Objectives: Once enamel is lost, dental pulp is exposed to physical, chemical and bacterial irritants through dentinal tubules. The outward fluid flow (OF) in dentin provides protection by preventing these irritants from entering the pulp via the tubules. We previously reported that lipopolysaccharide (LPS) diffusion was reduced to nearly zero in intact (ID) and demineralized dentin by OF in vitro. However, LPS is found in the tooth pulp beneath the exposed dentin in vivo. In this study, we examined the changes in hydraulic conductance (Lp) and LPS diffusion across dentin underneath early caries (ECD) compared to ID. Materials and Methods: Six ID and 11 ECD discs were prepared from the crown portion of freshly extracted human third molars. Lp of dentin was measured using a horizontally placed split chamber device. Simulation of the pulp interstitial pressure (1.47kPa) was used to produce the OF. Five of 11 ECD discs were discarded because LPS was detected before the experiment. LPS diffusion against OF through ID and ECD was measured and compared to that with non-outward flow (NF)(n=3 for each group) at 0, 1, 4 and 8h. Results: The Lp of ECD was significantly lower than that of ID (independent West, p<0.00l). The results of the amount of diffused LPS, independent of experimental period, in decreasing order are ID-NF, ECD-NF, ECD-OF, ID-OF(two-way ANOVA, p<0.001). OF reduced the diffused LPS to 1/10 in the ECD group and to 1/10
4-10
5 in the ID group. These results indicate that OF reduced the LPS diffusion of ID more than that of ECD. LPS was not detected from six of 11 ECD discs, suggesting that LPS entry may not cause reduction of the functional diameter of dentinal tubules. The hydrodynamic movement of the dentinal tubule fluid, which can cause deformation of the odontoblast cell membrane, may have triggered the reduction of the functional diameter of dentinal tubules.Conclusions: Caries is not a simple process of demineralization of hard tissues accompanied with collapse of collagen fibers, but a dynamic change in which tissue destruction and defense and repair mechanisms coexist. A decrease in outward volumetric flow rate caused by the reduced functional diameter of dentinal tubules in the inner dentin may coexist with an increase in diffusion by demineralization in the outer dentin. This breakdown of the protective mechanism is thought to result in LPS entry into the tooth pulp. Until complete obturation of dentinal tubules and/or atubular dentin formation or pulp necrosis occurs, the competition between pulpal defense mechanism and irritation entry will continue.
View full abstract