## 4 Discussion
\begin{table}
\begin{tabular}{c c c c c c c c c} \hline \hline  & **IL-23** & **sIL-23R** & **IL-17A** & **sIL-17 RA** & **IL-23-GT** & **IL-23R-GT** & **IL-17A-GT** & **IL-17 RA-GT** \\ \hline
**Power** & 0.99 * & 0.098 & 1 * & 0.99 * & 0.43 & 1 * & 0.99 * & 1 * \\
**Effect size** & 1.04 * & 0.075 & 2.02 * & 0.89 * & 0.37 & 2.61 * & 1.46 * & 2.55 * \\ \hline \hline \end{tabular}  
* GT: site of gingival tissue was obtained.
* power \(\geq\) 80 or effect size \(\geq\) 0.5.  
\end{table} 
Table 2: Power and effect size of IL-23/IL-17 axes in periodontitis. by mass spectrometric and grades of glycosylation of IL-23R [40], due to the fact that some IL-23R isoforms have been described in [PERSON]'s disease [41]. On the other hand, in plasma samples, there is a decrease in IL-17A in patients with periodontitis, similar to that reported by some authors regarding GCF [42] and plasma [22]. In contrast, other authors have described an increment in the concentration of IL-17A in different biological fluid samples from periodontitis patients [17; 18; 26], while others still failed to detect this cytokine in patients with periodontitis [12; 13]. However, IL-17A is a cytokine highly studied in inflammatory and autoimmune diseases such as Sjogren's syndrome and rheumatoid arthritis, among others [43; 44; 45; 46]. In this sense, [PERSON]. et al. [47] propose that several cytokines, such as IL-17A, are inversely proportional to the course and chronicity of rheumatoid arthritis. In addition, an increase in IL-17A was observed in the preclinical phase, and this cytokine decreases as the chronicity of RA enhances [47]. Although, periodontal disease affects the bone and periodontal tissue and is known to have a similarity to RA [48]. IL-17A in periodontitis may exhibit behavior similar to what [PERSON] et al. propose in rheumatoid arthritis. Contrary to plasma, in gingival tissue samples an increase in IL-17A was observed in periodontitis patients than HS, which coincides with that reported by [PERSON] et al., and [PERSON] et al., in gingival tissue [28; 31] as well as by [PERSON] et al., in gingival culture supernatant [21]. This increase in IL-17A can be attributed to the gingival microenvironment generated by the severity of periodontitis, since in this study all patients were between periodontal stages III and IV, being the most advanced of periodontitis [1]. This finding can apply the [PERSON] observation in some molecules, such as IL-17A that are overexpressed according to the severity and chronicity of rheumatoid arthritis [47]. Regarding sIL-17 RA in plasma, differences between HS and periodontitis patients were not found. An increase in sIL-17 RA was expected in periodontitis because in a previous study, this receptor was observed increased in the gingival tissue of patients with periodontitis [31], some considered that sIL-17 RA could be elevated in plasma because several soluble isoforms of sIL-17 RA can be secreted as a result of alternative splicing [12]. In addition, an increase in IL-17 RA has been observed in other pathologies [49; 50; 51]. On the other hand, sIL-17 RA positively correlated with the RBL%, which is a parameter that indicates the periodontal grade (severity); in this regard, the inhibitory effect of some IL-17A soluble receptors on IL-17A in vitro has been demonstrated [52; 53]. The study of the sIL-17 RA expression isoforms in periodontitis could elucidate the role that these molecules play in bone resorption in this disease. Regarding IL-17 RA in gingival tissue, an increase was observed in patients with periodontitis as reported by previous studies in patients with chronic and aggressive periodontitis [31]. It has been shown that there is an increase in RANKL produced by fibroblasts under the stimulus of IL-17A when binding to its receptor [54]. Therefore, the enhanced levels of IL-17A [21; 28; 55] and IL-17 RA [31] in the gingival tissue of patients with periodontitis reported by other authors agree with the increase in RANKL reported by [PERSON] et al. [54].