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IFN-γR2 is strongly expressed on endothelial cells of gingival tissues from patients with chronic periodontitis

Franco-Topete, Ramón; Zepeda-Nuño, José Sergio; Zamora-Perez, Ana Lourdes; Fuentes-Lerma, Martha Graciela; Gómez-Meda, Belinda Claudia; Guerrero-Velázquez, Celia.
J. appl. oral sci ; 26: e20170291, 2018. tab, graf
Artigo em Inglês | LILACS, BBO | ID: biblio-954515
Abstract Chronic periodontitis (CP) is characterized by gingival inflammation and bone destruction. It has been reported that interferon-gamma (IFN-γ) levels are high in CP patients; however, the IFN-γ receptor (IFN-γR) has not been studied in gingival tissue from these patients.

Objective:

To evaluate IFN-γ levels and IFN-γR expression in gingival tissue biopsies from chronic periodontitis patients compared with healthy subjects (HS). Material and

Methods:

Gingival tissues were obtained from all study subjects, CP (n = 18) and healthy subjects (HS) (n = 12). A tissue section of each study subject was embedded in paraffin blocks to determine the expression of IFN-γ R (IFN-γR1 and IFN-γR2) through immunohistochemistry. Another section of the tissue was homogenized and IFN-γ was measured by the ELISA technique.

Results:

No significant differences were found in the IFN-γR1 expression within the cell layers of the gingival tissue of the study groups. When analyzing the IFN-γR2 expression it was found that IFN-γR2 is strongly expressed in the endothelial cells of CP patients when compared to HS (p<0.05). IFN-γ concentrations in the gingival tissue were significantly higher in CP patients than in HS. No significant correlation between IFN-γ levels and the expression of IFN-γR1 and IFN-γR2 was found. However, a positive correlation between IFN-γ levels and clinical parameters [probing depth (PD) and clinical attachment level (CAL)] was found.

Conclusion:

The study of IFN-γR expression in gingival tissue samples from patients with CP showed an increase only in the IFN-γR2 chain in endothelial cells when compared to HS.
Biblioteca responsável: BR1.1