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Micro- and nanoplastics in periodontitis: mechanistic pathways and clinical implications
Summary
Tiny plastic particles from water, food, and even toothpaste may be doing more than just floating around your mouth, this review of existing research suggests they could worsen gum disease by fueling inflammation, disrupting the balance of oral bacteria, and interfering with how your body repairs bone and tissue. The evidence so far comes mostly from lab studies, not large human trials, so microplastics shouldn't be seen as a proven cause of gum disease, but they're a plausible piece of the puzzle worth watching, especially since periodontitis is linked to broader health issues like heart disease and diabetes.
Micro- and nanoplastics (MNPs) are increasingly recognized as pervasive environmental contaminants with potential relevance to oral and periodontal health. The oral cavity is continuously exposed to MNPs through water, food, air, oral-care products, and polymer-based dental materials, placing periodontal tissues at a plausible interface between environmental exposure and chronic inflammation. Emerging evidence suggests that MNPs can aggravate biologic processes central to periodontitis, including oxidative stress, mitochondrial dysfunction, inflammatory signaling, epithelial barrier disruption, dysbiosis, inflammasome activation, and imbalanced bone remodeling. MNPs may also act as colonization surfaces for biofilm development, alter microbial selection pressures, and contribute to antibiotic resistance gene enrichment, although direct evidence for an oral plastisphere remains limited. Epigenetic changes, including altered DNA methylation, histone marks, and microRNA profiles, provide an additional mechanism by which MNP exposure may sustain inflammatory priming. Current evidence remains predominantly preclinical, and contamination-controlled studies directly quantifying oral MNP burden in relation to periodontal phenotype are still lacking. This review summarizes current evidence on oral exposure pathways, mechanistic links between MNPs and periodontal breakdown, translational implications, and priorities for future research. Present data support viewing MNPs as plausible environmental modifiers of periodontitis rather than established independent causal agents.