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    Boric acid alleviates periodontal inflammation induced by IL-1? in human gingival fibroblasts
    (Elsevier Gmbh, 2024) Bozkurt, Serife Buket; Hakki, Sema S.; Nielsen, Forrest H.
    Background: Boric acid (BA) has been found to have therapeutic effects on periodontal disease through beneficially affecting antibacterial, anti-viral, and anti-inflammatory actions. Methods: This study was conducted to determine the effect of BA on cell viability and on mRNA expressions of proinflammatory and anti-inflammatory cytokines and on oxidative stress enzymes induced by IL-1 beta (1 ng/mL) in Human Gingival Fibroblasts (HGF) cultured for 24 and 72 h in DMEM media. The BA concentrations added to the media were 0.09 %, 0.18 %, 0.37 %, and 0.75 %. Results: All of the BA concentrations increased the viability of cell cultured in DMEM media only, indicating that these concentrations were not toxic and actually beneficial to cell viability. The addition of 1 ng/m: of IL-1 beta decreased cell viability that was overcome by all concentrations of BA at both 24 and 72 h. The IL-1 beta addition to the media increased the expressions of the proinflammatory cytokines IL-1 beta, IL-6, IL-8, and IL-17; the antiinflammatory cytokine IL-10; and the oxidative stress enzymes superoxide dismutase (SOD0 and glutathione peroxidase (GPX). The IL-1 beta induced increase mRNA expression of IL-1 beta was decreased at 24 h by the 0.37 % and 0.75 % BA additions to the media and decreased in a dose-dependent manner by all concentrations of BA at 72 h. The IL-1 beta induced increase in the expression of IL-6 was decreased in dose-dependent manner at 72 h by BA. All BA concentrations decreased the IL-1 beta induced expression of IL-8 at both 24 and 72 h. The induced increase in IL17 by IL-1 beta was not significantly affected by the BA additions. The increase in the anti-inflammatory cytokine IL10 induced by IL-1 beta was increased further by all BA additions in dose dependent manner at both 24 and 72 h. The mRNA expressions of SOD and GPX increased by IL-1 beta were further increased by the 0.37 % and 0.75 % BA concentrations at 72 h. Conclusions: These findings indicate that BA can significantly modulate the cytokines that are involved in inflammatory stress and reactive oxygen species action and thus could be an effective therapeutic agent in the treatment of periodontal disease.
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    Boric Acid Reverses Nicotine-Induced Cytokine Expressions of Human Gingival Fibroblasts
    (Springernature, 2023) Bozkurt, Serife Buket; Nielsen, Forrest H.; Hakki, Sema S.
    Nicotine, the major bioactive ingredient in tobacco, is a major risk factor for periodontal disease and destruction. Nicotine has been shown to stimulate the production of cytokines that are priming agents for inflammation that induces tissue destruction, such as IL-1 beta, IL-6, and IL-8, by gingival keratinocytes and human gingival fibroblasts (HGF). Boron as boric acid has been found to decrease pro-inflammatory cytokines and increase anti-inflammatory cytokines in cells with inflammatory stress. Thus, a study was performed to determine whether boric acid reverses negative effects of nicotine on human gingival fibroblasts (HGFs). The viability and cytokine expressions of HGFs cultured for 24 and 72 h in control medium with no nicotine or boric acid added and in media containing only nicotine, only boric acid, or a combination of BA and nicotine were determined. Nicotine in concentrations of 10(-1), 10(-2), 10(-3),10(-4), 10(-5), and 10(-6) mM significantly reduced cell viability compared to the control. Boric acid at 10 and 50 ng/mL in the media partially restored and 100 ng/mL in the media fully restored the nicotine-depressed HGF cell viability to the same level as the control group. Nicotine elevated the expression of pro-inflammatory cytokines TNF-alpha, IL-1 beta, IL-6, IL-8, and IL-17 and decreased the anti-inflammatory IL-10 in HGFs at 24 and 72 h. Boric acid at 100 ng/mL in the medium prevented the changes induced by nicotine alone. The findings indicate that boric acid can inhibit or reverse nicotine-induced pathology in periodontal tissue and thus may help maintain oral and periodontal health in tobacco users.