Rat peri-implant soft tissue specifically expressed CXCL2 on titanium implant during wound healing
Rat peri-implant soft tissue specifically expressed CXCL2 on titanium implant during wound healing
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DOI：
10.1002/jbm.a.37337
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发表时间：
2021-11-30
影响因子：
4.9
通讯作者：
Yajima, Yasutomo
中科院分区：
文献类型：
--
作者：
Asami, Yosuke;Sasaki, Hodaka;Yajima, Yasutomo
通过基因芯片分析，许多在种植体周软组织中特异表达的基因参与了炎症反应。本研究探讨创伤愈合过程中PIST特异性炎症标志物在PIST中的表达和定位。将纯钛种植体植入大鼠上颌窝，制作PIST模型。取PIST标本为实验组，口腔黏膜组织拔牙面积(OMT)和健康牙周组织(PT)为对照组。检测4种标准炎症标志物和9种PIST特异性炎症标志物，包括趋化因子(C-X-C基序)配体2(CXCL2)在创面愈合过程中的基因表达。比较CXCL2和免疫细胞在PIST和对照组织中的免疫反应。在创面愈合过程中，PIST特异性炎症标志物的基因表达高于OMT(p<；0.05)，但标准炎症标志物的表达差异无统计学意义。CXCL2分子在种植体-结缔组织界面局部表达，免疫细胞的定位与CXCL2的表达模式非常匹配。在PIST中，有7种PIST特异性炎症标志物在创面愈合过程中特异性和强表达，并且它们的表达一直维持到愈合结束。此外，CXCL2的表达是由于种植体-结缔组织界面的建立，它在PIST中建立了一种独特的防御机制，这在OMT或PT中并不明显。
Many of genes specifically expressed in peri-implant soft tissue (PIST) selected by microarray analysis are involved in the inflammatory response. This study investigated the gene expression and localization of PIST-specific inflammatory markers in PIST during wound healing. Pure titanium implants were implanted into the rat upper mandibular socket to create PIST. Samples were harvested from PIST as an experimental group, and tooth extracted area of oral mucosa tissue (OMT) and healthy periodontal tissue (PT) as control groups. The gene expressions of four standard inflammatory markers and nine PIST-specific inflammatory markers including chemokine (C-X-C motif) ligand 2 (CXCL2) during wound healing were examined. Immunoreactions of CXCL2 and immune cells in PIST and control tissues were compared. During wound healing, gene expression of PIST-specific inflammatory markers was higher in PIST than in OMT (p < .05), but there were no significant differences in the expression of standard inflammatory markers. The molecule CXCL2 was expressed locally at the implant-connective tissue interface, and localization of immune cells closely matched the CXCL2 expression pattern. In PIST, seven of PIST-specific inflammatory markers were expressed specifically and strongly during wound healing and their expression was maintained until the end of healing. Furthermore, CXCL2 expression was due to the creation of the implant-connective tissue interface, and it established a unique defense mechanism in PIST that was not apparent in OMT or PT.