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Epithelial cell response to challenge of bacterial lipoteichoic acids and lipopolysaccharides in vitro

M.T. PÖLLÄNEN, J.I. SALONEN^*, D. GRENIER and V.-J. UITTO

Institute of Dentistry, University of Turku, Finland, *Kuwait University, Faculty of Dentistry, Safat, Kuwait, Universite Laval, Quebec and University of British Columbia, Vancouver, Canada

Corresponding author: Dr M. T. Pöllänen (e-mail: marja.pollanen{at}utu.fi).

Received 8 March 1999; revised version accepted 13 Aug. 1999.

Abstract

Accumulating dental plaque at the gingival margin contains lipoteichoic acids (LTAs) from the cell walls of gram-positive bacteria. In subgingival plaque associated with periodontal disease the amount of lipopolysaccharides (LPSs) from gram-negative bacteria increases. As the gingival junctional epithelium (JE) is an important structural and functional tissue, participating in the first line defence against apical advancement of dental plaque, this study examined the direct effects of LTAs (from Streptococcus mutans and S. sanguis) and LPSs (from Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, Treponema denticola and Escherichia coli) on two epithelial cell lines (HaCaT and ERM) and a culture model for human JE. The cells were exposed to the LTAs or LPSs (10–50 µg/ml) for variable periods of time. None of the bacterial surface components had any effect on primary adhesion or on the epithelial attachment of the JE cultures. However, cell growth and mitotic activity were consistently reduced in all cultures treated with LTAs. In contrast, LPSs showed only slight or no effects on cell growth and mitotic activity depending on the epithelial cells used. This suggests that LPSs, despite their established role as modulators of inflammation, do not have direct harmful effects – at the concentrations found in dental plaque and gingival crevicular fluid – which would explain the mechanism of epithelial degeneration and detachment from the tooth surface. However, the LTAs appear to inhibit the renewal of epithelium and may thus contribute to degeneration of coronal JE and subgingival colonisation by periodontal pathogens.

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