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Shared Inflammatory Genetic Susceptibility Underlying Spontaneous Preterm Birth and Periodontitis: A Case-Control
Joana Couceiro1,2,3,4, Carlos Família3,4, José Brito3
1UCIBIO-Applied Molecular Biosciences Unit, Department of Life Sciences, NOVA School of Science and Technology, NOVA University Lisbon, 2829-516 Caparica, Portugal.
Journal of Clinical Medicine
|September 13, 2025
Summary
Genetic variants in inflammatory pathways may increase the risk for spontaneous preterm birth (SPTB) and periodontitis (PD). The TLR1 rs5743618 variant showed the strongest association, suggesting SPTB could stem from systemic inflammation.
Area of Science:
- Genetics
- Immunology
- Obstetrics
Background:
- Spontaneous preterm birth (SPTB) is a major global health concern with unknown causes.
- Chronic inflammatory conditions like periodontitis (PD) are potential risk factors for SPTB.
- This study investigates shared genetic predispositions to SPTB and PD, viewing SPTB as a potential manifestation of dysregulated inflammation.
Purpose of the Study:
- To explore shared genetic susceptibility between spontaneous preterm birth (SPTB) and periodontitis (PD).
- To identify specific genetic variants in inflammatory pathways associated with SPTB risk.
- To propose a new perspective on SPTB etiology, linking it to systemic inflammatory dysregulation.
Main Methods:
- A case-control study involving 126 Portuguese postpartum women.
- Screening of 56 single nucleotide polymorphisms (SNPs) in 36 inflammation-related genes.
- Detailed regression analysis of four selected variants (IL1RN rs4251961, TLR1 rs5743618, IL6 rs2069827, IL6R rs4845617), adjusting for covariates and interaction terms.
Main Results:
- The IL1RN rs4251961 variant was associated with SPTB risk.
- The IL6R rs4845617 variant demonstrated a protective effect.
- The TLR1 rs5743618 variant showed the strongest association with an "inflammation" phenotype, with CC homozygotes having a four-fold increased odds.
Conclusions:
- Shared genetic variants in inflammatory pathways, particularly TLR1 rs5743618, may contribute to susceptibility for both SPTB and PD.
- Findings suggest SPTB might result from systemic inflammatory dysregulation, not just comorbid conditions.
- Further validation in larger cohorts is recommended to confirm the role of these genetic markers.
