Abstract
BackgroundPeriodontopathic bacteria such as Porphyromonas gingivalis produce a large amount of butyric acid as a metabolite. Though butyric acid has been reported to have an anti-inflammatory effect on inflammatory diseases in the gastrointestinal tract, it has been suggested to contribute to the progression of periodontal disease in the oral cavity. The concentration of butyric acid in periodontal tissue of patients with periodontitis patients is reported to increase with the progress of the periodontal disease state. However, the influence of butyric acid on periodontal disease progression is not well known.Main textIn this review, we have considered the relationship between butyric acid and periodontal disease with respect to the findings reported till date and the knowledge we newly obtained [Shirasugi M et al. Biochem Biophys Res Commun, 2017]. We have studied the relationship between butyric acid and periodontal disease by analyzing the effect of butyric acid on normal human gingival fibroblasts, which are a major component of periodontal tissue. We observed that gingival fibroblasts underwent cytostasis and apoptosis via extrinsic and intrinsic pathways upon long-term exposure to butyric acid. In addition, we showed that TNF-α produced by gingival fibroblasts treated with butyric acid plays an important role in inducing exogenous apoptosis.ConclusionButyric acid produced by periodontopathic bacteria may promote progress of the periodontal disease state. Butyric acid is known to act as an HDAC inhibitor. Thus, we believe that advanced epigenetic analysis of the effects of butyric acid on gingival fibroblasts will help elucidate the periodontal disease pathology and facilitate discovery of new targets for periodontal disease treatment.
Highlights
In this review, we have considered the relationship between butyric acid and periodontal disease with respect to the findings reported till date and the knowledge we newly obtained [Shirasugi M et al Biochem Biophys Res Commun, 2017]
Past studies on periodontal diseases have been focused on pathogenic factors such as LPS from periodontal pathogens represented by the Red complex (Porphyromonas gingivalis, Treponema denticola, Tannerella forsythensis)
As periodontal disease is chronic in nature, we considered that periodontal tissues are exposed to pathogenic factors for a long time during periodontal disease progression
Summary
High concentration of butyrate-induced apoptosis in inflamed-human gingival fibroblasts High concentrations of butyric acid are reported to induce apoptosis in immune cells [17,18,19]. Ochiai et al have reported that high concentration of butyrate induces apoptosis in human gingival fibroblasts (HGFs) collected from inflamed sites of patients with periodontal disease [16]. It is considered that normal (healthy) human gingival fibroblasts are exposed to butyric acid for a long time in the process of periodontal disease progression. In the presence of TNF-α neutralizing antibody, activation of Caspase 8 and expression of IL-6 mRNA were not observed in HGFs despite butyric acid stimulation [23] These results suggest that TNF-α produced by HGFs exposed to butyric acid contributes to induce extrinsic apoptosis and enhance proinflammatory cytokine expression (Fig. 1). It is necessary to further investigate whether the susceptibility of HGFs to TNF-α is altered by butyric acid, using epigenetic analysis
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