Immunomodulatory Factors Gene Polymorphisms in Chronic Periodontitis

An Overview

Zahra Heidari; Bita Moudi; Hamidreza Mahmoudzadeh-Sagheb

Disclosures

BMC Oral Health. 2019;19(29) 

In This Article

Summary and Conclusions

Infections can be affected by host genetic factors. The aim of the current review is to provide prognostic genetic markers for detection of the susceptibility of an individual to the chronic periodontitis. Genetic varieties can affect the function of the immune system by changing the transcription of immune factors.

Complex diseases, such as inflammatory bowel disease, type 2 diabetes and many other immune-mediated diseases, share a number of genetic risk variants. In this regard, if a candidate gene has an effect on multiple phenotypes, the pleiotropy occurs. Recently, the effects of pleiotropy in the pathogenesis of complex diseases have been studied.[168] Pleiotropy is associated with many SNPs recorded in the National Human Genome Research Institute (https://www.genome.gov/) brochure. It is interesting to note that in the genes that mediate the immune diseases pleiotropy increases. This definition can improve identifying the risk factors for CP. Therefore, a gene that was recognized as a risk factor for an inflammatory infectious disease might have a similar effect in the process of developing periodontal diseases. For example, IL-10 and 28B, which are important risk factors for hepatitis B virus infection may also be associated with CP. Finally, the overlap of genetic risk factors among diseases may be a useful reason, to analysis such genetic variations in CP. These studies can identify precisely the heritability of CP. As mentioned above, there are a large number of host genetic factors that are believed to be associated with CP susceptibility. It seems that single allelic variants are responsible for disease susceptibility. The most successful example is the identification of SNPs in different cytokine genes in CP.

A genetic variation may be a risk factor for a disease in one population but not for other populations. As the genotype and allele frequencies are vary between different ethnic and geographical populations. With regard to this issue, the studies show that, the IL-1α − 889, IL-1β + 3954, IL1RN VNTR, IL-6-174, IL-10-1087, TNF-α-308, TGF-β1–29, IFN-γ + 874, VDR TaqI and BsmI SNPs were polymorphic in Caucasian in contrast to Asian populations. It means that, ethnic background can change the association between SNPs and disease susceptibility.

Another important point is the accurate disease phenotype definition. There are two forms of periodontitis, which have some similar clinical symptoms: chronic periodontitis and aggressive periodontitis. Therefore, correct disease classification should be used in patient selection.

The studies with regard to the identifying significant genetic factors for susceptibility to chronic periodontitis are not reproducible always. There are differences among the various studies for some SNPs. Nevertheless, there is some evidence that SNPs in the IL-1α, IL-1β, IL1RN, IL-6, IL-10, TNF-α, TGF-β1, IFN-γ and VDR may be associated with CP susceptibility. These SNPs can change the signaling pathways of Wnt/b-catenin, p53 and JAK/STAT and induce CP. Such signaling pathways are believed to modulate the host immune system and are considered as useful biomarkers for determining CP.

It should be noted that, genetic predisposing to CP is not the only risk factor for disease. The interaction between genetic, bacterial and lifestyle factors can also affect the disease susceptibility. In other words, individual habits, microorganisms and diet can affect the expression of the gene through the changing the individual's epigenome.

In conclusion, the study has implied the relationship between genetic variations and CP susceptibility and related traits. However, the real mechanism of interaction between these factors and host immunity functions not specified yet. Moreover, genetic factors alone cannot explain pathogenesis of inflammation. Therefore, further investigation of other host genetic and environment factors, by novel technologies are needed. This process provided therapeutic and preventive strategies for CP.

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