The overall analyses verified that the IL-10rs1800872 polymorphism was significantly associated with an increased risk of periodontitis in the allelic model, homozygote model, dominant model, and recessive model (A vs C: OR = 1.28, 95%CI = 1.11-1.49, P = .00, I = 56.87%; AA vs CC: OR = 2.06, 95%CI = 1.32-3.23, P = .00, I = 73.3%; AA + AC vs CC: OR = 1.42, 95%CI = 1.03-1.96, P = .03, I = 76.2%; AA vs AC + CC: OR = 1.78, 95%CI = 1.26-2.56, P = .00, I = 76.7%).
In the chronic migraine group, patients with periodontitis had greater levels of serum CGRP (19.7 ± 6.5 versus 15.3 ± 6.2 pg/mL, P < 0.0001) and IL-6 (15.1 ± 9.2 versus 9.6 ± 6.3 pg/mL, P < 0.0001) while non-significant differences were observed with IL-10 (2.0 ± 1.0 versus 2.8 ± 1.5 pg/mL, P = 0.675) concentrations than those without periodontitis.
However, the frequency of GG genotype in IL-10 -1082 (G/A) polymorphic region was higher in normal subjects and was associated with the decreased risk of periodontitis under recessive model [OR = 2.89, 95% CI (0.99-8.43), p = 0.039].
The studies reviewed support that the IL-10rs1800871 and rs1800872 polymorphisms may represent a potential genetic biomarker for periodontitis risk in Latin American populations.
Additionally, we found that B10 cell transfer into the experimental periodontitis ones resulted in increased IL-10 (P < 0.05), but decreased IL-17 (P < 0.05) and receptor activator for nuclear factor κB ligand (RANKL) (P < 0.05) gene and protein expression in local lesions.
The blockage of androgen receptor significantly increased radiographic bone loss and tissue levels of IL-1α (P <0.05), IL-1β (P <0.001) and IL-10 (P <0.01) compared with the periodontitis group.
We show herein that, ASA-BMMSCs treatment reduced inflammatory infiltration and alveolar bone loss in periodontitis rats, reflected by immunohistochemistry staining of OPG/RANK-L and Micro-CT. Levels of TNF-α and IL-17 decreased while IL-10 increased after the treatment of ASA-BMMSCs in periodontitis rats.
Contribution of Interleukin-10-592 (-590, -597) C>A Polymorphisms to Periodontitis Susceptibility: An Updated Meta-Analysis Based on 18 Case-Control Studies.
For individual studies, odds ratio (OR) and its 95%confidence interval (CI) were calculated to assess the strength of association between IL10 polymorphisms (- 1082 A > G, -819C > T, - 592 A > C) and the risk of periodontitis.
Protein analysis demonstrated higher levels of the TGFβ1 and IL10 cytokines in periodontitis tissues and in B-cell and plasma cell predominant gingival tissues than in healthy/gingivitis tissues and T-cell predominant gingival tissues.
Ligature-induced periodontitis exhibited similar patterns of bone loss and inflammatory cytokine profile in both groups of mice, except that the level of Il10 was elevated (P = .0114) whereas the Rankl/Opg ratio was not elevated (P = .9755) in Tlr2-KO mice compared with control mice.
More IL-1β, IL-6, IL-17A, and RANKL, and less IL-10 and TGF-β are also detected in the gingiva and CLNs from animals with periodontitis than the one from healthy animals.
The percentages of CD25<sup>+</sup>Foxp3<sup>+</sup> Treg significantly increased in the peripheral blood, which was consistent with gingival tissues study that Treg cells related transcription factor Foxp3 mRNA and cytokines IL-10 and TGF-β increased in the course of periodontitis.
This study was conducted to determine the effect of local B10 cell induction on periodontal inflammation and bone loss in ligature-induced experimental periodontitis in vivo Purified spleen B cells from C57BL/6J mice (8 to 10 weeks old) were cultured with CD40 ligand (CD40L) and the Toll-like receptor 9 (TLR9) agonist cytidine-phosphate-guanosine oligodeoxynucleotide (CpG) to determine effective IL-10 induction in vitro Silk ligatures (size 7-0) were tied around the mouse maxillary second molars on day 0, followed by the injection of CD40L and CpG into the palatal gingiva on days 3, 6, and 9.
The mRNA and protein levels of IL-10, IL-1β, and RANKL, as well as mRNA levels of TNF-α, were positively correlated with the number of IL-10 producing CD19<sup>+</sup> B cells, which highlights the importance of these factors in the development and progression of periodontitis.
Interleukin-10 gene promoter polymorphisms have been associated with interleukin-10 decreased production, thereby playing a role in the pathogenesis of periodontitis.
When comparing genotype/allele frequencies in periodontitis versus healthy and periodontitis versus gingivitis scenarios, the number of positive associations (2-4) and the degree of association (p and odds ratio values) were significantly increased by the new approach proposed (periodontitis versus gingivitis), suggesting the association of IL1B-3954, TNFA-308, IL10-592 and TLR4-299 with periodontitis risk.
We found that there was no association between IL-10 -1082 gene polymorphism and periodontitis risk (either CP or AgP), even when we separately investigated sub-group analysis among Caucasians.
The transcription factor Sp1 was present in large amounts in periodontitis lesions, and the local expression of Sp1 was related to the -1087 IL-10 SNP.
Interleukin-10 (-592 C/A) and interleukin-12B (+16974 A/C) gene polymorphisms and the interleukin-10 ATA haplotype are associated with periodontitis in a Taiwanese population.