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Polyethylene: an identified component of human dental calculus triggers cytotoxicity and inflammatory responses in gingival fibroblasts

Environment International 2025 1 citation ? Citation count from OpenAlex, updated daily. May differ slightly from the publisher's own count.
Zhanhong Wu, Yingjie Yi, Bing Yang, Xing Cui, Fa‐Ming Chen, Guofeng Wu

Summary

Researchers identified 26 types of microplastics in human dental calculus, with polyamide, polyethylene, and polyurethane as the most prevalent. Laboratory experiments showed that polyethylene micro- and nanoplastics reduced gingival cell viability, increased cell death, impaired cell migration, and activated inflammatory signaling pathways in a dose-dependent manner. The study suggests that microplastics accumulate in the oral cavity over time and may drive chronic inflammation in gum tissue.

Study Type In vitro

The oral cavity, the gateway to the digestive system, represents a critical entrance for micro- and nanoplastics (MNPs) to enter the human body. Few studies have assessed the long-term accumulation of MNPs in the oral cavity and their potential harm to resident cells. This study investigated the presence of MNPs in human dental calculus and evaluated the cytotoxic and inflammatory effects of polyethylene (PE) on human gingival fibroblasts (HGFs). Twenty-six types of microplastics were identified in human dental calculus, with polyamide (PA, 41.4 %), PE (32.7 %), and polyurethane (PU, 7 %) emerging as the predominant components. In vitro experiments revealed that PE-MNPs significantly reduced HGFs' viability, increased apoptosis rates, and impaired cell migration in a dose-dependent manner. Furthermore, PE-MNPs exposure activated the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway and upregulated mRNA expression of pro-inflammatory cytokines (interleukin [IL]-1β and IL-6), as evidenced by elevated phosphorylation of NF-κB. This study revealed that MNPs persistently accumulate in the oral cavity, potentially driving chronic inflammatory activation in gingival fibroblasts and compromising tissue repair mechanisms.

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