Beikler Thomas, Peters Ulrike, Prior Karola, Eisenacher Martin, Flemmig Thomas F
Department of Periodontics, University of Washington, Seattle, USA.
BMC Med Genomics. 2008 Jul 7;1:30. doi: 10.1186/1755-8794-1-30.
In periodontitis, treatment aimed at controlling the periodontal biofilm infection results in a resolution of the clinical and histological signs of inflammation. Although the cell types found in periodontal tissues following treatment have been well described, information on gene expression is limited to few candidate genes. Therefore, the aim of the study was to determine the expression profiles of immune and inflammatory genes in periodontal tissues from sites with severe chronic periodontitis following periodontal therapy in order to identify genes involved in tissue homeostasis.Gingival biopsies from 12 patients with severe chronic periodontitis were taken six to eight weeks following non-surgical periodontal therapy, and from 11 healthy controls. As internal standard, RNA of an immortalized human keratinocyte line (HaCaT) was used. Total RNA was subjected to gene expression profiling using a commercially available microarray system focusing on inflammation-related genes. Post-hoc confirmation of selected genes was done by Realtime-PCR.
Out of the 136 genes analyzed, the 5% most strongly expressed genes compared to healthy controls were Interleukin-12A (IL-12A), Versican (CSPG-2), Matrixmetalloproteinase-1 (MMP-1), Down syndrome critical region protein-1 (DSCR-1), Macrophage inflammatory protein-2beta (Cxcl-3), Inhibitor of apoptosis protein-1 (BIRC-1), Cluster of differentiation antigen 38 (CD38), Regulator of G-protein signalling-1 (RGS-1), and Finkel-Biskis-Jinkins murine osteosarcoma virus oncogene (C-FOS); the 5% least strongly expressed genes were Receptor-interacting Serine/Threonine Kinase-2 (RIP-2), Complement component 3 (C3), Prostaglandin-endoperoxide synthase-2 (COX-2), Interleukin-8 (IL-8), Endothelin-1 (EDN-1), Plasminogen activator inhibitor type-2 (PAI-2), Matrix-metalloproteinase-14 (MMP-14), and Interferon regulating factor-7 (IRF-7).
Gene expression profiles found in periodontal tissues following therapy indicate activation of pathways that regulate tissue damage and repair.
在牙周炎中，旨在控制牙周生物膜感染的治疗可使炎症的临床和组织学体征消退。尽管治疗后牙周组织中发现的细胞类型已有详细描述，但基因表达方面的信息仅限于少数候选基因。因此，本研究的目的是确定重度慢性牙周炎患者经牙周治疗后牙周组织中免疫和炎症基因的表达谱，以识别参与组织稳态的基因。在非手术牙周治疗后6至8周，采集了12例重度慢性牙周炎患者的牙龈活检组织，并采集了11例健康对照者的牙龈活检组织。使用永生化人角质形成细胞系（HaCaT）的RNA作为内标。使用市售的聚焦于炎症相关基因的微阵列系统对总RNA进行基因表达谱分析。通过实时聚合酶链反应对选定基因进行事后验证。
在分析的136个基因中，与健康对照相比，表达最强的5%的基因是白细胞介素-12A（IL-12A）、多功能蛋白聚糖（CSPG-2）、基质金属蛋白酶-1（MMP-1）、唐氏综合征关键区域蛋白-1（DSCR-1）、巨噬细胞炎性蛋白-2β（Cxcl-3）凋亡抑制蛋白-1（BIRC-1）、分化抗原簇38（CD38）、G蛋白信号调节因子-1（RGS-1）和Finkel-Biskis-Jinkins小鼠骨肉瘤病毒癌基因（C-FOS）；表达最弱的5%的基因是受体相互作用丝氨酸/苏氨酸激酶-2（RIP-2）、补体成分3（C3）、前列腺素内过氧化物合酶-2（COX-2）、白细胞介素-8（IL-8）、内皮素-1（EDN-1）、纤溶酶原激活物抑制剂2型（PAI-2）、基质金属蛋白酶-14（MMP-14）和干扰素调节因子-7（IRF-7）。
治疗后牙周组织中发现的基因表达谱表明调节组织损伤和修复的通路被激活。
