Department of Periodontology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.
J Periodontal Res. 2017 Feb;52(1):74-82. doi: 10.1111/jre.12370. Epub 2016 Mar 9.
The barrier function of long junctional epithelium is thought to be important after periodontal initial therapy and periodontal surgery. Although the difference between long junctional epithelium and normal junctional epithelium regarding their resistance to destruction of periodontal tissue has been investigated, the mechanism still remains unclear. Using our rat experimental periodontitis model in which loss of attachment and resorption of alveolar bone is induced by the formation of immune complexes, we investigated the resistance of periodontal tissue containing long junctional epithelium and normal junctional epithelium to destruction.
Rats were divided into four groups. In the immunized long junctional epithelium (I-LJE) group, rats were immunized with lipopolysaccharide (LPS), and curettage and root planing procedures were performed on the palatal gingiva of the maxillary first molars to obtain reattachment by long junctional epithelium. In the immunized normal junctional epithelium (I-JE) group, rats were immunized without curettage and root planing procedures. In the nonimmunized long junctional epithelium (nI-LJE) group, rats were not immunized but curettage and root-planing procedures were performed. In the control group, neither immunization nor curettage and root-planing was performed. In all rats, periodontal inflammation was induced by topical application of LPS into the palatal gingival sulcus of maxillary first molars. The rats were killed at baseline and after the third and fifth applications of LPS. Attachment loss and the number of inflammatory cells and osteoclasts in the four groups were compared histopathologically and histometrically.
After the third application of LPS in the I-LJE group, attachment loss showed a greater increase than in control and nI-LJE groups, and inflammatory cell infiltration and osteoclasts were increased more than in the other groups. After the fifth application of LPS, attachment loss was greater and there was a higher degree of inflammatory cell infiltration in nI-LJE and I-LJE groups than in control and I-JE groups.
Our findings suggest that the destruction of periodontal tissue is increased in tissue containing long junctional epithelium compared with normal junctional epithelium and that the immunized condition accelerates the destruction by forming immune complexes.
长结合上皮的屏障功能被认为在牙周初始治疗和牙周手术后很重要。尽管已经研究了长结合上皮与正常结合上皮在抵抗牙周组织破坏方面的差异，但机制仍不清楚。使用我们的大鼠实验性牙周炎模型，该模型通过形成免疫复合物诱导附着丧失和牙槽骨吸收，我们研究了含有长结合上皮和正常结合上皮的牙周组织对破坏的抵抗力。
大鼠分为四组。在免疫长结合上皮（I-LJE）组中，大鼠用脂多糖（LPS）免疫，并对上颌第一磨牙的腭侧牙龈进行刮治和根面平整以通过长结合上皮获得再附着。在免疫正常结合上皮（I-JE）组中，大鼠未经刮治和根面平整而免疫。在非免疫长结合上皮（nI-LJE）组中，大鼠未免疫但进行了刮治和根面平整。在对照组中，既不免疫也不进行刮治和根面平整。在所有大鼠中，通过将 LPS 局部应用于上颌第一磨牙的腭侧龈沟来诱导牙周炎症。在基线和 LPS 第三次和第五次应用后处死大鼠。在四个组中比较组织病理学和组织学附着丧失以及炎症细胞和破骨细胞的数量。
在 I-LJE 组第三次应用 LPS 后，与对照组和 nI-LJE 组相比，附着丧失增加更大，炎症细胞浸润和破骨细胞增加更多。在第五次应用 LPS 后，nI-LJE 和 I-LJE 组的附着丧失更大，炎症细胞浸润程度更高。
我们的发现表明，与正常结合上皮相比，含有长结合上皮的组织中牙周组织的破坏增加，并且形成免疫复合物会加速免疫状态下的破坏。
