# Role of αENaC in root resorption of adjacent teeth due to entirely impacted mandibular third molars

**Authors:** Jiaqi Tang, Weijun Yu, Lu Lin, Ruhan Yang, Guanglong Li, Min Jin, Yuting Gu, Bin Jiang, Eryi Lu

PMC · DOI: 10.1186/s12903-024-04040-z · BMC Oral Health · 2024-03-21

## TL;DR

This study explores how αENaC contributes to root resorption in adjacent teeth caused by impacted molars, suggesting it could be a new indicator for the disease.

## Contribution

The study identifies αENaC as a novel indicator for root resorption caused by impacted molars and its correlation with inflammation and disease severity.

## Key findings

- αENaC is upregulated and localized in fibroblasts of granulation tissues associated with root resorption.
- αENaC positively correlates with inflammation markers TNF-α and N-cadherin in resorption tissues.
- ROC analysis confirms αENaC as a potential indicator for the disease.

## Abstract

Entirely impacted mandibular third molar (EIM3M) concerns the pathological external root resorption (ERR) of the adjacent mandibular second molar (M2M) and formation of granulation tissue between two molars. The study aimed to clarify the effect of αENaC, a mechano-sensitive molecule, to explore the mechanical mechanism in this scenario.

The force EIM3M exerted on M2M was proved by finite element analysis. αENaC expressions were tested by real-time polymerase chain reaction (PCR), immunoblotting and immunofluorescence. Inflammatory and epithelial-mesenchymal transition (EMT)-related molecules expressions were also detected by real-time PCR. The correlation was analyzed by Spearman’s correlation analysis, and receiver-operator characteristic (ROC) curve was further exhibited.

The force was concentrated in the ERR area. αENaC was upregulated, positively correlated with ERR degree and localized to the fibroblasts in ERR granulation tissues. Moreover, αENaC was respectively and positively associated with elevated TNF-α and N-cadherin in ERR granulation tissues. More importantly, ROC analysis verified αENaC as a novel indication of the incidence of this disease.

Our finding revealed the force from EIM3M causing ERR of M2M, and elucidated the expression and localization of αENaC and its positive correlation with inflammation, EMT and disease severity, suggesting a novel indication in this disease.

The online version contains supplementary material available at 10.1186/s12903-024-04040-z.

## Linked entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124], CadN (Cadherin-N) [NCBI Gene 35070]

## Full-text entities

- **Genes:** SCNN1A (sodium channel epithelial 1 subunit alpha) [NCBI Gene 6337] {aka BESC2, ENaCa, ENaCalpha, LIDLS3, PHA1B1, SCNEA}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CDH2 (cadherin 2) [NCBI Gene 1000] {aka ACOGS, ADHD8, ARVD14, CD325, CDHN, CDw325}
- **Diseases:** Inflammatory (MESH:D007249), ERR (MESH:D012391)

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10956368/full.md

## References

40 references — full list in the complete paper: https://tomesphere.com/paper/PMC10956368/full.md

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Source: https://tomesphere.com/paper/PMC10956368