Periodontal Disease, Chronic Silent Inflammation, and Micro/Nanoplastics: An Environmental Microbiology Review of Oral Biofilm Retention, Dysbiosis, and Systemic Risk Pathways

Micro- and nanoplastics (MNPs) have now been detected in human blood, placenta, and arterial tissue, yet the oral cavity, which serves as the primary portal of environmental exposure, has received strikingly little mechanistic attention. This narrative review addresses that gap from an environmental microbiology perspective, synthesizing recent literature on periodontal disease, chronic low-grade inflammation, oral biofilms, dental materials, microbial–plastic interactions, and systemic chronic disease risk. Unlike prior reviews, we apply an explicit evidentiary framework that distinguishes what is directly demonstrated from what is biologically plausible but unproven, and we situate the periodontal environment specifically as a particle-retention and inflammatory-amplification niche. The strongest direct oral evidence shows that human dental calculus harbors at least 26 microplastic types, dominated by polyamide (41.4%), polyethylene (32.7%), and polyurethane (7.0%). Polyethylene isolated from calculus induces cytotoxicity, apoptosis, impaired migration, NF-κB activation, and upregulation of IL-1β and IL-6 in human gingival fibroblasts. The oral cavity is also a portal for environmental exposure and a local site of plastic generation: MNPs are released from chewing gum, oral care products, orthodontic appliances, and resin-based dental materials, while oral microorganisms have been documented to degrade methacrylate polymers. Across experimental systems, MNPs activate oxidative stress, inflammasome signaling, macrophage polarization, and barrier dysfunction — pathways that overlap extensively with the pathobiology of periodontitis. Environmental biofilm studies further indicate that plastic substrates can enhance extracellular polymeric substance production, quorum sensing, antibiotic resistance gene transfer, and pathogen persistence, suggesting a plausible but not yet proven oral plastisphere within plaque and calculus. We argue that periodontitis should be reconceptualized as a chronically inflamed particle-processing interface that may increase local MNP retention, cellular reactivity, and systemic inflammatory spillover, with implications for cardiovascular, metabolic, and other chronic disease risk pathways. Current evidence does not yet prove that environmental MNP exposure causes human periodontitis, and that evidentiary boundary is maintained throughout. A priority research agenda is proposed, centered on contamination-controlled subgingival biomonitoring stratified by periodontal status, spatially resolved multi-species biofilm models, polymer source attribution, and longitudinal clinical studies linking oral plastic burden to inflammatory and systemic outcomes.