BACTERIAL METABOLITES SODIUM-BUTYRATE AND PROPIONATE INHIBIT EPITHELIAL-CELL GROWTH IN-VITRO

The structural and functional barrier preventing the free advancement of microbial plaque subgingivally along the tooth surface is formed by the junctional epithelial (JE) cells directly attached to the tooth ( DAT cells). The mechanism leading to degeneration of the DAT cells is not known. In the present study we examined the possible role of short chain fatty acids (SCFAs) on epithelial cells by making use of 2 epit helial cell cultures (HaCaT and ERM) and an explant culture model of h uman JE. The SCFAs butyrate and propionate were used in concentrations found in human plaque and gingival crevicular fluid (0.25-16.0 mM). T he SCFAs had no effect on primary cell adhesion nor on the epithelial attachment apparatus (EAA). By contrast, even 0.25 mM of butyrate sign ificantly retarded epithelial cell growth. Similar effects with propio nate were first observed at concentrations higher than 1.0 mM. The ret ardation of epithelial cell growth was found to be due to inhibition o f cell. division. Furthermore, after butyrate treatment dense accumula tions of intermediate filaments and cytoplasmic vacuolization were cha racteristically seen in cells adjacent to cells of normal appearance. This suggests that some cells of the growing epithelial cell populatio n are more sensitive to the SCFAs than others, and agrees with previou s reports on the DAT cells of periodontally-involved teeth in vivo. Th e results suggest that SCFAs are microbial factors that play a role in the initiation and progression of periodontal pocket formation by imp airing epithelial cell function rather than having a direct effect on the EAA.