The Fcγ Receptor Genotype as a Severity Factor for Chronic Periodontitis in Japanese Patients

Kobayashi, Tetsuo; Yamamoto, Kouji; Sugita, Noriko; Pol, W‐Ludo van der; Yasuda, Keiko; Kaneko, Sawa; Winkel, Jan G. J. van de; Yoshie, Hiromasa

doi:10.1902/jop.2001.72.10.1324

Cited by 74 publications

(84 citation statements)

References 40 publications

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“…FcgRIIIAÀ158V and FcgRIIIB-NA2 were recently shown as a severity factor for CP. 28 In this study, we found no linkage disequilibrium between FcgRIIB-nt 646À184A/G and other FcgRIIA, IIIA and IIIB polymorphisms. These results suggested the FcgRIIB-nt 646À184A/G genotype to be a susceptibility factor for CP.…”

Section: Discussionmentioning

confidence: 40%

FcγRIIB gene polymorphisms in Japanese periodontitis patients

et al. 2003

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Human type II low-affinity receptor for immunoglobulin G (FcgRII) constitutes a clustered gene family consisting of FcgRIIA, IIB and IIC genes. FcgRIIB is unique in its ability to transmit inhibitory signals in B cells via immunoreceptor tyrosine-based inhibitory motif (ITIM). B-cell activation and subsequent elevated production of IgG are the immunopathological features of inflammatory disease such as periodontitis. To determine whether an association with periodontitis susceptibility exists, genetic polymorphisms of FcgRIIB were examined in Japanese patients with aggressive periodontitis (AGP) and chronic periodontitis (CP), and in the race-matched healthy controls (HCs). A significant difference was observed in the distribution of FcgRIIBÀ232I/T allele (exon 5) between the AGP and HC groups, with enrichment of the 232T in the AGP group (P¼0.006). In addition, the FcgRIIB-nt 646À184A/G allele (intron 4) distribution was significantly different between the CP and HC groups, with enrichment of the nt 646À184A in the CP group (P¼0.011). These results document the association of FcgRIIB gene polymorphisms with susceptibility to periodontitis in the Japanese.

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Section: Discussionmentioning

confidence: 40%

FcγRIIB gene polymorphisms in Japanese periodontitis patients

et al. 2003

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“…NA1 is found to a greater extent in Japanese patients who are resistant to chronic periodontitis (OR 1.87, 95% CI 1.07-3.28). 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).…”

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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“…27 In contrast, another Japanese researchers reported that the FcγRIIIa-158V allele was over-represented in patients with severe periodontitis versus subjects with moderate disease. 28 In this study, a significant association was observed between the FcγRIIIa-158V/F polymorphism and AgP patients. Moreover, the FcγRIIIa-158F allele was more frequently detected in AgP over healthy controls.…”

Section: Distribution Of Fcγriii Genotypes and Allelesmentioning

confidence: 50%