Kobayashi Tetsuo, Ito Satoshi, Yasuda Keiko, Kuroda Takeshi, Yamamoto Kouji, Sugita Noriko, Tai Hideaki, Narita Ichiei, Gejyo Fumitake, Yoshie Hiromasa
Division of Periodontology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
J Periodontol. 2007 Mar;78(3):467-74. doi: 10.1902/jop.2007.060194.
The pathobiology of systemic lupus erythematosus (SLE) is similar to that of periodontitis in that the immunoglobulin G Fc receptor (FcgammaR) and proinflammatory cytokines play an important role. Genetic variations of FcgammaR and interleukin (IL)-1 are associated with susceptibility to both diseases. Therefore, we evaluated whether the combination of FcgammaR or IL-1 polymorphic genes represents a common risk factor for SLE and periodontitis.
The study population consisted of Japanese adults with SLE and periodontitis (SLE+P group; n = 46), SLE only (SLE group; n = 25), periodontitis only (P group; n = 58), and healthy individuals with no systemic or oral disease (H group; n = 44). Clinical periodontal condition was evaluated by measurement of probing depth, clinical attachment level, and alveolar bone loss. Genomic DNA was isolated from peripheral blood and analyzed for determination of FcgammaR genotypes (FcgammaRIIA, FcgammaRIIB, FcgammaRIIIA, and FcgammaRIIIB) and IL-1 genotypes (IL-1A +4845 and IL-1B +3954) by allele-specific polymerase chain reactions or DNA sequencing.
A significant overrepresentation of the R131 allele of stimulatory FcgammaRIIA and the 232T allele of inhibitory FcgammaRIIB was found in the SLE+P group compared to the H group (P = 0.01 and P = 0.0009, respectively). The combination of FcgammaRIIA-R131 and FcgammaRIIB-232T alleles yielded a strong association with SLE and periodontitis (SLE+P group versus P group: P = 0.01, odds ratio: 3.3; SLE+P group versus H group: P = 0.0009, odds ratio: 11.2). Furthermore, SLE patients with the combined FcgammaR risk alleles exhibited more severe periodontal tissue destruction compared to other SLE patients. The frequencies of IL-1 polymorphic alleles were too low to assess the association with SLE or periodontitis.
The combination of stimulatory FcgammaRIIA and inhibitory FcgammaRIIB genotypes may increase susceptibility to SLE and periodontitis in the Japanese population.
系统性红斑狼疮(SLE)的病理生物学与牙周炎相似,免疫球蛋白G Fc受体(FcγR)和促炎细胞因子在其中发挥重要作用。FcγR和白细胞介素(IL)-1的基因变异与这两种疾病的易感性相关。因此,我们评估了FcγR或IL-1多态性基因的组合是否代表SLE和牙周炎的共同危险因素。
研究人群包括患有SLE和牙周炎的日本成年人(SLE+P组;n = 46)、仅患有SLE的患者(SLE组;n = 25)、仅患有牙周炎的患者(P组;n = 58)以及无全身性或口腔疾病的健康个体(H组;n = 44)。通过测量探诊深度、临床附着水平和牙槽骨丧失来评估临床牙周状况。从外周血中分离基因组DNA,并通过等位基因特异性聚合酶链反应或DNA测序分析以确定FcγR基因型(FcγRIIA、FcγRIIB、FcγRIIIA和FcγRIIIB)和IL-1基因型(IL-1A +4845和IL-1B +3954)。
与H组相比,SLE+P组中刺激性FcγRIIA的R131等位基因和抑制性FcγRIIB的232T等位基因显著过多(分别为P = 0.01和P = 0.0009)。FcγRIIA-R131和FcγRIIB-232T等位基因的组合与SLE和牙周炎有很强的相关性(SLE+P组与P组相比:P = 0.01,优势比:3.3;SLE+P组与H组相比:P = 0.0009,优势比:11.2)。此外,与其他SLE患者相比,具有FcγR风险等位基因组合的SLE患者表现出更严重的牙周组织破坏。IL-1多态性等位基因的频率过低,无法评估其与SLE或牙周炎的关联。
刺激性FcγRIIA和抑制性FcγRIIB基因型的组合可能会增加日本人群对SLE和牙周炎的易感性。