From mouth to brain: Linking periodontal and peri-implant dysbiosis to systemic inflammation and neuropathology.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Authors
Cafferata Cafferata, Schwarz Schwarz, DĂaz-ZĂșñiga DĂaz-ZĂșñiga, Kantarci Kantarci
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