The relationship between smoking and recurrent aphthous stomatitis: A Mendelian randomization study
Introduction Existing research suggests an association between smoking and the incidence of recurrent aphthous stomatitis (RAS); however, the causal relationship remains ambiguous. We employed Mendelian randomization (MR) to clarify the potential causal association between smoking and the risk of de...
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| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
European Publishing
2025-01-01
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| Series: | Tobacco Induced Diseases |
| Subjects: | |
| Online Access: | https://www.tobaccoinduceddiseases.org/The-relationship-between-smoking-and-recurrent-aphthous-stomatitis-A-Mendelian-randomization,199253,0,2.html |
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| Summary: | Introduction
Existing research suggests an association between smoking and the
incidence of recurrent aphthous stomatitis (RAS); however, the causal relationship
remains ambiguous. We employed Mendelian randomization (MR) to clarify the
potential causal association between smoking and the risk of developing RAS.
Methods
We utilized genome-wide association study (GWAS) sequencing data
related to smoking from the Finnish database as instrumental variables (IVs) and
GWAS data for RAS from the UK Biobank (UKB) as the outcome to perform a
two-sample MR analysis. The selection of IVs was rigorously controlled according
to the three principal assumptions of relevance, independence, and exclusivity. The
primary analytical methods utilized were inverse variance weighting (IVW) and
weighted median (WM), supplemented by MR-Egger, simple mode, and weighted
mode techniques to infer causality between smoking and RAS. Sensitivity analyses
were conducted using MR-PRESSO, Cochran's Q, and the MR-Egger intercept to
ensure the robustness of the findings.
Results
The findings from the IVW and WM analyses suggest a causal association
between smoking and an elevated risk of RAS (IVW: OR=1.003; 95% CI: 1.0002–
1.005, p=0.033; WM: OR=1.003; 95% CI: 1.00006–1.007, p=0.044). Compared
to non-smokers, smokers have a 0.3% increase in the risk of RAS. Furthermore,
the sensitivity analysis did not reveal any inconsistencies that would contradict
the MR results.
Conclusions
Our findings provide preliminary evidence of a potential causal
relationship between smoking and the risk of RAS, which may contribute to a
deeper understanding of the underlying mechanisms. Further research is needed
to confirm these results and explore their implications for clinical practice. |
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| ISSN: | 1617-9625 |