Yu Jinping, Lyu Jinglu, Zhu Tongxin, Li Yang, Xia Hanping, Liu Qing, Li Lili, Chen Bin
Department of Periodontology, Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University, Nanjing, China.
BMC Oral Health. 2025 Jun 3;25(1):894. doi: 10.1186/s12903-025-06269-8.
Periodontitis is a chronic inflammatory disease, having significant impact on systemic conditions. Ulcerative colitis (UC) is a chronic relapsing inflammatory disorder of the intestines. Studies have suggested a potential association between periodontitis and UC. This study aims to elucidate the influence of periodontitis on the progression of UC and to uncover the potential mechanistic pathways involved.
A total of 20 male C57BL/6J mice were randomly assigned to four groups: Sham, Periodontitis (P), UC, and Periodontitis + UC (P-UC). A chronic UC model was induced by alternating oral administration of 1% and 0.5% Dextran Sulfate Sodium Salt (DSS) solution, while periodontitis was induced by ligatures. Disease severity was accessed using Disease Activity Index (DAI), histopathology, and intestinal permeability assays. Gut microbiota and periodontal microbiota was analyzed using 16S rRNA sequencing. Tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) were measured by quantitative PCR (qPCR) to evaluate the systemic inflammation burden. Zonula occludens-1 (ZO-1) and occludin in intestinal tissues were assessed using qPCR and immunohistochemistry. Correlation analyses were performed between periodontal destruction indices and markers.
A chronic UC model closely resembling clinical conditions was successfully established. The P-UC group exhibited earlier and more pronounced body weight loss than the UC group. Colonic inflammation was exacerbated, with significantly elevated TNF-α and IL-6 expression (P < 0.05). In the P-UC group, intestinal barrier disruption was evident with reduced occludin protein levels (P < 0.01) and increased intestinal permeability (P < 0.05), indicated by serum diamine oxidase (DAO). Both the P-UC and UC groups exhibited notable dysbiosis of the gut microbiota, with the P-UC group showing significantly higher abundance of UC-associated bacteria, such as Muribaculum and Allobaculum (P < 0.05), compared to the UC group. A trend toward reduced abundance of the gut-protective bacterium Akkermansia was also observed (P = 0.06). Pearson correlation analysis confirmed the association between periodontitis and intestinal inflammation, suggesting that intestinal barrier dysfunction and gut microbiota dysbiosis may be key mediators in periodontitis-induced UC exacerbation.
Periodontitis may exacerbate UC by increasing harmful gut bacteria, reducing beneficial bacteria, and promoting the secretion of pro-inflammatory cytokines, thereby disrupting the intestinal barrier and worsening UC severity.
牙周炎是一种慢性炎症性疾病，对全身状况有重大影响。溃疡性结肠炎（UC）是一种肠道慢性复发性炎症性疾病。研究表明牙周炎与UC之间可能存在关联。本研究旨在阐明牙周炎对UC进展的影响，并揭示其中潜在的机制途径。
将20只雄性C57BL/6J小鼠随机分为四组：假手术组、牙周炎组（P）、UC组和牙周炎+UC组（P-UC）。通过交替口服1%和0.5%的葡聚糖硫酸钠（DSS）溶液诱导慢性UC模型，通过结扎诱导牙周炎。使用疾病活动指数（DAI）、组织病理学和肠道通透性测定评估疾病严重程度。使用16S rRNA测序分析肠道微生物群和牙周微生物群。通过定量PCR（qPCR）测量肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）以评估全身炎症负担。使用qPCR和免疫组织化学评估肠道组织中的紧密连接蛋白-1（ZO-1）和闭合蛋白。对牙周破坏指数与标志物之间进行相关性分析。
成功建立了与临床情况相似的慢性UC模型。P-UC组比UC组表现出更早、更明显的体重减轻。结肠炎症加剧，TNF-α和IL-6表达显著升高（P<0.05）。在P-UC组中，肠道屏障破坏明显，闭合蛋白水平降低（P<0.01），肠道通透性增加（P<0.05），血清二胺氧化酶（DAO）表明了这一点。P-UC组和UC组均表现出明显的肠道微生物群失调，与UC组相比，P-UC组中与UC相关的细菌，如穆里杆菌属和别杆菌属的丰度显著更高（P<0.05）。还观察到肠道保护菌阿克曼氏菌丰度有降低的趋势（P=0.06）。Pearson相关性分析证实了牙周炎与肠道炎症之间的关联，表明肠道屏障功能障碍和肠道微生物群失调可能是牙周炎诱导UC加重的关键介质。
牙周炎可能通过增加有害肠道细菌、减少有益细菌以及促进促炎细胞因子的分泌来加重UC，从而破坏肠道屏障并恶化UC严重程度。
