Polymorphisms of Fcγ-receptors RIIa, RIIIa, and RIIIb in patients with adult periodontal diseases

Meisel, Peter; Carlsson, LE; Sawaf, Hazem; Fanghaenel, J.; Greinacher, Andreas; Kocher, Thomas

doi:10.1038/sj.gene.6363777

Cited by 51 publications

(57 citation statements)

References 25 publications

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“…41,42 However, whereas in the other studies, these results were referable to LD, in the present analysis when the frequencies of the combined genotypes FCGR2A*C and FCGR3B* C were evaluated, the statistical analysis indicated an increased effect on the disease susceptibility for the combined genotype (w 2 ¼ 8,656; P ¼ 0.0033). This effect does not seem to be a consequence of LD, as the two markers of the Fc-g receptors are in complete equilibrium (D 0 ¼ 0.108; r 2 ¼ 0.0) in our sample.…”

Section: Gene-gene Interaction and Agp Susceptibility C Scapoli Et Alcontrasting

confidence: 76%

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

et al. 2011

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Aggressive periodontitis (AgP) is a multifactorial disease. The distinctive aspect of periodontitis is that this disease must deal with a large number of genes interacting with one another and forming complex networks. Thus, it is reasonable to expect that gene-gene interaction may have a crucial role. Therefore, we carried out a pilot case-control study to identify the association of candidate epistatic interactions between genetic risk factors and susceptibility to AgP, by using both conventional parametric analyses and a higher order interactions model, based on the nonparametric Multifactor Dimensionality Reduction algorithm. We analyzed 122 AgP patients and 246 appropriate periodontally healthy individuals, and genotyped 28 polymorphisms, located within 14 candidate genes, chosen among the principal genetic variants pointed out from literature and having a role in inflammation and immunity. Our analyses provided significant evidence for gene-gene interactions in the development of AgP, in particular, present results: (a) indicate a possible role of two new polymorphisms, within SEPS1 and TNFRSF1B genes, in determining host individual susceptibility to AgP; (b) confirm the potential association between of IL-6 and Fc g-receptor polymorphisms and the disease; (c) exclude an essential contribution of IL-1 cluster gene polymorphisms to AgP in our Caucasian-Italian population.

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Section: Gene-gene Interaction and Agp Susceptibility C Scapoli Et Alcontrasting

confidence: 76%

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

et al. 2011

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“…Several studies have found associations of FCGR2A polymorphisms with susceptibility to meningococcal disease, 23 periodontal disease 24 recurrent bacterial respiratory tract infection in children with low IgG2 anticarbohydrate antibodies 25 bacteremic pneumococcal pneumonia, 26 and invasive pneumococcal infections in patients with SLE. 27 The FCGR2A 131 H/R SNP strongly influences the ability of the receptor to bind human IgG 2 , the isotype often made in response to encapsulated bacteria.…”

Section: Discussionmentioning

confidence: 99%

Genetic risk factors for infection in patients with early rheumatoid arthritis

et al. 2004

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We analyzed clinical and genetic factors contributing to infections in 457 subjects with early rheumatoid arthritis (RA) enrolled in a prospective, 1-year clinical trial of methotrexate and the TNF inhibitor etanercept. Subjects were genotyped for the following single nucleotide polymorphisms (SNPs): (TNF À308, À238, and þ 488); lymphotoxin-a (LTA) (LTA þ 249, þ 365, and þ 720); and Fc gamma receptors FCGR2A 131 H/R; FCGR3A 176 F/V; and FCGR3B NA 1/2 and genotypes were correlated with infections. At least one URI was noted in 52% of subjects (99/191) with the NA2/NA2 genotype of the neutrophil-specific FCGR3B gene, compared to 42% (77/181) of those with the NA1/NA2 genotype and 39% (23/59) of those with the NA1/NA1 genotype (P ¼ 0.038). Urinary tract infection (UTI) was associated with the TNF À238 A (odds ratio(OR) 2.56, 95% confidence interval (CI) 1.05-6.25) and LTA þ 365 C (OR 1.73, 95% CI 1.07-2.79) alleles, and marginally with the FCGR3A F allele (OR 1.72, 95% CI 0.99-3.00). There was a striking linear correlation between UTI and the number of risk alleles defined by these three SNPs (Po0.001), suggesting an additive effect on susceptibility. These findings have important implications for the role of genetics in susceptibility to bacterial and viral infections.

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“…Kobayashi et al (2001) reported that 2 Fc␥RIII alleles may be associated with severity of chronic periodontitis in a Japanese population. Meisel et al (2001) analyzed the association between Fc␥RIIIa (high-affinity receptor) and Fc␥RIIIb (low-affinity receptor) and chronic periodontitis (CP). They found that Fc␥RIIIa was associated with CP (OR 5.3, 95% CI 1.4-26.2) but that this is in linkage disequilibrium with Fc␥RIIIb, which is also associated with CP.…”

Section: (9) Fc-gamma Receptormentioning

confidence: 99%

Genes and Gene Polymorphisms Associated with Periodontal Disease

Kinane

Hart

2003

Critical Reviews in Oral Biology & Medicine

293

252

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ABSTRACT:The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.

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Polymorphisms of Fcγ-receptors RIIa, RIIIa, and RIIIb in patients with adult periodontal diseases

Cited by 51 publications

References 25 publications

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

Gene–gene interaction among cytokine polymorphisms influence susceptibility to aggressive periodontitis

Genetic risk factors for infection in patients with early rheumatoid arthritis

Genes and Gene Polymorphisms Associated with Periodontal Disease

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