Search

In the process of host defence against microbial challenge, neutrophils release granule contents with the potential side effect of damaging structural tissues. In the junctional epithelium such damage may contribute to the degeneration and renewal of the epithelial cells attached directly to the tooth (DAT cells), and subsequently to periodontal pocket formation. This study reports on lactoferrin, one of the substances released by neutrophils, and its effects on epithelial cell adhesion, growth, DNA synthesis and spreading of cell colonies at concentrations recorded in the crevicular fluid. We show that, in opposition to what has been reported on bacterial cells, lactoferrin has no effect on the DNA synthesis of attached epithelial cells in model systems attempting to simulate the DAT cells in vivo. However, both iron-saturated and unsaturated lactoferrin hampered cell adhesion, growth and spreading of cell colonies in a dose-dependent manner. These findings suggest that lactoferrin does not affect epithelial cell proliferation but it may have a role in delaying the repair of the DAT cell population during inflammation by interfering with cell adhesion.

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. [ABSTRACT FROM AUTHOR]

This study examined the directly attached cells (DAT cells) of the human junctional epithelium from teeth extracted for advanced periodontal disease. The monolayer nature of the DAT cells remaining on the tooth surface after extraction offers a unique opportunity to study their morphology and activity in situ. We collected DAT cells and examined them by transmission electron microscopy and by autoradiography of cells labeled with ³H-thymidine. Our morphological results suggest that degenerative changes associated with pocket formation affect individual cells rather than regions of the DAT cell population at one time. The epithelial attachment apparatus (EAA) appeared to be the most resistant structure persisting on the tooth surface during the degeneration of the individual DAT cells. The new technique developed for two-dimensional observation of the sheet of DAT cells labeled in situ on the tooth surface in culture showed that the attached cells, even in periodontal disease, exhibit proliferative ability, suggesting a regenerative role for the DAT cells. [ABSTRACT FROM AUTHOR]