Abstract
Purpose: To elucidate the effects of butyric acid (BA), a metabolite of bacteria involved in periodontitis, and a possible enhancer of the junctional epithelial cells. Methods: A murine junctional epithelial cell line, JE-1, was used to assess the effects of sodium butyrate (NaB) as BA. Cell proliferation, migration and attachment were analyzed. Additionally, gene and promoter expression analysis was performed, i.e., cap analysis of gene expression (CAGE) and gene ontology (GO) term enrichment analysis. Results: NaB affected junctional epithelial cell proliferation, migration and attachment. A high concentration of NaB caused cell death and a low concentration tended to promote migration and adhesion. CAGE analysis revealed 75 upregulated and 96 downregulated genes in the cells after 0.2 mM NaB stimulation for 3 h. Regarding GO term enrichment, the genes upregulated >4-fold participated predominantly in cell migration and proliferation. The results of this study suggest that BA produced from periodontopathic bacteria is involved in periodontal tissue destruction at high concentrations. Furthermore, at low concentrations, BA potentially participates in periodontal disease progression by increasing proliferation, migration and attachment of the junctional epithelium and thereby increasing epithelial down-growth.
Highlights
Periodontitis is a chronic multifactorial inflammatory disease associated with dysbiotic dental plaque biofilms [1]
The results of the present study show that butyric acid (BA) participates in the progression of periodontitis by increasing the proliferation, migration and attachment of the junctional epithelium
We investigated the effects on tissue destruction involved in the progression of periodontal disease
Summary
Periodontitis is a chronic multifactorial inflammatory disease associated with dysbiotic dental plaque biofilms [1]. Previous studies have associated periodontal diseases with the risk of various human malignant neoplasms, such as poorly differentiated oral squamous cell carcinoma [13,14], as well as preterm birth and low birth weight [15,16]. The periodontal ligament is destroyed by inflammation and the junctional epithelium enters a state of attachment loss in which the epithelium progresses and propagates onto the cementum towards the root apex side. Thereafter, attachment loss continues from the crown side, and a periodontal pocket is formed between the tooth surface and the gingiva [17,18]. The majority of previous studies have focused on pathogenic factors, such as fimbriae, lipopolysaccharides and exotoxins, of periodontopathic bacteria represented by the “red complex” species
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