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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]

Objectives/hypothesis: The objective of this study was to describe the long-term outcomes of tracheoplasty for distal tracheal stenosis, demonstrate the utility of cardiopulmonary bypass for intraoperative airway management, and compare perioperative morbidity and mortality of slide tracheoplasty for distal tracheal stenosis to costochondral graft, and resection with end-to-end anastomosis., Study Design: Retrospective chart review., Methods: A retrospective chart review of all patients undergoing tracheoplasty for distal obstruction and also requiring the use of cardiopulmonary bypass for intraoperative airway management from 1994 to 2009 was performed. The setting for the study was a tertiary care children's hospital., Results: A total of 11 patients, aged 1 month to 12 years, were identified. Four patients underwent slide tracheoplasty, two had end-to-end anastomosis, and five had costochondral graft. Average cardiopulmonary bypass time was 120 minutes, 60 minutes, and 63 minutes, respectively. The only complication of cardiopulmonary bypass was a superficial wound infection. There was one late death due to airway obstruction after repair of severe cardiac anomalies. The numbers of bronchoscopies required for resolution of granulation tissue in the slide tracheoplasty and end-to-end anastomosis groups were less than for the cartilage graft group. Three patients in the cartilage graft group required tracheostomy, and one remained tracheostomy dependent at last follow-up. None in the slide tracheoplasty or end-to-end anastomosis groups required a tracheostomy during management., Conclusions: Improvements in operative techniques and perioperative management have led to significant decreases in morbidity and mortality. At our institution, slide tracheoplasty has become the preferred technique for all except very short segment stenosis, and cardiopulmonary bypass is used in all cases involving the distal trachea., (Copyright © 2011 The American Laryngological, Rhinological, and Otological Society, Inc.)

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.