International endodontic journal · 2026
Differential Expressions of Inflammatory, Dentinogenic, Regulatory, Proliferative and Stemness Genes in Non-Carious and Carious Human Dental Pulp Tissues: An Ex Vivo Proof-of-Concept Study.
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Arora Shelly, Cooper Paul R, Friedlander Lara T, Ratnayake Jithendra T, Rizwan Shakila B, Seo Benedict, Rich Alison M, Hussaini Haizal M
Аннотация
BACKGROUND: Dental caries demineralises the enamel and dentine of the teeth, and as infection progresses it can lead to pulpal inflammation, infection and severe pain.
AIM: To determine and compare the level of mRNA expression of Toll-like receptors ((TLR)-2, TLR-4 and TLR-9), tumour necrosis factor (TNF)-α, interleukins ((IL)-1α, IL-1β, IL-4, IL-6, IL-8, IL-17 and IL-23) as well as markers of dentinogenic (dentine matrix protein (DMP)-1, dentine sialophosphoprotein (DSPP)), regulatory (nuclear factor-kappa B (NF-κB1), mitogen activated protein kinase (MAPK1)), proliferative (mitogen activated protein kinase (MKi)) and stemness (sex determining region Y-box 2 (SOX2)) between non-carious and carious dental pulp tissues.
METHODOLOGY: This study undertook a comprehensive analysis of inflammatory markers including TLR-2, TLR-4, TLR-9, TNF-α, IL-1α, IL-1β, IL-4, IL-6, IL-8, IL-17 and IL-23, as well as markers of dentinogenic DMP-1, DSPP, NF-κB1, MAPK1, proliferative MKi and stemness SOX2 processes in healthy and carious pulp tissues using quantitative real-time reverse-transcription polymerase chain reaction.
RESULTS: We found higher levels of TLR-2, TLR-4, IL-6, IL-8, IL-17A, IL-23A, along with NF-κB1 and MKi67 in the carious pulps (p < 0.05). The concurrent upregulation of IL-17A and IL-23A may suggest the activation of the IL-23/IL-17 signalling axis in the carious pulps, a point underreported in the literature.
CONCLUSION: These findings highlight the crucial role of the immune system in pulpal inflammation and potential implications in developing targeted molecular treatments, supporting the need for further translational research.
AIM: To determine and compare the level of mRNA expression of Toll-like receptors ((TLR)-2, TLR-4 and TLR-9), tumour necrosis factor (TNF)-α, interleukins ((IL)-1α, IL-1β, IL-4, IL-6, IL-8, IL-17 and IL-23) as well as markers of dentinogenic (dentine matrix protein (DMP)-1, dentine sialophosphoprotein (DSPP)), regulatory (nuclear factor-kappa B (NF-κB1), mitogen activated protein kinase (MAPK1)), proliferative (mitogen activated protein kinase (MKi)) and stemness (sex determining region Y-box 2 (SOX2)) between non-carious and carious dental pulp tissues.
METHODOLOGY: This study undertook a comprehensive analysis of inflammatory markers including TLR-2, TLR-4, TLR-9, TNF-α, IL-1α, IL-1β, IL-4, IL-6, IL-8, IL-17 and IL-23, as well as markers of dentinogenic DMP-1, DSPP, NF-κB1, MAPK1, proliferative MKi and stemness SOX2 processes in healthy and carious pulp tissues using quantitative real-time reverse-transcription polymerase chain reaction.
RESULTS: We found higher levels of TLR-2, TLR-4, IL-6, IL-8, IL-17A, IL-23A, along with NF-κB1 and MKi67 in the carious pulps (p < 0.05). The concurrent upregulation of IL-17A and IL-23A may suggest the activation of the IL-23/IL-17 signalling axis in the carious pulps, a point underreported in the literature.
CONCLUSION: These findings highlight the crucial role of the immune system in pulpal inflammation and potential implications in developing targeted molecular treatments, supporting the need for further translational research.