, apical periodontitis, periodontitis.<br />Competing Interests: The authors declare that they have no competing interests.<br /> (© 2024 Chen et al.)

Details

Language :
English
ISSN :
2167-8359
Volume :
12
Database :
MEDLINE
Journal :
PeerJ
Publication Type :
Academic Journal
Accession number :
39221277
Full Text :
https://doi.org/10.7717/peerj.17953