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.
Highlights
Chronic periodontitis (CP) is a strong immunoinflammatory response to periodontal pathogens influenced by metabolic disorders,[1,2] as well as genetic[3,4] and environmental factors.[5]Chronic gingival and periodontal inflammations lead to attachment loss with a periodontal pocket formation and progressive alveolar bone destruction.[6,7]Responding to the bacterial infection in periodontitis, antigen-presenting cells (APC) produce IL-12 and IL18.8 Subsequently, IL-12 and IL-18 synergize and stimulate the production of interferon-gamma (IFN-g) in T and NK cells.[9-11]
probing depth (PD) and clinical attachment level (CAL) were significantly higher in CP patients when compared to healthy subjects (HS) (Table 1)
Little is known about the intracellular trafficking of IFN-gR2, it seems that on certain cell types, IFN-γ regulates the expression of IFN-gR2 and determines the ability of these cells to respond to subsequent exposure to IFN-g
Summary
Chronic periodontitis (CP) is a strong immunoinflammatory response to periodontal pathogens influenced by metabolic disorders,[1,2] as well as genetic[3,4] and environmental factors.[5]Chronic gingival and periodontal inflammations lead to attachment loss with a periodontal pocket formation and progressive alveolar bone destruction.[6,7]Responding to the bacterial infection in periodontitis, antigen-presenting cells (APC) produce IL-12 and IL18.8 Subsequently, IL-12 and IL-18 synergize and stimulate the production of interferon-gamma (IFN-g) in T and NK cells.[9-11]. IFN-g and IFN-gR are known to be fundamental in the pathophysiology of several chronic and infectious diseases. In this sense, a deregulation in the expression of IFN-g and IFN-gR levels in patients with lepromatous leprosy has been described.[8,13]. A deregulation in the expression of IFN-g and IFN-gR levels in patients with lepromatous leprosy has been described.[8,13] In this regard, an increase in mRNA and IFN-g protein has been reported in gingival tissue, gingival crevicular fluid (GCF), and serum samples from CP patients compared to healthy subjects (HS).[14-19]. The objective of this study was to evaluate IFN-g levels and the expression of IFN-gR in gingival tissue samples from CP patients compared to healthy subjects Regarding the expression of IFN-gR in CP, only studies of IFNgR1 polymorphisms exist and no association has been found for periodontitis.[20,21] the objective of this study was to evaluate IFN-g levels and the expression of IFN-gR in gingival tissue samples from CP patients compared to healthy subjects
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