The Fcγ receptor III genotype as a risk factor for aggressive periodontitis in Korean patients

Abstract

Aggressive periodontitis (AgP) represents an inflammatory disease with pathogenic features, such as onset in the juvenile or early adults years and severe and rapid destruction of periodontal tissue. It is now recognized that microbial factors can not solely be held responsible for AgP, although these are important in the initiation of periodontitis. 1 Genetically determined variance in host immune response bacteria has been identified in individuals with AgP. Many AgP (especially those with localized form) patients display defective neutrophil chemotaxis due to changes in chemotactic receptors or activation pathways. 2,31) It was after only the Kormann’s study4 on the genetic polymorphism of interleukin (IL) that many researchers were really being interested in the genetic factors and trying to find the scientific evidences of genetic factors that affect the pathogenesis of periodontitis. Since then, the wide spectrum of genes that might affect the progression of the peridontal disease, such as IL, tumor necrosis factor-α (TNF-α), Fcγ receptor (Fcγ R), vitamine D receptor, Nformyl receptor, matrix metalloproteinase (MMP) promoter, Toll-like receptor 2 (TLR2) and TLR4 have been studied for their role in the various types of periodontitis. Leukocyte receptors for the constant (or Fc-) part of immunoglobulins (FcR) link cellular and humoral branches of the immune systems, which are considered essential for host defense against periodontopathic bacteria. FcR for IgG (FcγR) may play a crucial role in the host defense against periodontopathic bacteria. 6-7 Three receptor