Hong Qing, Ren Yu, Tang Xin, Mao Bingyong, Zhang Qiuxiang, Zhao Jianxin, Cui Shumao, Liu Zhenmin
State Key Laboratory of Dairy Biotechnology, Shanghai Engineering Research Center of Dairy Biotechnology, Dairy Research Institute, Bright Dairy & Food Co., Ltd., Shanghai 200436, China.
State Key Laboratory of Food Science and resources, Jiangnan University, Wuxi 214122, China.
Microorganisms. 2025 Jul 20;13(7):1701. doi: 10.3390/microorganisms13071701.
Periodontitis is a chronic inflammatory disease caused by periodontopathic bacteria such as (), which leads to alveolar bone destruction and systemic inflammation. Emerging evidence suggests that probiotics may mitigate periodontal pathology. To systematically evaluate the alleviative effects and mechanisms of different forms of probiotics, including live bacteria and postbiotics, on periodontitis, we first screened and identified CCFM1332 ( CCFM1332) through in vitro antibacterial and anti-biofilm activity assays. Subsequently, we investigated its therapeutic potential in a rat model of experimental periodontitis. The results demonstrated that both live CCFM1332 (PL) and its postbiotics (PP) significantly reduced the gingival index (GI) and probing depth (PD) in rats, while suppressing oral colonization of . Serum pro-inflammatory cytokine levels were differentially modulated: the PL group exhibited reductions in interleukin-17A (IL-17A), interleukin-6 (IL-6), and interleukin-1β (IL-1β) by 39.31% ( < 0.01), 17.26% ( < 0.05), and 14.74% ( < 0.05), respectively, whereas the PP group showed decreases of 34.79% ( < 0.05), 29.85% ( < 0.01), and 19.74% ( < 0.05). Micro-computed tomography (Micro-CT) analysis demonstrated that compared to the periodontitis model group (PM), the PL group significantly reduced alveolar bone loss (ABL) by 30.1% ( < 0.05) and increased bone volume fraction (BV/TV) by 49.5% ( < 0.01). In contrast, while the PP group similarly decreased ABL by 32.7% ( < 0.05), it resulted in a 40.4% improvement in BV/TV ( > 0.05). Histological assessments via hematoxylin and eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining confirmed that both the PL group and the PP group alleviated structural damage to alveolar bone-supporting tissues and reduced osteoclast-positive cell counts. This study suggests that live CCFM1332 and its postbiotics reduce alveolar bone resorption and attachment loss in rats through antibacterial and anti-inflammatory pathways, thereby alleviating periodontal inflammation in rats.
牙周炎是一种由诸如()等牙周病原菌引起的慢性炎症性疾病,会导致牙槽骨破坏和全身炎症。新出现的证据表明,益生菌可能减轻牙周病变。为了系统评估不同形式的益生菌,包括活菌和后生元,对牙周炎的缓解作用及机制,我们首先通过体外抗菌和抗生物膜活性试验筛选并鉴定了CCFM1332(CCFM1332)。随后,我们在实验性牙周炎大鼠模型中研究了其治疗潜力。结果表明,活菌CCFM1332(PL)及其后生元(PP)均显著降低了大鼠的牙龈指数(GI)和探诊深度(PD),同时抑制了(此处原文缺失相关细菌名称)的口腔定植。血清促炎细胞因子水平受到不同程度的调节:PL组中白细胞介素-17A(IL-17A)、白细胞介素-6(IL-6)和白细胞介素-1β(IL-1β)分别降低了39.31%(<0.01)、17.26%(<0.05)和14.74%(<0.05),而PP组则分别降低了34.79%(<0.05)、29.85%(<0.01)和19.74%(<0.05)。显微计算机断层扫描(Micro-CT)分析表明,与牙周炎模型组(PM)相比,PL组显著减少了牙槽骨吸收(ABL)30.1%(<0.05),并使骨体积分数(BV/TV)增加了49.5%(<0.01)。相比之下,虽然PP组同样使ABL降低了32.7%(<0.05),但其使BV/TV提高了40.4%(>0.05)。通过苏木精和伊红(H&E)染色以及抗酒石酸酸性磷酸酶(TRAP)染色进行的组织学评估证实,PL组和PP组均减轻了牙槽骨支持组织的结构损伤,并减少了破骨细胞阳性细胞计数。本研究表明,活菌CCFM1332及其后生元通过抗菌和抗炎途径减少大鼠牙槽骨吸收和附着丧失,从而减轻大鼠牙周炎症。