## 1 Introduction  
Periodontitis is caused by multiple risk factors such as bacterial dysbiosis, destructive host immune responses, and environmental factors such as smoking [1]. It is distinguished by an immuno-inflammatory solid response characterized by gingival inflammation, periodontal pockets (sites with deep probing depths), attachment loss, and radiographic bone loss [1, 2]. However, dysbiosis is not sufficient to induce loss of attachment or erosion of the alveolar bone [3]. In this context, dendritic cells and macrophages stimulated by periodontal pathogenic bacteria produce IL-23 which plays an important role in the innate immune responses to bacterial and fungal infections diseases [4, 5]. IL-23 binds to IL-23R which is expressed in several cells such as macrophages, dendritic cells, and natural killer (NK) cells, but principally on Th17 cells [6]. After binding of IL-23 to IL-23R, Th17 cells become activated and release IL-17A, IL-17F, IL-6, IL-22, and tumor necrosis factor \(\alpha\) (TNF-\(\alpha\)) [6, 7], and the receptor activator of the NF-\(\kappa\)B ligand (RANKL) [8]. IL-17 activates cells such as fibroblasts through the IL-17A receptor (IL-17 RA/RC) and induces the release of RANKL [9]. RANKL released by fibroblasts and Th17 cells binds to RANKexpressed on osteoclast precursor and induces their maturation to initiate bone destruction in periodontitis [9].  
Significantly, IL-23R and IL-17 RA can be in soluble form (sIL-23R and sIL-17 RA) [10]. IL-23 binds to IL-23R and forms a complex (IL-23-IL-23R), acting as an inhibitor or activator of Th17 cell signaling [10; 11] while sIL-17 RA can function as a blocker of IL-17A signaling [12].  
IL-23/IL-17 axis in periodontitis has been studied in different biological samples. Regarding IL-23 in gingival crevicular fluid (CGF), high concentrations have been reported in patients with periodontitis [13; 14], as well as in saliva [15]. Contrary to [PERSON] et al., who found decreased IL-23 when compared to healthy subjects (HS) [16]. On the other hand, some study groups did not observe significant differences in IL-23 between HS and periodontitis in GCF samples [17; 18]. Other study groups demonstrated that patients with periodontitis have higher levels of IL-23 compared in serum and plasma [19; 20]. Regarding IL-17 concentrations, elevated concentrations have been reported in CGF samples from patients with periodontitis compared to HS [17; 21; 22; 23]. Elevated concentrations of IL-17A were reported in serum, plasma, and saliva samples in patients with periodontitis compared to HS [13; 14; 15; 24; 25]. Contrarily, [PERSON] et al., found higher IL-17 in the saliva of HS compared to patients with periodontitis [26], but in other study however, in another study, there were no significant differences [27].  
In gingival tissue samples, few working groups have evaluated the IL-23/IL-17 axis, of which IL-17 is elevated in patients with periodontitis compared to healthy subjects [21; 28]. However, [PERSON] et al. only detected IL-17A in 10 of 16 gingival tissue samples from patients with periodontitis [29]. [PERSON] [PERSON] et al., reported higher IL-23 and IL-23R mRNA expression in early and advanced periodontal lesions compared to biopsies from healthy sites of periodontitis [30].  
Regarding the receptors of IL-23R and IL-17 RA, our study group have described that IL-23R is diminished and IL-17 RA increased in gingival tissue from chronic and aggressive periodontitis patients [31]. Based on studies conducted on gingival tissue of the IL-23/IL-17 axis in periodontitis patients diagnosed according to the 1999 classification, we hypothesized that the molecules of the IL-23/IL-17A axis are increased in the gingival tissue in periodontitis coupled with the progression and severity of periodontitis based on the classification of periodontal disease (2018).