Background: The pathobiology of systemic lupus erythematosus (SLE) is similar to that of periodontitis in that the immunoglobulin G Fc receptor (FcγR) and proinflammatory cytokines play an important role. Genetic variations of FcγR and interleukin (IL)-1 are associated with susceptibility to both diseases. Therefore, we evaluated whether the combination of FcγR or IL-1 polymorphic genes represents a common risk factor for SLE and periodontitis.
Methods: 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 FcγR genotypes (FcγRIIA, FcγRIIB, FcγRIIIA, and FcγRIIIB) and IL-1 genotypes (IL-1A +4845 and IL-1B +3954) by allele-specific polymerase chain reactions or DNA sequencing.
Results: A significant overrepresentation of the R131 allele of stimulatory FcγRIIA and the 232T allele of inhibitory FcγRIIB was found in the SLE+P group compared to the H group (P = 0.01 and P = 0.0009, respectively). The combination of FcγRIIA-R131 and FcγRIIB-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 FcγR 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.
Conclusion: The combination of stimulatory FcγRIIA and inhibitory FcγRIIB genotypes may increase susceptibility to SLE and periodontitis in the Japanese population.
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