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.
In this experiment, the periodontal bone defects were established in periodontitis rats; recombinant human progranulin (rhPGRN), tumor necrosis factor alpha inhibitor (anti-TNF-α), or phosphate buffer saline (PBS)-loaded collagen membrane scaffolds were implanted within defects and the rats were sacrificed at scheduled time points.
Inflammatory periodontitis induced by P. gingivalis increased alveolar bone resorption and increased expression of TNF-α and IL-1β, while BV treatment resulted in decreased bone loss and pro-inflammatory cytokines.
Leukocyte and macrophage number and protein level of tumor necrosis factor <i>α</i> (TNF-<i>α</i>) in periodontium and serum interleukin-6 level were downregulated by HF diet in periodontitis mice (<i>P</i> < 0.05).
Individuals with periodontitis have increased systemic levels of acute phase proteins, plasma antibody levels, coagulation factor, total white blood cell count, neutrophils, C reactive protein (CRP), and cytokines such as INF- gamma (Interferon gamma), TNF-α (Tumor necrosis Factor- Alpha), IL (Interleukin)-1β, IL-2 and IL-6.
The results suggest that the evolution of gingivitis to periodontitis is related to the accumulation of activated Th1 cells (IFN-γ and TNF-α) associated with the presence of increased IL-17.
Increased GCF HIF-1α, VEGF, and TNF-α levels in both chronic and aggressive form of periodontitis might suggest the role of TNF-α/HIF-1α/VEGF pathway in the pathogenesis of periodontal diseases.
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.
One hundred and eight male Wister rats were randomly assigned into three groups: control (healthy) group, periodontitis group, and periodontitis plus human tumor necrosis factor receptorII:IgG Fc fusion protein (rhTNFR:Fc) group.
In addition, individuals with diabetes and periodontitis exhibit high levels of circulating TNF-α, CRP and mediators of oxidative stress, and successful periodontal treatment reduces their levels.
Women with periodontitis exhibited significantly higher levels (<i>p</i> = 0.001) of salivary IL-6 and TNF-α compared with the healthy group: 25.1 (±11.2) pg/mL vs. 16.3 (±5.0) pg/mL and 29.7 (±17.2) pg/mL vs. 16.2 (±7.6) pg/mL, approximately 1.5 and 1.8 times more, respectively.
This study aimed to investigate the chemical characteristics and the effects of an orabase gel with Cashew Gum Polysaccharide (CG-P) from Anacardium occidentale L. on alveolar bone loss and relative mRNA expression of TNF-α, IL-1β, RANK, RANKL, and OPG in the periodontal tissue of Wistar rats (Rattus norvegicus) subjected to ligature-induced periodontitis.
The aim of this study is to compare periodontitis prevalence between controls and patients with OSA by assessing clinical periodontal parameters and gingival crevicular fluid (GCF) levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and high-sensitive C-reactive protein (hs-CRP); serum hs-CRP was also sampled.
Root resorption is a common phenomenon presented in periodontitis and orthodontic treatment, both of which are accompanied by an elevated TNF-α expression level in the periodontal tissues.
In addition, human gingival fibroblasts (HGFs) were tested for production of IL-6 and MMP-2 after stimulation with hydrocortisone (HC), MIF, tumour necrosis factor-alpha (TNF-α), or Fusobacterium nucleatum, a pathogen known to elicit immune responses during periodontitis.
Denervation effectively aggravates ligature-induced rat periodontitis by the NF-κB signaling pathway for excessive production of IL-1β and TNF-α and increased osteoclasts for decreased OPG/RANKL ratio.
The objective of this study was to determine the effect of TNF-α expression of osteocytic RANKL and sclerostin in type 1 diabetes rats with periodontitis using infliximab (IFX), a TNF-α antagonist.
Visfatin was positively correlated with the levels of NF-κB<sub>1</sub> (r = 0.549, P < 0.05), NF-κB<sub>2</sub> (r = 0.636, P < 0.05), PI3k (r = 0.682, P < 0.01), TNF-α (r = 0.558, P < 0.05), and IL-1β (r = 0.686, P < 0.01) in the tissues with periodontitis.
Tumor necrosis factor alpha (TNF-α)-induced osteoclastogenesis have profound effects in states of inflammatory osteolysis such as rheumatoid arthritis, periprosthetic implant loosening, and periodontitis.