Interferon gamma (IFN-γ) is an immunoregulatory cytokine that, when activated by its receptor, plays an important role in the activation of inflammatory processes, which are the basis of periodontal disease.
Th1-polarized host response, mediated by IFN-γ, has been associated with increased severity of periodontal disease as well as control of periodontal infection.
The aim of our investigations was to determine whether periodontal disease might aggravate atherosclerosis and whether interferon-gamma (IFNG), widely recognized as a potent multifunctional cytokine, might serve as a marker of the process.
The goal of this investigation was to determine whether epigenetic modifications in the IFNG promoter are associated with an increase of IFNG transcription in different stages of periodontal diseases.
Our results showed no significant difference in the allele and genotype frequencies of interleukin-4 (C-590T) and interferon-gamma (G5644A) gene polymorphisms between patients with periodontal disease and controls.
We utilized a jacalin-IgA capture assay to determine the IgA1 titers in total saliva and reverse transcriptase-polymerase chain reaction to detect mRNA for interferon gamma (IFN-gamma) and tumor necrosis factor alpha (TNF-alpha) in total saliva samples of 13 patients with chronic moderate periodontal disease and 10 with chronic severe periodontal disease.