Induced mineral growth for mechanical recovery of caries affected dentin

Introduction: It has been suggested that mechanical properties of dentin are related to the presence of intrafibrillar mineral (Kinney et al, JDR 2003). Remineralization of dentin can occur either by precipitation of mineral between the collagen fibrils or functionally, bound to its structure. Objective: We sought to restore the properties of artificial dentin carious lesions by inducing the formation of apatite (AP) from calcium and phosphate metastable solutions. Methods: Experiments used dentin substrates (12 mm²) partially demineralized with a 0.05M acetate buffer in pH 5.0 for 8 hours. Calcium and phosphate solutions with approximated constant composition saturated for HAP (37ºC, pH 7.4) were used for remineralization experiments. Samples were stored for 5 days, and removed at 24 hr intervals (n=5). Elastic moduli (E) of the fully hydrated tissues were measured using nanoindentation before and after experiments; mean values were analyzed by ANOVA and Tukey HSD (p<.05). Microstructural changes in the specimens were studied using AFM and SEM. Mineral formation was evaluated by infrared (FTIR) spectroscopy. Results: All specimens showed improvement in E during the remineralization process. The recovery of elastic properties was highest (65%) in samples remineralized at low crystallization rates but recovered only about 20% when remineralized at high crystallization rates. FTIR indicated the presence of apatite on the samples. SEM showed mineralized layers covering the surfaces of samples remineralized at high crystallization rates, while AFM showed little precipitate and changes in the collagen topography of samples exposed to low crystallization rates. Conclusions: Slow rates of mineral formation under constant composition allowed more recovery of dentin properties (65%) which may be related to association of mineral with the organic matrix of dentin. The results suggest insight into conditions that are required to provide functional mineralization of carious dentin lesions.

Supported by NIH/NIDCR R01DE16849.