PM2.5 exposure induces oral tissue alterations and exacerbates experimental periodontitis via oxidative stress and mast cell activation

Abstract Exposure to fine particulate matter (PM2.5) is a well-established environmental risk factor associated with systemic inflammatory and oxidative effects. However, its impact on oral tissues and periodontal homeostasis remains incompletely understood. This study investigated the effects of PM2.5 exposure on oral tissues under physiological and experimentally induced inflammatory conditions. Male mice were exposed to PM2.5, with or without concurrent inflammatory stimulation, and periodontal and lingual tissues were analyzed for histopathological and inflammatory alterations. PM2.5 exposure was associated with increased inflammatory cell infiltration and tissue structural changes, particularly under inflammatory conditions, indicating an exacerbation of pre-existing tissue injury. These effects are consistent with a model in which PM2.5 acts as a disease-modifying environmental factor rather than a primary etiological agent. The observed tissue alterations may be driven by a combination of local epithelial stress responses and systemic inflammatory and oxidative mediators derived from pulmonary exposure. Although specific intracellular signaling pathways were not directly assessed, the findings are consistent with previously described mechanisms involving redox imbalance and innate immune activation in response to particulate matter exposure. Importantly, PM2.5 exposure enhanced the inflammatory profile of oral tissues, suggesting increased susceptibility to environmental and inflammatory stressors. Mast cell activity and cytokine changes likely reflect participation in a broader inflammatory microenvironment rather than isolated mechanistic drivers. In conclusion, PM2.5 exposure contributes to oral tissue inflammation and structural alterations, particularly under pre-existing inflammatory conditions. These findings support the relevance of environmental air pollution as a modifying factor in oral and periodontal disease pathogenesis and reinforce the importance of considering systemic environmental exposures in oral health research.