Recurrent oral ulceration (RAU) is also known as recurrent aphthous stomatitis, with characters of recurrent episodes of oral ulcers. Reports indicated that RAU affects about 20% of populations [1,2]. The etiology of RAU is multifactorial, genetic, immune, nutritional, and microbial factors and local trauma might contribute to the occurrence. In addition, family history of RAU is confirmed to be a risk factor for RAU [3].
The etiology of RAU is not well demonstrated clearly, previous studies indicated that inflammatory factors play an key role in the development of RAU [4,5]. Borra et al revealed that cytokine genes in peripheral blood mononuclear cells, such as IL-2, TNF-α and IL-6, contribute to the development of RAU [6]. Other research indicated that IL-10 mRNA levels decreased in RAU patients, which suggests a failure of suppressing inflammatory reaction to oral mucosa in immune system [7].
So far, few studies reported the association between polymorphism of inflammatory genes and risk of RAU. The polymorphisms of IL-1β -3954 C/T (rs1143634), IL-6-174G/C (rs1800795), IL-10-1082A/G (rs1800896), and IL-10-819C/T (rs1800871) have been reported correlated with risk of RAU in a Chinese population [1]. While no association study about IL-17 polymorphisms and RAU was reported.
IL 17 play an important role in adaptive and innate immune systems. Five confirmed receptors (IL-17RA-RD and SEF) and six members (IL-17A-F) [8,9] of IL 17 have been identified so far. Among them, IL-17A and IL-17F are secreted by Th17 cells, and composed a distinct lineage of CD4 + effector cells [10]. As a pro-inflammatory cytokine, IL-17 could trigger the release of chemokines, cytokines, antimicrobial peptides, and matrix metalloproteinases (MMPs) from mesenchymal and myeloid cells [11]. On the other hand, IL-17 is expressed in synovial tissues, and could participate in the process of cartilage breakdown and synovial infiltration in RAU through inducing the release of chemokines from chondrocytes [12]. IL-17 also augments nitric oxide production via nuclear factor kappa B activation in RAU cartilage [13].
Compelling studies indicated that genetic polymorphisms of IL-17 are related to the susceptibility of a scope of inflammation-related diseases, including ulcerative colitis, gastric cancer, breast cancer, and rheumatoid arthritis [14–17]. So far, there is no relative report about association of IL-17 polymorphism with RAU in the publicly available Genome database, we hypothesize that IL-17 is a potential risk factor for RAU, and aim to explore the correlation between the polymorphisms of IL-17A and IL-17F with risk of RAU among Chinese population. The polymorphs of IL-17A rs2275913 and IL-17F rs763780 with the risk factors of RAU were evaluated in our recruited subjects. This case-control study was designed to explore the relationship of these two SNPs with the morbidity and severity of RA.