Altered gene expression in leukocyte transendothelial migration and cell communication pathways in periodontitis-affected gingival tissues.

BACKGROUND AND

OBJECTIVE

Gene expression is related to the pathogenesis of periodontitis and plays a crucial role in local tissue destruction and disease susceptibility. The aims of the present study were to identify the expression of specific genes and biological pathways in periodontitis-affected gingival tissue using microarray and quantitative real-time RT-PCR analyses.

MATERIAL AND

METHODS

Healthy and periodontitis-affected gingival tissues were taken from three patients with severe chronic periodontitis. Total RNAs from six gingival tissue samples were used for microarray analyses. Data-mining analyses, such as comparisons, gene ontology and pathway analyses, were performed and biological pathways with a significant role in periodontitis were identified. In addition, quantitative real-time RT-PCR analysis was performed on samples obtained from 14 patients with chronic periodontitis and from 14 healthy individuals in order to confirm the results of the pathway analysis.

RESULTS

Comparison analyses found 15 up-regulated and 13 down-regulated genes (all of which showed a change of more than twofold in expression levels) in periodontitis-affected gingival tissues. Pathway analysis identified 15 up-regulated biological pathways, including leukocyte transendothelial migration, and five down-regulated pathways, including cell communication. Quantitative real-time RT-PCR verified that five genes in the leukocyte transendothelial migration pathway were significantly up-regulated, and four genes in the cell communication pathway were significantly down-regulated, which was consistent with pathway analysis.

CONCLUSION

We identified up-regulated genes (ITGB-2, MMP-2, CXCL-12, CXCR-4 and Rac-2) and down-regulated genes (connexin, DSG-1, DSC-1 and nestin) in periodontitis-affected gingival tissues; these genes may be related to the stimulation of leukocyte transendothelial migration and to the the impairment of cell-to-cell communication in periodontitis.