Periodontitis is a chronic inflammatory disease that destroys the supporting structures of the teeth and ultimately leads to tooth loss. Beyond local effects, it is recognized as a risk factor for systemic conditions, including diabetes, cardiovascular disease, and cognitive impairment. Systemic inflammation initiated by periodontitis may disrupt the blood–brain barrier and activate neuroinflammatory pathways, contributing to neuronal damage and cognitive decline. Although its prevalence increases with age, younger individuals are also susceptible due to poor oral hygiene, genetic predisposition, and immune dysregulation. In this study, we established a model of chronic periodontitis–associated cognitive decline in young adult mice by bilaterally ligating the maxillary molars. Periodontitis was confirmed by micro-computed tomography and histological analysis, which revealed alveolar bone loss and periodontal tissue destruction. Astrocyte activation and inflammatory gene expression in the hippocampus were examined following ligature placement, and cognitive function was evaluated using behavioral tests. In addition, gene expression profiling was conducted to identify molecular alterations related to cognitive dysfunction in the prefrontal cortex and hippocampus. This model provides the first evidence that chronic periodontitis can impair cognitive function in young adult mice, indicating that the impact of the disease extends beyond older populations. It also provides a practical platform to explore mechanistic links between periodontal inflammation and neurocognitive outcomes, offering insights for developing targeted therapeutic strategies.