ADHESION MOLECULE EXPRESSION IN CHRONIC INFLAMMATORY PERIODONTAL-DISEASE TISSUE
ADHESION MOLECULE EXPRESSION IN CHRONIC INFLAMMATORY PERIODONTAL-DISEASE TISSUE
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DOI：
10.1111/j.1600-0765.1994.tb01090.x
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发表时间：
1994-01-01
影响因子：
3.5
通讯作者：
SEYMOUR, GJ
中科院分区：
文献类型：
--
作者：
GEMMELL, E;WALSH, LJ;SEYMOUR, GJ
淋巴细胞群的差异已被证明在牙龈炎和牙周炎病变。粘附分子的差异表达可能在这些组织中的淋巴细胞运输中发挥作用。间接抗生物素蛋白生物素免疫过氧化物酶技术被用来染色的范围内的粘附分子在组织切片的21牙龈活检牙龈炎和牙周炎的主题。根据浸润的大小将这些标本分为三组。ICAM-1、PECAM-1和LECAM-1在炎性浸润组织中的表达随浸润范围的增大而显著增加。这些单核细胞中约50%为LFA-1+和CD 29+。当标本分组，根据其假定的疾病状态有单核细胞粘附分子表达之间没有显着差异，无论是牙龈炎或成人牙周炎的小浸润。两个临床组的较大病变也是如此。因此，牙龈炎和牙周炎组织中淋巴细胞上的粘附分子似乎没有差异表达。内皮细胞ICAM-1、PECAM-1、CD 29、GMP-140阳性，ELAM-1阴性。角质形成细胞表达的ICAM-1的增加而增加的浸润的大小，虽然在重度浸润，在该地区的交界上皮细胞，在小病灶呈阳性，成为ICAM-1阴性。在小浸润中，口腔上皮的上层为LECAM-1阳性，并且随着浸润大小的增加，下层和许多沟上皮和结合上皮角质形成细胞为阳性。下层基底上皮和角质形成细胞均为CD 29+，较大浸润区上层也为阳性。这项研究表明，如果特定的归巢不同的淋巴细胞克隆发生在牙龈炎相比，牙周炎，这是没有反映在本调查中观察到的粘附分子的表达模式。本研究可能有助于阐明炎症组织中内皮细胞和角质形成细胞在淋巴细胞运输中所起的作用。
Differences in lymphocyte populations have been demonstrated in gingivitis and periodontitis lesions. A differential expression of adhesion molecules may play a role in lymphocyte trafficking in these tissues. An indirect avidin biotin immunoperoxidase technique was used to stain a range of adhesion molecules in tissue sections of 21 gingival biopsies from both gingivitis and periodontitis subjects. These specimens were placed into three groups according to the size of the infiltrate. ICAM-1, PECAM-1 and LECAM-1 expression on mononuclear cells in the inflammatory infiltrates increased significantly with increasing size of infiltrate. Approximately 50% of these mononuclear cells were LFA-1+ and CD29+. When specimens were grouped according to their putative disease status there were no significant differences between mononuclear cell adhesion molecule expression in small infiltrates from either gingivitis or adult periodontitis subjects. This was also the case with larger lesions from both clinical groups. Therefore there does not appear to be a differential expression of adhesion molecules on lymphocytes in gingivitis and periodontitis tissue. Endothelial cells were positive for ICAM-1, PECAM-1, CD29, GMP-140 but negative for ELAM-1. Keratinocyte expression of ICAM-1 increased with increasing size of infiltrate although in heavy infiltrates, cells in the region of the junctional epithelium which were positive in small lesions, became ICAM-1 negative. The upper layers of the oral epithelium were positive for LECAM-1 in small infiltrates and with increasing size of infiltrate, the lower layers and many of the sulcular and junctional epithelium keratinocytes were positive. The basal epithelium and keratinocytes in the lower layers were CD29+ and in larger infiltrates, the upper layers were also positive. This study suggests that if specific homing of different lymphocyte clones occurs in gingivitis compared with periodontitis, this is not reflected in the pattern of adhesion molecule expression observed in this investigation. The present study may help to elucidate the roles played by endothelial cells and keratinocytes in lymphocyte trafficking in inflamed tissues.