## 3 Results  
A total of 26 studies were positioned as a result of the preliminary search. Of these, following screening and application of the inclusion and exclusion criteria, only three clinical studies remained after all the filters and crosswords were applied, and these were the ones that made up the final sample (Tables 2 and 3). Figure 1 displays the flowchart (PRISMA) of the bibliographic searches and demonstrates the results obtained initially and after applying the filters \"in vivo,\" \"clinical study,\" and \"period from 2000 to 2022,\" indicating the scarcity of clinical trials on the topic. After applying filters based on sources of data collection, a total of three papers emerged as relevant for this section and were considered for analysis. The selection process is outlined in Figure 1. The three studies that fulfilled the eligibility criteria (Table 3) were observational (one cross-sectional and two case-control studies) and examined the role of the NRLP3 in mediating the relationship between periodontitis and diabetes. Unfortunately, these studies presented their results in various formats, making meta-analysis impossible.  
\begin{table}
\begin{tabular}{c c c c c c c} \hline
**Author** & **Year** & **Study Design** & **Population** & **Samples** & **Experimental Analysis** & **Main Findings** \\ \hline [PERSON] et al. (2017) & 2015 & Case-control & \begin{tabular}{c} 20 healthy individuals; \\ 20 patients diagnosed with \\ predictions; 12 subjects presenting \\ periodontitis and \\ type 2 diabetes. \\ \end{tabular} & \
\begin{tabular}{c} Human ging/val epithelial \\ cells (HCCs). \\ \end{tabular} & Immunohistochemistry (HC). & Expression levels of NLBP3, \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\  & & & & & & \\ \end{tabular} &
\begin{tabular}{c} A significant elevation in the expression of \\ inflammatory changes (H-c, L-1,1-10) was \\ observed affect affect classifications for NLBP3. \\ \(P\)-HC (\(\%\)) of the NLBP3 and NLBP3.  
Figure 2 shows a schematic illustration of the mechanisms of NLRP3 activation in periodontitis and diabetes.  
Periodontal pathogens and hyperglicemia promote the expression of NLRP3 inflammatory leading to an inflammatory response, pyproptosis, periodontal bone resorption, and development of diabetes.  
The number of participants/samples in each study ranged from 40 to 60, and a total of 32 patients with periodontitis and diabetes completed the studies until the end. The number was not specified in one study. In two of the three studies, immunochemical analysis was used, while PCR and Quantitative real-time polymerase chain reaction (qRT-PCR), Enzyme-linked immunosorbent assay (ELISA), and Western blot (WB) were used in 1 study each. As shown in Table 3: [PERSON] et al. [27] revealed that NLRP3 inflammosome was upregulated in patients with periodontitis and diabetes and significantly increased IL-1\(\beta\) levels; [PERSON] et al. [28] showed that NLRP3 mRNA as well as its protein was overexpressed in patients manifesting both diseases in comparison with the healthy group; the findings of [PERSON] et al. [28] suggested that enhanced expression and activation of proteins related to the NLRP3 inflammasome may promote the impairment of periodontal inflammation and pathogenesis manifested in T2D because the protein levels of NLRP3, ASC, caspase-1, and IL -1 were higher in patients with periodontitis and diabetes.  
\begin{table}
\begin{tabular}{c c c} \hline \hline  & **Number** & **Reference:** & **Summary Comment for Exclusion** \\ \hline  
len [PERSON] et al., 2015 [52] & Study not relevant to the research question and outcomes \\ \hline \hline \end{tabular}
\end{table}
Table 3: Excluded studies with rationale.