From mouth to brain: Linking periodontal and peri-implant dysbiosis to systemic inflammation and neuropathology.

BACKGROUND/AIM: Growing evidence suggests that imbalances occurring within the human microbiota and deregulation of the host immune response may play a significant role in the development of neurodegenerative diseases. MATERIALS AND METHODS: A comprehensive narrative review of the latest experimental, clinical, and epidemiological insights was conducted to explore the associations among oral dysbiosis, including periodontitis and peri-implantitis, a low-grade inflammatory phenotype, and biological pathways that may contribute to the onset of neuroinflammation and neuropathologies. RESULTS: Periodontitis is a chronic inflammatory non-communicable disease driven by subgingival dysbiosis, increasingly linked not only to progressive bone and tooth loss but also to a broad range of systemic chronic non-communicable diseases. Indeed, the persistent burden of deregulated chronic inflammation not only exacerbates periodontal tissue destruction but also promotes a low-grade inflammatory phenotype that may predispose patients to a spectrum of degenerative diseases, such as neurodegenerative disorders. In contrast, evidence regarding peri-implantitis remains comparatively limited and indirect, although emerging data indicate potential systemic inflammatory and cognitive implications. CONCLUSION: Elucidating the intricate interactions between oral dysbiosis, periodontal diseases, chronic inflammation, and neurodegeneration is essential for understanding oral health's systemic implications for neurodegenerative and age-related diseases. Current evidence supports an association between oral dysbiosis, chronic oral inflammation, and pathways relevant to neurodegeneration, particularly for periodontitis. However, important knowledge gaps remain, especially concerning peri-implant diseases, where human data are limited. CLINICAL RELEVANCE: Effective management strategies targeting periodontal and peri-implant dysbiosis and restoring the immune imbalance may offer novel avenues for promoting healthy aging and preventing neuropathic morbidities.