Genetic polymorphisms and periodontal disease in populations of African descent: A review

Abstract

Aggressive periodontitis is a rare but rapidly progressing form of periodontal disease that usually affects otherwise systemically healthy individuals, at a young age. It usually affects first molars and incisors, which are usually lost if treatment is not properly and early rendered. Although of low prevalence, it affects individuals of African descent at a higher prevalence, and usually multiple members within the same family. Several studies have been performed in the attempt to evaluate specific single nucleotide polymorphisms (SNPs) that could be associated with this disease. To the best of our knowledge, the present article provides the first review of the literature focusing on studies that evaluated SNPs in patients of African descent with aggressive periodontitis. Several SNPs have been evaluated in different genes according to their role in the pathogenesis of the disease, with positive and negative associations (such as IL1, FCGR3B, FPR1, LTF, CYBA, GLT6D1, TLR4) with both the localized and generalized forms of aggressive periodontitis. Given the complexity of periodontitis, the difficulty in gathering large cohorts diagnosed with this rare form of disease, and the fact that candidate gene studies may only determine part of the genetic risk of a disease, the search for specific SNPs associated with aggressive periodontitis seems to be a long one, most likely to result in the combination of multiple SNPs, in multiple genes.

Magnoliae Cortex and maize modulate Porphyromonas gingivalis-induced inflammatory reactions

“…The primary etiology of periodontal disease is infection by periodontal pathogens such as P. gingivalis , P. intermedia, and A. actinomycetemcomitans [ 1 2 4 22 ]. Conversely, periodontal disease progresses in response to the host immune inflammatory reaction to periodontal pathogens and their products [ 2 4 22 ]. TLR ligands from pathogens such as P. gingivalis stimulate immune cells, such as neutrophils, monocytes, and macrophages, and immune cells produce cytokines by multiple processes ( Figure 9 ) [ 4 23 ].…”

“…TLR ligands from pathogens such as P. gingivalis stimulate immune cells, such as neutrophils, monocytes, and macrophages, and immune cells produce cytokines by multiple processes ( Figure 9 ) [ 4 23 ]. These inflammatory mediators, such as IL-1β, IL-6, and TNF-α, cause local tissue destruction and alveolar bone loss [ 2 4 22 ].…”

“…Aggressive periodontitis generally involves rapid attachment loss and bone destruction inconsistent with the amount of the microbial deposit [ 3 22 24 ]. Single nucleotide polymorphisms on genes encoding cytokines, receptors, and metabolic modulators and proteins result in increased disease susceptibility or overexpression of the host innate inflammatory reaction [ 22 ].…”

“…Aggressive periodontitis generally involves rapid attachment loss and bone destruction inconsistent with the amount of the microbial deposit [ 3 22 24 ]. Single nucleotide polymorphisms on genes encoding cytokines, receptors, and metabolic modulators and proteins result in increased disease susceptibility or overexpression of the host innate inflammatory reaction [ 22 ]. Modulators of inflammatory mediators, such as SDD, may be especially beneficial for slowing the progression of periodontal disease, especially aggressive periodontitis, along with the mechanical removal of oral pathogens [ 2 4 25 ].…”

Identification and clinical relevance of phenotype modifying genetic factors in monogenic diseases

“…The comparison of the WES data of the HMS and PLS patients identified a putative phenotype-modifying genetic variant (rs34608771 SNP) in the SH2D4A gene, which encodes a T-cell-expressed adapter protein that is expressed in T-cells, Bcells, macrophages and dendritic cells (Hashimoto et al, 2000). SH2D4A regulates T-cell receptor (TCR) signal transduction in T-cells, and, in human T-cells, its expression increased in response to T-cell activation (Gonçalves et al, 2018).…”