IntroductionThe worldwide prevalence of periodontitis is considerably high, and its pathogenic mechanisms must be investigated and understood in order to improve clinical treatment outcomes and reduce the disease prevalence and burden. The exacerbation of the host immune system induced by oral microbial dysbiosis and the subsequent tissue destruction are the hallmarks of the periodontitis. However, the oral bacteria involved in periodontitis are not fully understood. We used the Oxford Nanopore Technologies (ONT) sequencing system to analyze metagenomic information in subgingival dental plaque from periodontitis and non‐periodontitis patients. The number of Lactobacillus zeae (L. zeae) in the periodontitis patients was 17.55‐fold higher than in the non‐periodontitis patients, suggesting that L. zeae is a novel periodontitis‐associated pathogen. Although several Lactobacillus species are used in vivo as probiotics to treat periodontitis and compete with Porphyromonas gingivalis (P. gingivalis), the roles of L. zeae in periodontitis progression, and the relationship between L. zeae and P. gingivalis needs to be investigated.MethodsBoth L. zeae and P. gingivalis were inoculated in the ligature‐implant site of periodontitis mice. We collected mouse gingival crevicular fluid to analyze inflammatory cytokine secretion using a multiplex assay. Intact or sliced mouse maxilla tissue was used for micro‐computed tomography analysis or hematoxylin and eosin staining, immunohistochemistry, and tartrate‐resistant acid phosphatase staining to evaluate alveolar bone loss, neutrophil infiltration, and osteoclast activation, respectively.ResultsWe observed that L. zeae competed with P. gingivalis, and it increased inflammatory cytokine secretion at the ligature‐implant site. Similar to P. gingivalis, L. zeae promoted ligature‐induced neutrophile infiltration, osteoclast activation, and alveolar bone loss.DiscussionWe, therefore, concluded that L. zeae accelerated the progression of periodontitis in the ligature‐induced periodontitis mouse model.

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口腔玉米乳杆菌加剧小鼠模型牙周炎的病理表现

简介世界范围内牙周炎的患病率相当高，必须调查和了解其致病机制，以改善临床治疗结果并减少疾病患病率和负担。口腔微生物失调引起的宿主免疫系统恶化以及随后的组织破坏是牙周炎的标志。然而，与牙周炎有关的口腔细菌尚不完全清楚。我们使用牛津纳米孔技术（ONT）测序系统来分析牙周炎和非牙周炎患者龈下牙菌斑的宏基因组信息。牙周炎患者体内玉米乳杆菌（L. zeae）的数量是非牙周炎患者的17.55倍，表明玉米乳杆菌是一种新型的牙周炎相关病原体。尽管有几种乳杆菌在体内用作益生菌来治疗牙周炎并与牙龈卟啉单胞菌（P.gingivalis）竞争，但玉米乳杆菌在牙周炎进展中的作用以及玉米乳杆菌和牙龈卟啉单胞菌之间的关系仍需要研究。方法将玉米乳杆菌和牙龈卟啉单胞菌接种于牙周炎小鼠的结扎种植体部位。我们收集了小鼠龈沟液，使用多重测定分析炎症细胞因子的分泌。使用完整或切片的小鼠上颌骨组织进行显微计算机断层扫描分析或苏木精和伊红染色、免疫组织化学和抗酒石酸酸性磷酸酶染色，分别评估牙槽骨丢失、中性粒细胞浸润和破骨细胞活化。与牙龈卟啉单胞菌竞争，它增加结扎种植部位炎症细胞因子的分泌。与牙龈卟啉单胞菌类似，玉米乳杆菌促进结扎诱导的中性粒细胞浸润、破骨细胞活化和牙槽骨丢失。因此，我们得出结论，玉米乳杆菌加速了结扎诱导的牙周炎小鼠模型中牙周炎的进展。