In our study, we found that 3 hub DElncRNAs (LINC00687, LBX2-AS1 and LINC01566) may be involved in the pathogenesis of periodontitis based on WGCNA and Limma analysis.
Patients with PD exhibited higher mean SBP [weighted mean difference (WMD) of 4.49 mmHg; 95% CI: 2.88-6.11] and DBP (2.03 mmHg; 95% CI: 1.25-2.81) when compared with non-PD.
Patients with PD exhibited higher mean SBP [weighted mean difference (WMD) of 4.49 mmHg; 95% CI: 2.88-6.11] and DBP (2.03 mmHg; 95% CI: 1.25-2.81) when compared with non-PD.
Thus, the data suggest that SH3BP2-SYK is a novel signaling axis for regulating alveolar bone loss in periodontitis and that SYK can be a potential therapeutic target to suppress alveolar bone resorption in periodontal diseases.
Our findings suggest that due to CATR domains, LMP1 contributes to the progression of periodontitis via IL8 production attributable to NF-ĸB activation.
Thus, the data suggest that SH3BP2-SYK is a novel signaling axis for regulating alveolar bone loss in periodontitis and that SYK can be a potential therapeutic target to suppress alveolar bone resorption in periodontal diseases.
Promotive effect on osteogenic activities by microRNA-335-5p (miR-335-5p) has been well demonstrated, but its role involved in the pathogenesis of periodontitis remains elusive.
Patients with PD exhibited higher mean SBP [weighted mean difference (WMD) of 4.49 mmHg; 95% CI: 2.88-6.11] and DBP (2.03 mmHg; 95% CI: 1.25-2.81) when compared with non-PD.
In our study, we found that 3 hub DElncRNAs (LINC00687, LBX2-AS1 and LINC01566) may be involved in the pathogenesis of periodontitis based on WGCNA and Limma analysis.
The results of the present study agree with previous studies in the literature showing an up-regulated trend in the levels of azurocidin in periodontitis patients.
Significant positive correlation between PD and both CD103 and CD69 epithelial expression was observed in tissue specimens from periodontitis patients (P < .001).
The total amounts and concentrations of SLIT3 and RANKL were significantly higher in periodontitis than those in healthy, while the level of OPG was significantly lower (p < .05).
The infiltration of macrophages, TLR9, autophagy proteins (TFEB and LC3) and inflammatory cytokines increased in the periodontitis-with-RA group and was reduced by the inhibition of Ctsk in the periodontal region.
Clinical (PI, plaque index; GI, gingival index; PD, probing depth; CAL, clinical attachment loss; and BOP, bleeding on probing scores) and ultrasonographic (thickness and elasticity of the masseter muscle) measurements of periodontitis were performed.
Lastly, the leading SNP rs2723183 (p = 3.93E-07) was predicted to regulate local gene IL-37 expression in PD (p = 2.64E-05; in GSE10334) and change regulatory motif RXRA.
In addition, miR-22-3p also upregulated the expression levels of the inflammatory cytokines tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-8 in PDLSC through SIRT1 pathway and downregulated the expression of TLR-2 and TLR-4. miR-22-3p is a new target either for the treatment of periodontitis or the improvement of inflammation caused by orthodontics.
Lastly, the leading SNP rs2723183 (p = 3.93E-07) was predicted to regulate local gene IL-37 expression in PD (p = 2.64E-05; in GSE10334) and change regulatory motif RXRA.
Also, a combination of the four key biomarkers (IL-1β, IL-6, MMP-8 and MIP-1α) showed promising results for distinction between gingivitis and periodontitis, as well as for periodontitis compared with gingival health.