Periodontitis is a prevalent chronic inflammatory disease due to the host response (IL-1β, IL-6, TNF-α and IL-17A) to oral bacteria such as Porphyromonas gingivalis.
Interleukin-1 beta (IL-1 beta) mRNA-expressing cells in human gingival crevicular washings (GCW) obtained from patients with periodontitis and healthy controls were examined by in situ hybridization.
Interleukin-1 beta (IL-1 beta) is a potent regulator of osteoprogenitor cells and fibroblasts, and is believed to be responsible for the bone loss and connective tissue breakdown that occurs in periodontitis.
A total of 106 patients hospitalized with ACS or angina were compared to a group of 1,959 individuals tested for susceptibility to periodontitis by profiling the IL-1 gene.
A total of 52 teeth (3.3%) out of 1,566 were lost due to periodontitis between T0 and T2; 28 of 957 (2.9%) in the IL-1 genotype negative group and 24 of 609 (3.9%) in IL-1 genotype positive group.
Also, we found three negative associated haplotypes with PE: IL-1α + 4845 G/IL-1β -511 A, IL-1β + 3954 C/IL-1β -511 A and interestingly IL-1α -889 C/IL-1β -511 A also with a positive association with RA.
Another IL-1 genetic pattern, characterized by the IL-1B (-511) and IL-1RN (+2018) markers, is associated with atherosclerotic plaque formation, as measured by angiography and arterial wall thickness, but not periodontitis.
Are selected IL-1 polymorphisms and selected subgingival microorganisms significantly associated to periodontitis in type 2 diabetes patients? a clinical study.
As an in vitro model for gingivitis and periodontitis, immortalized human gingival keratinocytes (IHGK) were stimulated with the proinflammatory cytokine interleukin-1beta.
As one of the most important primary proinflammatory cytokines, interleukin 1β (IL1β) plays an essential role during the early stage of periodontitis and its amounts simultaneously increase dramatically during this stage.
Decreased salivary trappin-2 and increased IL-1β levels in individuals with periodontitis, compared with healthy individuals, may implicate a potential antiprotease/proinflammatory cytokine imbalance, resulting in impaired host protective capacity.
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.
Diabetic conditions such as HG induce IL-1β and sIL-6R production from macrophages in inflammatory periodontal tissues and may exacerbate the periodontitis synergistically via MMP-1 production from HGFs.
Functionally, the specific periodontitis-associated IL-1 genotype comprises a variant in the IL-1B gene that is associated with high levels of IL-1 production.
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.