牙周炎是一种常见的炎症性口腔疾病，与结肠癌风险增加有关。实验动物模型是研究牙周炎对结肠癌影响和机制的重要工具。数种小鼠牙周炎模型已经在研究中被使用，包括口服、牙周病原体注射和外科缚带模型。丝线结扎所致实验性牙周炎对结肠癌的作用尚不清楚。本研究分别在溃疡性结肠炎相关结肠癌模型和自发模型上使用实验性牙周炎模型。我们观察到在需要系固结扎诱导牙周炎小鼠组中的结肠癌促进，相比于对照组的2个模型，评估肿瘤数量、肿瘤大小和肿瘤负荷。由于细菌失调是 牙周炎的一个重要特征，我们接下来使用16S核糖体RNA基因测序分析口腔和肠道微生物组。我们发现实验性牙周炎模型重塑了口腔和肠道微生物群落。此外，我们发现在牙周炎组的肿瘤样本中，程序化死亡1（PD-1）阳性CD8+T细胞浸润程度比对照组高，通过免疫荧光染色。关于潜在的分子机制，我们将牙周炎患者的粪便微生物移植到小鼠体内，并观察到在牙周炎组中促进肿瘤的效果，通过肿瘤体积和肿瘤重量进行评估，同时也观察到皮下肿瘤小鼠中INF-γ+ CD8+ T细胞浸润水平较低。综上所述，我们展示了牙周炎模型通过微生物群落重塑和免疫反应抑制来促进结肠癌。

Periodontitis is a prevalent inflammatory oral disease associated with an increased risk of colorectal cancer. Experimental animal models are critical tools to investigate the effects and mechanisms of periodontitis on colorectal cancer. Several murine periodontitis models have been used in research, including oral gavage, periodontal pathogen injection, and ligature models. The role of experimental periodontitis caused by silk ligation in colorectal cancer remains unclear. In this study, we used an experimental periodontitis model on a colitis-associated colorectal cancer model and a spontaneous model, respectively. We observed the promotion of colorectal cancer in ligature-induced periodontitis mice compared to those control mice in 2 different models, as assessed by tumor number, tumor size, and tumor load. Since bacterial dysbiosis is an important feature of periodontitis, we next analyzed the oral and gut microbiomes using 16S ribosomal RNA gene sequencing. We found that the experimental periodontitis model reshaped the microbial community in the oral cavity and gut. In addition, we found a higher extent of programmed death 1 (PD-1)-positive CD8+ T-cell infiltration in tumor samples of the periodontitis group than in controls by immunofluorescence staining. Regarding the potential molecular mechanism, we transplanted the fecal microbiota of the periodontitis patient into mice and observed a tumor-promoting effect in the periodontitis group, assessed by tumor volume and tumor weight, together with a low level of INF-γ+ CD8+ T-cell infiltration in subcutaneous tumor mice. Taken together, we show that ligature-induced periodontitis model promotes colorectal cancer by microbiota remodeling and suppression of the immune response.