Bacterial metabolites sodium butyrate and propionate inhibit epithelial cell growth in vitro.
Department of Periodontology, University of Turku, Finland. marja.pollanen@utu.fi
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 epithelial cell cultures (HaCaT and
ERM) and an explant culture model of human JE. The SCFAs butyrate and
propionate were used in concentrations found in human plaque and
gingival crevicular fluid (0.25-16.0 mM). The SCFAs had no effect on
primary cell adhesion nor on the epithelial attachment apparatus (EAA).
By contrast, even 0.25 mM of butyrate significantly retarded epithelial
cell growth. Similar effects with propionate were first observed at
concentrations higher than 1.0 mM. The retardation of epithelial cell
growth was found to be due to inhibition of cell division. Furthermore,
after butyrate treatment dense accumulations of intermediate filaments
and cytoplasmic vacuolization were characteristically seen in cells
adjacent to cells of normal appearance. This suggests that some cells
of the growing epithelial cell population are more sensitive to the
SCFAs than others, and agrees with previous reports on the DAT cells of
periodontally-involved teeth in vivo. The results suggest that SCFAs
are microbial factors that play a role in the initiation and
progression of periodontal pocket formation by impairing epithelial
cell function rather than having a direct effect on the EAA.
PMID: 9138199 [PubMed - indexed for MEDLINE]
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