Gingival tissue transcriptomes in experimental gingivitis

Gingival tissue transcriptomes in experimental gingivitis
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DOI:
10.1111/j.1600-051x.2011.01719.x
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发表时间:
2011-07-01
影响因子:
6.7
通讯作者:
Papapanou, Panos N.
Papapanou, Panos N.
中科院分区:
医学1区
文献类型:
--
作者:
Joensson, Daniel;Ramberg, Per;Papapanou, Panos N.

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目的研究实验性牙龈炎诱导和消退过程中龈内基因序列表达的变化。材料和方法20名牙周和全身健康的非吸烟志愿者参加了为期3周的实验性牙龈炎方案,随后进行清创和2周的常规菌斑控制。我们记录了一半参与者的临床指标,并在基线、第7天、第14天和第21天(“诱导期”)以及另一半参与者的第21天、第25天、第30天和第35天(“消退期”)采集了四个近端腭间部位的牙龈组织样本。使用Affymetrix Human Genome U133Plus2.0微阵列对RNA进行提取、扩增、反转录、扩增、标记和杂交。配对t检验比较连续时间点之间基因表达的变化。基因本体论分析将表达模式归纳为生物学相关的类别。结果基线时牙龈指数中位数为0,第21天为2,第35天为1。差异基因调控在诱导第3周和分离后第4天达到高峰。白细胞迁移、细胞粘附和抗原加工/呈递是主要的差异调控途径。结论转录组学研究增强了我们对可逆性炎症性牙龈病变病理生物学的理解,并提供了实验性牙龈炎诱导和消退过程中动态组织反应的详细描述。
P>AimsWe investigated the sequential gene expression in the gingiva during the induction and resolution of experimental gingivitis.Material and MethodsTwenty periodontally and systemically healthy non-smoking volunteers participated in a 3-week experimental gingivitis protocol, followed by debridement and 2-week regular plaque control. We recorded clinical indices and harvested gingival tissue samples from four interproximal palatal sites in half of the participants at baseline, Day 7, Day 14 and Day 21 (the "induction phase"), and at Day 21, Day 25, Day 30 and Day 35 in the other half (the "resolution phase"). RNA was extracted, amplified, reversed transcribed, amplified, labelled and hybridized using Affymetrix Human Genome U133Plus2.0 microarrays. Paired t-tests compared gene expression changes between consecutive time points. Gene ontology analyses summarized the expression patterns into biologically relevant categories.ResultsThe median gingival index was 0 at baseline, 2 at Day 21 and 1 at Day 35. Differential gene regulation peaked during the third week of induction and the first 4 days of resolution. Leucocyte transmigration, cell adhesion and antigen processing/presentation were the top differentially regulated pathways.ConclusionsTranscriptomic studies enhance our understanding of the pathobiology of the reversible inflammatory gingival lesion and provide a detailed account of the dynamic tissue responses during the induction and resolution of experimental gingivitis.