Research Article

Environmental factors and polymorphisms of interleukin genes contribute to susceptibility to chronic periodontal disease

Published: September 30, 2020
Genet. Mol. Res. 19(3): GMR18568 DOI: https://doi.org/10.4238/gmr18568
Cite this Article:
J.A.X. Manso, R. Hannum, J.S. Fortes, S.S.M. Duarte, A.S. da Cruz, L.B. Minasi, A.D. da Cruz, C.C. da Silva (2020). Environmental factors and polymorphisms of interleukin genes contribute to susceptibility to chronic periodontal disease. Genet. Mol. Res. 19(3): GMR18568. https://doi.org/10.4238/gmr18568
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Abstract

Chronic periodontal disease (CPD) is described as a recurrent inflammatory condition of tooth supporting tissues, caused by bacterial infections and self-destructive processes of immune activity mediated by pro-inflammatory cytokines, of which the interleukins 1β, 6 and 8 stand out; together with other biomolecules these cytokines mediate innate immunity. These molecules may have variations in their genes, such as single nucleotide polymorphisms, which together with environmental factors, can affect susceptibility to this disease condition. We investigated how polymorphisms of the IL1B, IL6 and CXCL8 genes, as well as sociodemographic and lifestyle aspects, affect susceptibility to chronic periodontal disease in a group of volunteers in Goiânia city. Peripheral blood samples from 152 volunteers were obtained via venipuncture and grouped into controls and a case group (CPD), according to the result of the periogram, previously elaborated, together with a questionnaire concerning habits and life style. The DNA of the samples was genotyped using PCR-RFLP and qPCR, for each molecular marker. A significant trend to develop CPD was detected for individuals who brush their teeth less than twice a day. The allele of minor frequency of the variants rs1143634, rs1800796, and rs2227539 were associated with CPD, revealing a significant predictive effect (P < 0.05). The most significant findings involved the T (rs1143634) and C (rs1800796) alleles, which were associated with increased risk, when examined individually and together. We concluded that this is a multifactorial disease, although the the genetic influence was predominant.

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