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Abstract：
BACKGROUND: Periodontitis is a chronic inflammation of periodontal supporting tissue caused by local factors. Periodontal surgery can change the gene expression of peripheral blood mononuclear cells. However, little is known about the potential mechanism of surgical treatment for periodontitis.
OBJECTIVE: To explore the potential molecular mechanism of surgical treatment for periodontitis.
METHODS: First, based on the expression profiles of genes related to surgical treatment for periodontitis, a set of expression disorder modules related to surgical treatment for periodontitis were obtained by enrichment analysis. Subsequently, based on crosstalk analysis, we proved that there was a significant crosstalk relationship between module 3 and module 5. Finally, based on predictive analysis of multidimensional regulators, we identified a series of regulatory factors, such as endogenous genes, non-coding RNAs (ncRNAs), and transcription factors, which have potential regulatory effects on periodontitis.
RESULTS: A total of 337 genes related to surgical treatment for periodontitis were obtained, and 3896 genes related to periodontitis were amplified. Eight expression modules of periodontitis were obtained, involving the aggregation of 2672 gene modules. These modules are mainly involved in G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger, and adenylate cyclase-modulating G-protein coupled receptor signaling pathway. In addition, eight endogenous genes (including EGF, RPS27A, and GNB3) were screened by network connectivity analysis. Finally, based on this set of potential dysfunction modules, 94 transcription factors (including NFKB1, SP1, and STAT3) and 1198 ncRNAs (including MALAT1, CRNDE, and ANCR) were revealed. These core regulators are thought to be involved in the potential molecular mechanism of periodontitis after surgical treatment.
CONCLUSIONS: Based on the results of this study, we can show biologists and pharmacists a new idea to reveal the potential molecular mechanism of surgical treatment for periodontitis, and provide valuable reference for follow-up treatment programs.
OBJECTIVE: To explore the potential molecular mechanism of surgical treatment for periodontitis.
METHODS: First, based on the expression profiles of genes related to surgical treatment for periodontitis, a set of expression disorder modules related to surgical treatment for periodontitis were obtained by enrichment analysis. Subsequently, based on crosstalk analysis, we proved that there was a significant crosstalk relationship between module 3 and module 5. Finally, based on predictive analysis of multidimensional regulators, we identified a series of regulatory factors, such as endogenous genes, non-coding RNAs (ncRNAs), and transcription factors, which have potential regulatory effects on periodontitis.
RESULTS: A total of 337 genes related to surgical treatment for periodontitis were obtained, and 3896 genes related to periodontitis were amplified. Eight expression modules of periodontitis were obtained, involving the aggregation of 2672 gene modules. These modules are mainly involved in G-protein coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger, and adenylate cyclase-modulating G-protein coupled receptor signaling pathway. In addition, eight endogenous genes (including EGF, RPS27A, and GNB3) were screened by network connectivity analysis. Finally, based on this set of potential dysfunction modules, 94 transcription factors (including NFKB1, SP1, and STAT3) and 1198 ncRNAs (including MALAT1, CRNDE, and ANCR) were revealed. These core regulators are thought to be involved in the potential molecular mechanism of periodontitis after surgical treatment.
CONCLUSIONS: Based on the results of this study, we can show biologists and pharmacists a new idea to reveal the potential molecular mechanism of surgical treatment for periodontitis, and provide valuable reference for follow-up treatment programs.
摘要：
背景：牙周炎是由局部因素引起的牙周支持组织的慢性炎症。牙周手术可以转变外周血单个核细胞的基因表达。然而,关于牙周炎手术治疗的潜在机制知之甚少。
目的：探讨牙周炎外科治疗的分子机制。
方法：首先，根据牙周炎手术治疗相关基因的表达谱，通过富集分析获得了一组与牙周炎手术治疗相关的表达障碍模块。随后，基于串扰分析，我们证明了模块3和模块5之间存在显著的串扰关系。最后,基于对多维调节器的预测分析，我们确定了一系列调节因素，例如内源性基因，非编码RNA（ncRNAs），和转录因子，对牙周炎有潜在的调节作用。
结果：共获得337个与牙周炎手术治疗相关的基因，扩增3896个牙周炎相关基因。获得8个牙周炎表达模块,涉及2672个基因模块的聚集。这些模块主要参与G蛋白偶联受体信号通路,与环核苷酸第二信使偶联，和腺苷酸环化酶调节G蛋白偶联受体信号通路。此外,八个内源基因(包括EGF，RPS27A,和GNB3)通过网络连接分析进行筛选。最后,基于这组潜在的功能障碍模块，94个转录因子（包括NFKB1，SP1和STAT3）和1198个ncRNAs（包括MALAT1，CRNDE，和ANCR）被揭露。这些核心调节剂被认为与手术治疗后牙周炎的潜在分子机制有关。
结论：根据本研究的结果，我们可以向生物学家和药剂师展示一个新的想法，以揭示牙周炎外科治疗的潜在分子机制，为后续治疗方案提供有价值的参考。
目的：探讨牙周炎外科治疗的分子机制。
方法：首先，根据牙周炎手术治疗相关基因的表达谱，通过富集分析获得了一组与牙周炎手术治疗相关的表达障碍模块。随后，基于串扰分析，我们证明了模块3和模块5之间存在显著的串扰关系。最后,基于对多维调节器的预测分析，我们确定了一系列调节因素，例如内源性基因，非编码RNA（ncRNAs），和转录因子，对牙周炎有潜在的调节作用。
结果：共获得337个与牙周炎手术治疗相关的基因，扩增3896个牙周炎相关基因。获得8个牙周炎表达模块,涉及2672个基因模块的聚集。这些模块主要参与G蛋白偶联受体信号通路,与环核苷酸第二信使偶联，和腺苷酸环化酶调节G蛋白偶联受体信号通路。此外,八个内源基因(包括EGF，RPS27A,和GNB3)通过网络连接分析进行筛选。最后,基于这组潜在的功能障碍模块，94个转录因子（包括NFKB1，SP1和STAT3）和1198个ncRNAs（包括MALAT1，CRNDE，和ANCR）被揭露。这些核心调节剂被认为与手术治疗后牙周炎的潜在分子机制有关。
结论：根据本研究的结果，我们可以向生物学家和药剂师展示一个新的想法，以揭示牙周炎外科治疗的潜在分子机制，为后续治疗方案提供有价值的参考。
