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Advances in Dental Research, Vol 15, Issue 1, 72-75
Copyright © 2001 by International & American Associations for Dental Research


Articles

The effects of high levels of glucose and insulin on type I collagen synthesis in mature human odontoblasts and pulp tissue in vitro

L Valikangas, E Pekkala, M Larmas, J Risteli, T Salo, and L Tjaderhane

Institute of Dentistry, University of Oulu, PO Box 5281, FIN-90014, University of Oulu, Finland. liisa.valikangas@oulu.fi

High levels of dietary sucrose affect the metabolism of the pulp-dentin complex and enhance the caries process in dentin. The high-sucrose diet reduces dentin formation in young rats (Tjaderhane et al., 1994; Hietala and Larmas, 1995; Tjaderhane, 1996) and in pups of rat dams fed high-sucrose diet during lactation (Pekkala et al., 2000a). However, the mechanisms behind the effects are unknown. A direct effect of elevated blood glucose or an indirect effect via insulin has been suggested. We investigated the effects of high glucose and insulin on type I collagen synthesis in human odontoblasts and pulp tissue in vitro, using an organ culture method for functional post-mitotic odontoblasts. Odontoblasts and pulp tissue were cultured separately for 10 days in DMEM with 15% FBS containing additional glucose (G) (4.45 g/L) or insulin (I) (0.6 microgram/mL) or both together (GI). We evaluated type I collagen synthesis with RIA, measuring the level of N-terminal propeptide of type I collagen (PINP) secreted into the culture media. PINP secretion decreased in odontoblasts and pulp tissue in G and GI groups when compared with the control and insulin samples (p = 0.001 in both groups in the pulp samples). Insulin alone did not affect PINP secretion distinctly. The results indicate that high levels of glucose, but not insulin, directly down-regulate the type I collagen synthesis in young, differentiated human odontoblasts and pulp tissue. Insulin does not affect the inhibitory effect of high sucrose. These in vitro findings indicate that the high-sucrose diet may alter odontoblast function independently of insulin.


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