# Potential roles and mechanisms of bacterial peptidylarginine deiminase in dental biofilm mediated by Porphyromonas gingivalis

## TL;DR

This review explores how an enzyme from a harmful oral bacterium contributes to dental biofilms and may link gum disease to rheumatoid arthritis.

## Contribution

The paper synthesizes current understanding of PPAD's roles in oral biofilm dynamics and systemic inflammation.

## Key findings

- PPAD modulates biofilm pathogenicity through pH changes and virulence factor citrullination.
- PPAD-generated citrullinated antigens may trigger autoimmune responses linking periodontitis to rheumatoid arthritis.
- PPAD is proposed as a potential biomarker and therapeutic target for oral-systemic diseases.

## Abstract

Porphyromonas gingivalis, a keystone oral pathogen, secretes the enzyme peptidylarginine deiminase (PPAD), which catalyzes protein citrullination and is implicated in both dental biofilm formation and the pathogenesis of systemic inflammatory diseases.

This review aims to synthesize current knowledge on PPAD, with a specific focus on its mechanistic roles in oral biofilm dynamics and its potential contribution to the development of periodontitis and rheumatoid arthritis (RA).

A comprehensive literature search was conducted using the PubMed database up to August 2025, employing keywords including ‘PPAD’, ‘Porphyromonas gingivalis’, ‘citrullination’, ‘dental biofilm’, ‘periodontitis’, and ‘rheumatoid arthritis’.

PPAD contributes critically to biofilm pathogenicity by modulating microbial pH, citrullinating virulence factors, and facilitating polymicrobial interactions. It promotes bacterial adhesion, disrupts host immunity, and sustains local inflammation. Systemically, PPAD-generated citrullinated antigens may trigger autoimmune responses, potentially linking periodontitis to RA.

PPAD represents a promising biomarker and therapeutic target for mitigating oral-systemic disease progression. Future research should prioritize elucidating its spatiotemporal regulation within biofilms and its immune-dysregulating effects to guide precision interventions.