1. In total 213 DEGs in CP and 45 DEGs in RP were identified in blood and saliva tissues.
2. The DEGs were involved in ribosome antigen processing and presentation pathways.
3. CD24 EST1, MTSS1, ING3, CCND2 and SYNE2 might be potential targets for CP.
The authors declare that they have no competing interests and financial interests to disclose.
BZ participated in the design of this study. TL performed the statistical analysis. HH carried out the study together with TL, and collected important background information. BZ drafted the manuscript. HH conceived of this study, participated in the design and helped to draft the manuscript. All of the authors read and approved the final manuscript.
This study aimed to identify characteristic representative genes through a comparative analysis of gene expression profiles in the blood and saliva of chronic periodontitis (CP) and refractory periodontitis (RP) patients to provide new treatment strategies that may be helpful in the treatment of different forms of periodontitis.
GSE43525 was downloaded from Gene Expression Omnibus. In the dataset, thirteen samples were from blood including 4 controls, 4 CP and 5 RP samples, and ten samples were from saliva including 3 controls, 4 CP and 3 RP samples. After comparing the CP and RP samples, differentially expressed genes (DEGs) between these two types of periodontitis in the blood and saliva samples were identified by an LIMMA package. Then, functional and pathway enrichment analyses were performed by DAVID and KOBAS, respectively. The significantly associated miRNAs in CP and RP were searched by WebGestalt.
In total, 213 DEGs in CP and 45 DEGs in RP were identified. Functional enrichment showed that the DEGs of CP were mainly enriched in ribosome and regulation of apoptosis-related pathways in blood as well as saliva, while the DEGs of RP were significantly enriched in immune responses and response to organic substance-related pathways. Several miRNAs, such as miR-381 and miR-494, were identified as being closely associated with CP. In addition, CD24, EST1, MTSS1, ING3, CCND2 and SYNE2 might be potential targets for diagnosis and treatment of CP.
The identified DEGs and miRNAs might be potential targets for the treatment of chronic and refractory periodontitis.
TP C. Uses of turmeric in dentistry: An update. Indian J Dent Res. 2009;20:107–9. CrossRef
Shusterman A, Salyma Y, Nashef A, Soller M, Wilensky A, Mott R, et al. Genotype is an important determinant factor of host susceptibility to periodontitis in collaborative cross and inbred mouse population. BMC Genet. 2013;14:68.
Teumer A, Holtfreter B, Völker U, Petersmann A, Nauck M, Biffar R, et al. Genome-wide association study of chronic pe riodontitis in general German population. J Clin Periodontol. 2013;40:977–85.
Chapple ILC GR, on behalf of working group 2 of the joint EFP/AAP workshop. Diabetes and periodontal disease:consensus report of the joint EFP/AAP workshop on peri-odontitis and systemic diseases. J Clin Periodontol. 2013;40:S106–12. CrossRef
Luciana M, Shaddox CBW. Treating chronic periodontitis: current status, challenges, and future directions. Clin Cosmet Investig Dent. 2010;2:79–91.
Colombo APV, Bennet S, Cotton SL, Goodson JM, Kent R, Haffajee AD, et al. Impact of periodontal therapy on the subgingival microbiota of severe periodontitis: comparison between good responders and individuals with refractory periodontitis using the human oral microbe identification microarray. J Periodontol. 2012;83:1279–87. PubMedPubMedCentralCrossRef
Colombo APV, Boches SK, Cotton SL, Goodson JM, Kent R, Haffajee AD, et al. Comparisons of subgingival microbial profiles of refractory periodontitis, severe periodontitis, and periodontal health using the human oral microbe identification microarray. J Periodontol. 2009;80:1421–32.
Socransky SSSC, Haffajee AD. Subgingival microbial profiles in refractory periodontal disease. J Clin Periodontol. 2002;29:206–68.
Marja L, Laine BGL, Crielaard W. Gene Polymorphisms in Chronic Periodontitis. Int J Dent. 2010;2010:324719.
Indriolo SG A, Ravelli P, Fagiuoli S. What can we learn about biofilm host interaction from the study of inflammatory bowel disease. J Clin Periodontol. 2011;38:36–43. CrossRef
Hajime Sasaki NS, Emad AS, Yan X, Ricardo B, Leslie M. 0: 18beta-Glycyrrhetinic Acid Inhibits Periodontitis Via Glucocorticoid-Independent NF–κB Inactivation In IL-10 Deficient Mice. J Periodontal Res. 2011;45:757–63. CrossRef
Ph.D. ZFSMSBHH. Study the role of proinflammatory and anti-inflammatorycytokines in Iraqi chronic periodontitis patients. J Bagh Coll Dent. 2012;24:164–9.
Smyth GK. limma: Linear Models for Microarray Data. 2005.
Huang DW, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc. 2009;4:44–57. CrossRef
Lu J, Getz G, Miska EA, Alvarez-Saavedra E, Lamb J, Peck D, et al. MicroRNA expression profiles classify human cancers. Nature, 2005;435:834–838.
Calin GA, Croce CM. MicroRNA signatures in human cancers. Nat Rev Cancer. 2006;6:857–866.
Wang J, Duncan D, Shi Z, Zhang B. WEB-based Gene SeT AnaLysis Toolkit (WebGestalt): update 2013. Nucleic Acids Res. 2013;41:77–83. CrossRef
Liu Y-CG, Lerner UH, Teng Y-TA. Cytokine responses against periodontal infection: protective and destructive roles. 2010. p. 52–206.
French EDS CK, Simon SL, Eklund SM, Chen MC, Klotz LC, Vaccaro K. DNA probe detection of periodontal pathogens. Oral Microbiol Immunol. 2007;1:58–62. CrossRef
Jochen U. The expression of metastasis suppressor MIM/MTSS1 is regulated by DNA methylation. Int J Cancer. 2006;119:2287–93. CrossRef
Suzuki S, Nozawa Y, Tsukamoto S, Kaneko T, Imai H, Minami N. ING3 Is Essential for Asymmetric Cell Division during Mouse Oocyte Maturation. Plos One. 2013;8:e74749.
- Comparative analysis of blood and saliva expression profiles in chronic and refractory periodontitis patients
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