Abstract
BackgroundPeriodontitis is a multi-factorial disease and several risk-factors such as infections, inflammatory responses, oral hygiene, smoke, aging and individual predisposition are involved in the disease. Pathogens trigger chronic inflammation with cytokines release which in turn leads to the destruction of the connective and the teeth supporting bone. The identification of genetic factors controlling oral inflammation may increase our understanding of genetic predisposition to periodontitis.Single nucleotide polymorphisms in the promoter region of Vascular Endothelial Growth Factor, Alpha-1-Antichymotripsin, hydroxy-methyl-glutaryl CoA reductase, Interferon alpha, Interleukin-1 Beta, Interleukin 10, Interleukin 6 and Tumor Necrosis Factor- alpha genes from a case/control study were investigated.ResultsThe C allele of Vascular Endothelial Growth Factor, A allele of Interleukin 10 and GG genotype of Tumor Necrosis Factor-α were individually associated with chronic periodontitis. However, the concomitant presence of the three genetic markers in the same subjects appeared to play a synergistic role and increased several folds the risk of the disease.ConclusionsOur findings offer new tools to implement the screening of unaffected subjects with an increased susceptibility of periodontitis and increase our understanding regarding the genetic inflammatory background related to familiarity of the disease.
Highlights
Periodontitis is a multi-factorial disease and several risk-factors such as infections, inflammatory responses, oral hygiene, smoke, aging and individual predisposition are involved in the disease
The percentage of Vascular Endothelial Growth Factor (VEGF) C carriers was significantly higher in the patients with periodontitis than in the CTR (94.8% vs 84.6%, p = 0.021; Odds ratio (OR) = 3.327; ci = 1.138-9.726), whereas the percentage of A carriers was significantly lower in the patients with periodontitis than CTR (27.3% vs 66.4%, p = 0.0001; OR = 0.190; ci = 0.107-0.338)
The GG genotype was more frequent in CTR than in the patients with periodontitis (19.8% vs 9.3%, p = 0.027; OR = 0.412; ci = 0.183-0.926), on the other hand the AA genotype was more represented in patients than in CTR (52% vs 35.7%, p = 0.008; OR = 1.929; ci = 1.181-3.151)
Summary
Periodontitis is a multi-factorial disease and several risk-factors such as infections, inflammatory responses, oral hygiene, smoke, aging and individual predisposition are involved in the disease. The identification of genetic factors controlling oral inflammation may increase our understanding of genetic predisposition to periodontitis. Periodontitis is a multi-factorial disease and several riskcomponents, such as environmental, metabolic, genetic, microbial factors, aging and poor oral hygiene status are involved in the pathogenesis of the disease [1]. It has been initially suggested that susceptibility to periodontitis could be genetically determined by the immune responsiveness to bacterial lipopolysaccharides [3]. Chronic inflammation and cytokines have been suggested to play a pivotal role in destructive processes occurring in periodontitis [5]. Chronic periodontitis is associated with systemic disease where altered control of inflammation may play a role. Inherited altered regulation of inflammatory responses may contribute to the pathogenesis of the disease
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