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Microplastics in the Pathogenesis of Periodontal Diseases: A Narrative Review

Annals of Global Health 2025 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Delfin Lovelina Francis, Saravanan Sampoornam Pape Reddy

Summary

This narrative review examines emerging evidence on how microplastics may contribute to the development and progression of periodontal diseases. Researchers found that microplastics have been detected in oral tissues and may promote inflammation, oxidative stress, and disruption of the oral microbiome. The study suggests that microplastic exposure could represent a previously unrecognized risk factor for gum disease.

Body Systems
Study Type In vitro

Introduction: Microplastics, plastic particles <5 mm in size, are a new class of environmental pollutants and have a role in systemic and oral health. Their implication in the pathogenesis of periodontal diseases has only recently been addressed. Objective: This review will discuss recent evidence of the modes of action by which microplastics may be involved in the onset and development of periodontal diseases. Methods: A systematic search of PubMed, Scopus, and Web of Science was performed up to May 2025 using keywords "microplastics," "nanoplastics," "oral health," "periodontal disease," "oxidative stress," "dysbiosis," "DNA damage response," and "immune response" in the title, abstract, or keywords. According to PRISMA guidelines, 235 articles were retrieved, and 210 remained after duplicates were discarded. A total of 150 were removed after title/abstract screening. Sixty full-text articles were reviewed, and 30 were included in the qualitative synthesis. Results: The existing evidence indicates that microplastics may induce periodontal pathology via several potential mechanisms, including (i) mechanical irritation of the surface of the gingival tissues, (ii) emission of toxic additives that cause oxidative stress, (iii) activation of DNA damage response (DDR) pathways, (iv) imbalance in the microbial community, and (v) immune regulation. These pathways intersect to enhance inflammation, tissue destruction, and dysbiosis, which culminate in the progression of periodontal disease. Conclusions: It is suggested that microplastics are one of the potential epiphenomena of periodontal diseases. However, original experimental data are limited, especially with reference to immunological interactions. Future in-vitro and clinical investigations are urgently needed to confirm these mechanistic hypotheses and to foster preventive and therapeutic approaches.

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