Periodontal Biology Laboratory, Faculty of Dentistry, Universidad de Chile, Chile.
Translational Allergy and Immunology Laboratory, Faculty of Medicine, Pontificia Universidad Católica de Chile, Chile.
J Periodontol. 2019 May;90(5):522-534. doi: 10.1002/JPER.18-0079. Epub 2018 Dec 20.
Encapsulation of Porphyromonas gingivalis has been demonstrated as responsible of several host immunological changes, which have been associated with the pathogenesis of periodontitis. Using a murine model of periodontitis and two isogenic non-capsulated mutants of P. gingivalis, this study aimed to analyze whether P. gingivalis encapsulation induces more severe alveolar bone resorption, and whether this bone loss is associated with a T-helper (Th)1 and Th17-pattern of immune response.
Experimental periodontal infections were generated by oral inoculation with the encapsulated W50 wild-type strain or isogenic non-encapsulated ΔPG0116-PG0120 (GPA) and ΔPG0109-PG0118 (GPC) mutants of P. gingivalis. Periodontal infections induced with the encapsulated HG184 or non-encapsulated ATCC 33277 strains of P. gingivalis were used as controls. Alveolar bone resorption was analyzed using microcomputed tomography and scanning electron microscopy. The expression levels of Th1, Th2, Th17, or T regulatory-associated cytokines and RANKL, as well as the periodontal bacterial load, were quantified by quantitative polymerase chain reaction. The detection of Th1 and Th17 lymphocytes was analyzed by flow cytometry.
In the periodontal lesions, both capsular-defective knockout mutant strains of P. gingivalis induced less alveolar bone resorption than the encapsulated W50 wild-type strain. This decreased bone loss was associated with a dismissed RANKL expression, decreased Th1- and Th17-type of cytokine expression, reduced Th1 and Th17 lymphocyte detection, and low osteoclast finding.
These data demonstrate that encapsulation of P. gingivalis plays a key role in the alveolar bone resorption induced during periodontitis, and this bone loss is associated with a Th1- and Th17-pattern of immune response triggered in the periodontal lesions.
有研究表明,牙龈卟啉单胞菌(Porphyromonas gingivalis)的囊膜包裹作用与牙周炎的发病机制有关,可导致宿主发生多种免疫变化。本研究使用牙周炎的小鼠模型和牙龈卟啉单胞菌的两个遗传上相同的非囊膜突变株,旨在分析 P. gingivalis 的囊膜包裹是否会导致更严重的牙槽骨吸收,以及这种骨丢失是否与 Th1 和 Th17 免疫反应模式相关。
通过口腔接种包裹的 W50 野生型菌株或遗传上相同的非包裹的 ΔPG0116-PG0120(GPA)和 ΔPG0109-PG0118(GPC)牙龈卟啉单胞菌突变株,建立实验性牙周感染。使用包裹的 HG184 或非包裹的 P. gingivalis ATCC 33277 菌株诱导的牙周感染作为对照。通过微计算机断层扫描和扫描电子显微镜分析牙槽骨吸收情况。通过定量聚合酶链反应定量分析 Th1、Th2、Th17 或 T 调节相关细胞因子和 RANKL 的表达水平,以及牙周细菌负荷。通过流式细胞术分析 Th1 和 Th17 淋巴细胞的检测。
在牙周病变中,两种缺乏囊膜包裹的牙龈卟啉单胞菌突变株引起的牙槽骨吸收均少于包裹的 W50 野生型菌株。这种骨丢失减少与 RANKL 表达下降、Th1 和 Th17 型细胞因子表达减少、Th1 和 Th17 淋巴细胞检测减少以及破骨细胞减少有关。
这些数据表明,牙龈卟啉单胞菌的囊膜包裹在牙周炎引起的牙槽骨吸收中起着关键作用,这种骨丢失与牙周病变中触发的 Th1 和 Th17 免疫反应模式有关。