Periodontitis has been linked to an increased risk of various chronic non-communicable diseases, including gastrointestinal cancers. Indeed, dysbiosis of the oral microbiome and immune-inflammatory pathways related to periodontitis may impact the pathophysiology of the gastrointestinal tract and its accessory organs through the so-called “gum–gut axis”. In addition to the hematogenous spread of periodontal pathogens and inflammatory cytokines, recent research suggests that oral pathobionts may translocate to the gastrointestinal tract through saliva, possibly impacting neoplastic processes in the gastrointestinal, liver, and pancreatic systems. The exact mechanisms by which oral pathogens contribute to the development of digestive tract cancers are not fully understood but may involve dysbiosis of the gut microbiome, chronic inflammation, and immune modulation/evasion, mainly through the interaction with T-helper and monocytic cells. Specifically, keystone periodontal pathogens, includingPorphyromonas gingivalisandFusobacterium nucleatum, are known to interact with the molecular hallmarks of gastrointestinal cancers, inducing genomic mutations, and promote a permissive immune microenvironment by impairing anti-tumor checkpoints. The evidence gathered here suggests a possible role of periodontitis and oral dysbiosis in the carcinogenesis of the enteral tract. The “gum–gut axis” may therefore represent a promising target for the development of strategies for the prevention and treatment of gastrointestinal cancers.
牙周炎与多种慢性非传染性疾病风险增加相关，包括胃肠道癌症。事实上，口腔微生物群失调及牙周炎相关的免疫炎症通路可能通过所谓的"牙龈-肠道轴"影响胃肠道及其附属器官的病理生理过程。除牙周病原体和炎症细胞因子的血行播散外，最新研究表明口腔致病共生菌可能通过唾液易位至胃肠道，进而影响胃肠道、肝脏和胰腺系统的肿瘤进程。口腔病原体促进消化道癌症发展的具体机制尚未完全阐明，但可能涉及肠道微生物群失调、慢性炎症及免疫调节/逃逸，主要通过辅助性T细胞和单核细胞的相互作用实现。特别是包括牙龈卟啉单胞菌和具核梭杆菌在内的关键牙周病原体，已知能与胃肠道癌症的分子特征相互作用，诱导基因组突变，并通过破坏抗肿瘤检查点促进免疫许可微环境的形成。本文收集的证据表明牙周炎和口腔菌群失调可能在肠道癌变过程中发挥作用。因此，"牙龈-肠道轴"有望成为胃肠道癌症防治策略开发的重要靶点。
The Gum–Gut Axis: Periodontitis and the Risk of Gastrointestinal Cancers
肿瘤(癌症)患者之家