# Familial Patterns of Oral–Gut Dysbiosis and Systemic Markers in Periodontitis

**Authors:** Hélvis E. S. Paz, Mabelle F. Monteiro, Camila S. Stolf, Cássia F. Araújo, Angelika Silbereisen, Mauro P. Santamaria, Nagihan Bostanci, Renato C. V. Casarin

PMC · DOI: 10.1111/jcpe.70047 · 2025-10-09

## TL;DR

The study found that parents with periodontitis have altered gut bacteria and systemic markers, which are also seen in their children.

## Contribution

This study reveals a potential oral–gut microbial transmission pathway linked to systemic health markers in families.

## Key findings

- Parents with periodontitis had distinct faecal microbiota profiles shared with their children.
- Elevated claudin-2 levels were observed in both parents and children with periodontitis.
- Claudin-2 levels correlated with oral dysbiosis and the faecal Firmicutes/Bacteroidetes ratio.

## Abstract

To investigate whether periodontitis in parents is associated with differences in the faecal microbiome and systemic markers in both themselves and their children.

Eighty participants were divided into four groups (n = 20): parents with periodontitis (PP); healthy parents (PC); and their respective children (CP, CC). Clinical periodontal parameters were recorded. Saliva and faecal bacterial DNA were analysed via 16S rRNA sequencing. Salivary lactoferrin, faecal calprotectin, gingival crevicular fluid cytokines (IFN‐γ, IL‐10, IL‐17, IL‐1β, IL‐4, TNF‐α) and urinary intestinal permeability markers (claudin‐2, ‐3, ‐4, haptoglobin) were quantified.

Parents with periodontitis showed distinct faecal microbiota profiles, which were mirrored in their children and significantly differed from controls. Claudin‐2 levels were elevated in both PP and CP groups (p < 0.05) and positively correlated with the oral dysbiosis index and the faecal Firmicutes/Bacteroidetes ratio.

Parental periodontal health appears to influence the faecal microbiome and systemic markers in the offspring. These findings highlight a potential pathway for oral–gut microbial transmission and its relevance to systemic health, warranting further investigation.

## Linked entities

- **Proteins:** tf.S (transferrin S homeolog), IFNG (interferon gamma), IL10 (interleukin 10), IL17A (interleukin 17A), IL1B (interleukin 1 beta), IL4 (interleukin 4), TNF (tumor necrosis factor), CLDN2 (claudin 2), CLDN3 (claudin 3), Claudin-4 (claudin-4)
- **Diseases:** periodontitis (MONDO:0005076)

## Full-text entities

- **Genes:** IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL10 (interleukin 10) [NCBI Gene 3586] {aka CSIF, GVHDS, IL-10, IL10A, TGIF}, CLDN2 (claudin 2) [NCBI Gene 9075] {aka OAZON, claudin-2}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, HP (haptoglobin) [NCBI Gene 3240] {aka HP2ALPHA2, HPA1S}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}
- **Diseases:** CP (MESH:D002972), Oral-Gut Dysbiosis (MESH:D064806), Periodontitis (MESH:D010518)

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12803660/full.md

---
Source: https://tomesphere.com/paper/PMC12803660