Analysis of the DNA methylation status in the SOCS1 gene in aggressive periodontite patients

Abstract

Periodontal inflammation represents a complex and multifactorial disease that results from the interaction of the host-defense mechanisms with plaque microorganisms. Methylation is the addition of methyl groups to the C5 position of DNA cytosines almost exclusively in CpG dinucleotides sites along the genome in differentiated cells. This mechanism is essential for the regulation of the gene expression. Since there are few studies in this area, a new study which investigates methylation patterns in genes that participate in the inflammatory pathways of periodontitis seems to be very valuable. There are a wide range of genes which are responsible for the expression of molecules, as proinflammatory and anti-inflammatory cytokines, which participate and conduct the host response during periodontitis. The SOCS gene family is involved in the cytokine regulation and participates in the periodontal disease, through JAK/STAT signaling pathway. An increase of the gene expression of SOCS1, 2 and 3 was demonstrated by studies focused on its role in the periodontitis process, probably taking part in the pathway signaling control of the inflammatory cytokines. However, epigenetic studies of SOCS genes focusing on the periodontitis have not yet been performed. Since the inflammation process is fundamental during the course of periodontitis, the SOCS proteins are involved in the inflammatory process regulation and the methylation process seems to be a very interesting and promising area in periodontitis disease, it is relevant to have studies focused on the relation between these factors.(AU)