# Desquamative Gingivitis and the Oral Microbiome: Insights into Immune–Microbial Interactions in Mucosal Inflammation

## TL;DR

This review explores how changes in the oral microbiome may influence immune responses in desquamative gingivitis and related diseases.

## Contribution

The paper highlights the role of microbial dysbiosis in immune activation and mucosal inflammation in desquamative gingivitis.

## Key findings

- Microbial dysbiosis in OLP includes reduced diversity and increased pro-inflammatory genera like Fusobacterium and Prevotella.
- Dysbiosis may activate Toll-like receptors and skew T cell responses, contributing to immune tolerance breakdown.
- Early evidence suggests microbial involvement in MMP and PV, though data is limited compared to OLP.

## Abstract

Desquamative gingivitis (DG) is a clinical presentation characterized by erythema, epithelial desquamation, and mucosal fragility, commonly associated with immune-mediated diseases such as oral lichen planus (OLP), mucous membrane pemphigoid (MMP), and pemphigus vulgaris (PV). While traditionally viewed as a manifestation of immune dysregulation, growing evidence suggests that the oral microbiome may modulate disease onset, persistence, and severity. This review summarizes current knowledge on the oral microbiota in DG and its underlying diseases, explores mechanistic links between dysbiosis and immune activation, and discusses clinical and research implications. A narrative literature review was conducted using PubMed and Scopus, focusing on studies analyzing the oral microbiome in OLP, MMP, and PV. Emphasis was placed on molecular microbiology techniques, immune profiling, and functional or longitudinal approaches. In OLP, microbial dysbiosis is consistently reported, including reduced diversity and increased abundance of pro-inflammatory genera such as Fusobacterium, Prevotella, and Capnocytophaga. These shifts correlate with epithelial barrier disruption and inflammatory cytokine production. Although data on MMP and PV are limited, early findings suggest microbial involvement in sustaining inflammation, delaying healing, and possibly amplifying autoimmune responses. Dysbiosis may activate Toll-like receptors, skew T cell responses, and contribute to the breakdown of immune tolerance. DG may reflect a dynamic interplay between immune mechanisms and microbial ecology. While evidence is strongest for OLP, preliminary data suggest broader microbial contributions across DG-associated diseases. Microbiome-informed approaches could enhance diagnostic accuracy and support the development of adjunctive therapies.