Propionic and acetic acids potentially compromise junctional epithelial barrier function and contribute to periodontitis progression.

OBJECTIVES

Periodontitis, a leading cause of tooth loss, is driven by pathogenic bacteria through classical virulence factors, including lipopolysaccharides, fimbriae, and proteases, and metabolic products such as short-chain fatty acids (SCFAs). Among these, butyric acid (BA) and lactic acid (LA) impair proliferation, migration, and inflammatory responses of gingival or junctional epithelial cells. However, the effects of other SCFAs, particularly propionic acid (PA) and acetic acid (AA), on the junctional epithelium remain unclear. In this study, the effects of PA and AA on murine JE-1 cells derived from the gingival junctional epithelium were examined.

METHODS

JE-1 cells were treated with PA or AA. Wound healing, proliferation, viability, and cell cycle distribution were evaluated. The mRNA expression of adhesion molecules and cell cycle regulators was analyzed using quantitative reverse-transcription polymerase chain reaction.

RESULTS

PA and AA markedly delayed wound closure and inhibited cell proliferation, without affecting cell viability. Both acids downregulated Integrin α6 and Integrin β4, induced G0/G1 arrest, decreased Ccnd1 expression, and increased p21 expression.

CONCLUSIONS

PA and AA impair wound repair, proliferation, and adhesion of junctional epithelial cells by altering the progression of the cell cycle and expression of adhesion-related genes. Together with prior findings on BA and LA, these results indicate that multiple SCFAs from periodontopathic bacteria contribute to weakening of the epithelial barrier, in vitro, highlighting the requirement for in vivo studies to confirm their roles in the pathogenesis of periodontitis.