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The Interleukin‐1 and Fcγ Receptor Gene Polymorphisms in Japanese Patients With Rheumatoid Arthritis and Periodontitis
Author(s) -
Kobayashi Tetsuo,
Ito Satoshi,
Kuroda Takeshi,
Yamamoto Kouji,
Sugita Noriko,
Narita Ichiei,
Sumida Takayuki,
Gejyo Fumitake,
Yoshie Hiromasa
Publication year - 2007
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2007.070136
Subject(s) - periodontitis , rheumatoid arthritis , medicine , genotype , immunology , proinflammatory cytokine , allele , odds ratio , interleukin , aggressive periodontitis , chronic periodontitis , arthritis , population , gastroenterology , gene , cytokine , biology , inflammation , genetics , environmental health
Background: The pathobiology of rheumatoid arthritis (RA) is similar to that of periodontitis in that proinflammatory cytokines and immunoglobulin G Fc receptor (FcγR) play an important role. Functional polymorphisms of interleukin (IL)‐1 and FcγR were shown to be associated with susceptibility to both diseases. Therefore, we evaluated whether the IL‐1 and FcγR gene polymorphisms represent a common risk factor for RA and periodontitis. Methods: The study population consisted of Japanese adults with RA (RA group; N = 100), periodontitis only (P group; N = 100), and healthy individuals with no systemic or oral disease (H group; N = 100). Clinical periodontal condition was defined by measurements of probing depth, clinical attachment level, and bleeding on probing. Genomic DNA was isolated from peripheral blood and analyzed for determination of IL‐1 genotypes (IL‐1A+4845, IL‐1B+3954, and IL‐1RN+2028) and FcγR genotypes (FcγRIIA, FcγRIIIA, and FcγRIIIB) by allele‐specific polymerase chain reactions. Results: Among 100 patients with RA, 86% showed periodontal tissue destruction. However, the RA group exhibited milder levels of periodontal tissue destruction than the P group ( P <0.01). There was a significant difference in the distribution of IL‐1B+3954 C/T genotypes between the RA and P groups and between the RA and H groups ( P = 0.03 for both comparisons), with enrichment of the T allele in the RA group ( P = 0.04; odds ratio, 2.9 for both comparisons). The combination of IL‐1A+4845 T and IL‐1+3954 T alleles yielded a strong association with RA and periodontitis (RA versus P group: P = 0.00001; RA versus H group: P = 0.00001). Conclusions: These results failed to show that IL‐1 and FcγR gene polymorphisms constitute a common risk factor for RA and periodontitis. However, it was suggested that the distributions of IL‐1B+3954 genotypes and IL‐1A+4845 and IL‐1B+3954 haplotypes were unique to the patients with RA and periodontitis.