Molecular-biological analysis by DNA microarray for diagnosis of occlusal trauma

DNA 微阵列分子生物学分析用于诊断咬合创伤

基本信息

批准号：
15390646
负责人：
KITAMURA Masahiro
金额：
$ 9.34万
依托单位：
Osaka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2005
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15390646/
关键词：
DNA microarray Occlusal trauma Periodontal diseases

项目摘要

This study was designed to investigate the mechanisms involved occurrence of occlusal trauma and search the diagnostic makers of occlusal trauma by cDNA microarray and semi-measurable reverse transcription-polymerase chain reaction (RT-PCR). In the in vitro occlusal trauma model utilizing cell-stretcher (Scholertec NS-200), we detected up-regulation of the gene expressions in the stretched human periodontal ligament cell (HPDL), such as cyclooxygenase-2 (Cox-2), c-fos, integrin β-1, β-actin and adenosine deaminase genes. In another way, the genes associated with periodontal ligament, such as periodontal ligament associated protein-1 (PLAP-1) and periostin, did not showed the change of gene expressions by the mechanical stress. Furthermore, in order to clarify the diagnostic makers of occlusal trauma, we detected the mRNA of inflammatory cytokines and mediators by RT-PCR in the gingival tissues with occlusal trauma and without occlusal trauma collected by needle-punched biopsy methods. In result, IL-1β, IL-6, IL-8 and Cox2 mRNA expression were decreased and IFN-γ mRNA expression was elevated in the periodontal lesions decreased the occlusal trauma by occlusal adjustment. In another way, the mRNA of inflammatory cytokines and mediators detected in this study did showed no change or slight elevation of the expression in the periodontal lesions with occlusal trauma treated with no occlusal adjustment. Present results show that the mechanical stress promotes the various gene expressions associated with inflammatory reactions and bone destruction in HPDL and suggest that the inflammatory cytokines and mediators detected in this study, such as IL-1β, IL-6, IL-8 and Cox2 and IFN-γ, could be the potential diagnostic makers of occlusal trauma.

这项研究旨在研究咬合创伤的发生的机制，并通过cDNA微阵列和半高衡量的逆转录 - 聚合酶链（RT-PCR）搜索咬合创伤的诊断制造商。在利用细胞牵引器（Scholertec NS-200）的体外咬合创伤模型中，我们在拉伸的人牙周膜膜细胞（HPDL）中检测到基因表达的上调，例如环氧酶-2（COX-2），C-FOS，C-FOS，C-FOS，C-FOS，C-FOS，整合性β-1，β-1，β-肌动蛋白和Adenose nisenase nesosine nisenase nisenine nisenine niwsine nisenine nisenine nisenine niwsine niwsine nisenine nigine nigine niginin inin。另一种方式，与牙周韧带相关的基因（例如牙周韧带相关蛋白-1（PLAP-1）和odecin）并未显示机械应力的基因表达变化。此外，为了澄清咬合创伤的诊断制造商，我们通过RT-PCR在具有咬合创伤的牙龈组织中检测到炎性细胞因子和介质的mRNA，并且没有针头锻造的活检方法收集的咬合创伤。结果，改善了IL-1β，IL-6，IL-8和COX2 mRNA表达，牙周病变中IFN-γmRNA表达升高，通过咬合调节降低了咬合创伤。从另一种方面来看，这项研究中检测到的炎性细胞因子和介质的mRNA确实表明在牙周病变中没有变化或略微升高，未经咬合调节治疗的咬合创伤。目前的结果表明，机械应力促进了HPDL中与炎症反应和骨骼破坏相关的各种基因表达，并表明这项研究中检测到的炎性细胞因子和介质（例如IL-1β，IL-6，IL-6，IL-8和COX2和COX2和IFN-γ）可能是潜在的闭孔诊断者。