Dental microplastics as emerging neurotoxicants: a systematic review on human data

Microplastics and compounds linked to plastic have recently emerged as potential contaminants that might affect brain function; nevertheless, results from these investigations have been inconsistent across epidemiological, clinical, and mechanistic research. Whether in people or in vitro models, this systematic review sought to compile the most recent data on the link between exposures to microplastics and neurological effects.

A comprehensive search of PubMed, Scopus, MEDLINE, EBSCO, and ScienceDirect was performed to identify studies published from January 2015 to December 2025. Eligible studies assessed the relationships between microplastics, nanoplastics, or associated chemical markers (e.g., bisphenols, phthalates) and neurological outcomes, including cognitive function, neurodegenerative biomarkers, or neuronal injury mechanisms. Two evaluators independently conducted study screening, data extraction, and quality assessment utilizing the Newcastle-Ottawa Scale for human studies and the ToxRTool for in-vitro studies.

Out of 477 records, 18 research fulfilled the inclusion criteria: nine human observational studies, one postmortem analytical study, and eight in-vitro mechanistic investigations. Human investigations indicated correlations between elevated internal exposure to microplastics or plastic-associated compounds and altered cognitive function or neurodegenerative biomarkers; yet, all were cross-sectional and failed to demonstrate causality. The postmortem study revealed microplastics buildup in brain tissue, but in vitro investigations elucidated molecular mechanisms including oxidative stress, mitochondrial malfunction, autophagy disruption, and protein aggregation that may contribute to neurotoxic consequences. Because of heterogeneity, results were synthesized within exposure and outcome specific subgroups instead of being merged.

Current evidence indicates possible neurological effects of microplastics-related exposures, corroborated by similar molecular pathways in in-vitro research and connections identified in human cross-sectional data. Nevertheless, the primarily observational and experimental characteristics of existing studies hinder definitive conclusions about clinical causation. Additional longitudinal, standardized human investigations are required to elucidate dose-response relationships and the applicability of in-vitro findings to real-world exposure.