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Gene expression in periodontal tissues following treatment

机译：治疗后牙周组织中的基因表达

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Background 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. Results 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-2β (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). Conclusion Gene expression profiles found in periodontal tissues following therapy indicate activation of pathways that regulate tissue damage and repair.
机译：背景技术在牙周炎中，旨在控制牙周生物膜感染的治疗导致炎症的临床和组织学症状的缓解。尽管已经很好地描述了治疗后在牙周组织中发现的细胞类型，但是有关基因表达的信息仅限于少数候选基因。因此，该研究的目的是确定牙周治疗后严重慢性牙周炎部位牙周组织中免疫和炎性基因的表达谱，以鉴定参与组织体内稳态的基因。在非手术性牙周治疗后六至八周对12例重度慢性牙周炎患者进行了牙龈活检，并对11例健康对照进行了牙龈活检。作为内标，使用了永生化的人角质形成细胞系（HaCaT）的RNA。使用可商购的专注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。对选定基因的事后确认是通过实时PCR进行的。结果在分析的136个基因中，与健康对照相比，表达最强的5％基因是白细胞介素12A（IL-12A），Versican（CSPG-2），基质金属蛋白酶-1（MMP-1）和唐氏综合症关键区蛋白-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蛋白信号传导1（RGS）的调节剂-1）和Finkel-Biskis-Jinkins鼠骨肉瘤病毒癌基因（C-FOS）;强度最低的5％表达基因是受体相互作用的丝氨酸/苏氨酸激酶2（RIP-2），补体成分3（C3），前列腺素-过氧化物合成酶2（COX-2），白介素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）。结论治疗后在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途径的激活。

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