Wang Yuqi, Ma Jun, Wang Haoyu, Yi Jingzheng, Bai Yuxin, Hu Min, Yan Jiaqing
School and Hospital of Stomatology, Jilin University, Changchun, China.
Jilin Provincial Key Laboratory of Tooth Development and Bone Remodeling, Hospital of Stomatology, Jilin University, Changchun, China.
Front Microbiol. 2025 Jan 22;16:1531258. doi: 10.3389/fmicb.2025.1531258. eCollection 2025.
Periodontitis and inflammatory bowel disease are chronic inflammatory diseases with shared epidemiological, biological, and therapeutic associations. Given the similarities in their pathogenic factors, this study hypothesized that mesalazine, a key treatment agent for inflammatory bowel disease, could also be effective in managing periodontitis.
The antimicrobial effect of mesalazine on was investigated , including observations of morphological changes on the surface of . Additionally, the impact of mesalazine on both the formation and established plaque biofilms was examined. The antimicrobial mechanism was elucidated by assessing the expression of virulence genes and by determining the disruptive effect on cell membranes. An rat model of periodontitis was constructed to evaluate mesalazine's efficacy and its influence on the periodontal bacterial flora in the context of periodontitis.
Our results demonstrated that mesalazine concentrations ranging from 0.5 to 2 mg/mL significantly inhibited proliferation over 72 h. Flow cytometry revealed a marked reduction in the number of viable cells following mesalazine treatment. At the nanometer scale, mesalazine induced crumpling and rupture of the surface, compromising cell membrane integrity. Mesalazine not only suppressed the formation of plaque biofilms by and polymicrobial communities but also disrupted pre-existing biofilms. The data also suggested that mesalazine could disrupt the integrity of the cell membrane and inhibit the expression of virulence factors. An animal model of periodontitis in rats was successfully constructed . Mesalazine treatment inhibited alveolar bone resorption, alleviated inflammation of periodontal tissues, and improved the composition of the periodontal flora to a healthier state. This study establishes that mesalazine can treat periodontitis through modulation of the periodontal flora and its anti-inflammatory properties, thus broadening its classical therapeutic applications.
牙周炎和炎症性肠病是具有共同流行病学、生物学及治疗关联的慢性炎症性疾病。鉴于其致病因素的相似性，本研究推测，作为炎症性肠病关键治疗药物的美沙拉嗪，可能对牙周炎的治疗也有效。
研究了美沙拉嗪对[具体研究对象]的抗菌作用，包括观察[具体研究对象]表面的形态变化。此外，还检测了美沙拉嗪对菌斑生物膜形成及已形成生物膜的影响。通过评估[具体研究对象]毒力基因的表达及对[具体研究对象]细胞膜的破坏作用，阐明其抗菌机制。构建了[具体动物]大鼠牙周炎模型，以评估美沙拉嗪在牙周炎背景下的疗效及其对牙周细菌菌群的影响。
我们的结果表明，浓度范围为0.5至2毫克/毫升的美沙拉嗪在72小时内显著抑制了[具体研究对象]的增殖。流式细胞术显示，美沙拉嗪处理后活细胞数量明显减少。在纳米尺度上，美沙拉嗪导致[具体研究对象]表面起皱和破裂，损害细胞膜完整性。美沙拉嗪不仅抑制了[具体研究对象]和多微生物群落形成菌斑生物膜，还破坏了已存在的生物膜。数据还表明，美沙拉嗪可破坏[具体研究对象]细胞膜的完整性并抑制毒力因子的表达。成功构建了大鼠牙周炎动物模型。美沙拉嗪治疗抑制了牙槽骨吸收，减轻了牙周组织炎症，并将牙周菌群组成改善至更健康的状态。本研究证实，美沙拉嗪可通过调节牙周菌群及其抗炎特性来治疗牙周炎，从而拓宽了其经典治疗应用范围。
