Topical application of lipopolysaccharide into gingival sulcus promotes periodontal destruction in rats immunized with lipopolysaccharide
Topical application of lipopolysaccharide into gingival sulcus promotes periodontal destruction in rats immunized with lipopolysaccharide
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DOI：
10.1111/j.1600-0765.2012.01486.x
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发表时间：
2012-10-01
影响因子：
3.5
通讯作者：
Hara, Y.
中科院分区：
文献类型：
--
作者：
Yoshinaga, Y.;Ukai, T.;Hara, Y.
Yoshinaga Y，Ukai T，Kaneko T，Nakatsu S，Shiraishi C，Kuramoto A，Oshino K，Ichimura I，Hara Y。将脂多糖局部应用于牙龈沟可促进脂多糖免疫大鼠的牙周破坏。牙周病研究杂志，2012； 47: 674680. (C) 2012 John Wiley & Sons A/S 背景和目的：牙周炎的病因是细菌和宿主免疫系统，但免疫系统在牙周病发生和进展中的作用仍不清楚。我们之前的报告表明，龈沟中免疫复合物的形成会引起牙周破坏。这项研究的目的是调查免疫系统，特别是免疫系统，如何参与牙周破坏。材料与方法：以脂多糖（LPS）腹腔注射免疫的动物作为免疫组。未免疫组仅接受磷酸盐缓冲盐水。加强注射后1天，每天将LPS涂抹到两组的腭龈沟处。测定抗LPS IgG的血清水平。通过组织病理学和组织计量学研究附着丧失和牙槽骨水平。对携带 RANKL 的细胞和 C1qB 的表达进行免疫组织学评估。结果：免疫组实验早期血清抗LPS IgG水平升高。免疫组中附着丧失、牙槽骨水平和携带 RANKL 的细胞数量显着增加。在交界上皮和邻近结缔组织中观察到 C1qB。当抗LPS IgG血清水平升高时和之后，未免疫组显示出相似的发现。结论：当LPS免疫大鼠血清抗LPS IgG水平升高时，局部应用LPS作为抗原可诱导牙周破坏。 C1qB 的存在表明免疫复合物的形成参与了这种破坏。
Yoshinaga Y, Ukai T, Kaneko T, Nakatsu S, Shiraishi C, Kuramoto A, Oshino K, Ichimura I, Hara Y. Topical application of lipopolysaccharide into gingival sulcus promotes periodontal destruction in rats immunized with lipopolysaccharide. J Periodont Res 2012; 47: 674680. (C) 2012 John Wiley & Sons A/S Background and Objective: The causes of periodontitis are bacteria and the host immune system, but the role of the immune system in the onset and progression of periodontal disease is still unclear. Our previous report showed that the formation of an immune complex in the gingival sulcus induces periodontal destruction. This study was carried out to investigate how the immune system, particularly immunization, is involved in periodontal destruction. Material and Methods: Animals immunized intraperitoneally with lipopolysaccharide (LPS) were used as the immunized group. The nonimmunized group received only phosphate-buffered saline. LPS was applied daily onto the palatal gingival sulcus in both groups 1 d after the booster injection. Serum levels of anti-LPS IgG were determined. Loss of attachment and the level of alveolar bone were histopathologically and histometrically investigated. RANKL-bearing cells and the expression of C1qB were immunohistologically evaluated. Results: The serum levels of anti-LPS IgG were elevated in the early experimental period in the immunized group. There were significant increases in loss of attachment, level of alveolar bone and the number of RANKL-bearing cells in the immunized group. C1qB was observed in the junctional epithelium and adjacent connective tissue. The nonimmunized group showed similar findings at and after the time when the serum level of anti-LPS IgG was elevated. Conclusion: Topical application of LPS as an antigen induced periodontal destruction when the serum level of anti-LPS IgG was elevated in rats immunized with LPS. The presence of C1qB suggests that the formation of immune complexes is involved in this destruction.