The Protective Effect of Histatins on Tooth Human Enamel Demineralization

The selective adsorption of salivary components results in the formation of an organic film on tooth surfaces known as the acquired enamel pellicle. Among several biological functions, the acquired enamel pellicle forms a selective permeable barrier that regulates mineralization/demineralization processes. While histatins are mostly known for their anti-microbial activities they are also considered to be the precursor proteins for the formation of the acquired enamel pellicle. Their functional properties after being adsorbed to the enamel surface are not well investigated. Objective: The aim of this study was to evaluate the effects of histatins on in vitro enamel demineralization. Methods: Enamel surfaces were coated with native histatin 1, histatin 3, and histatin 5, synthetic histatin 1 lacking phosphate and synthetic histatin 3 phosphorylated at residue 2. Adsorption was allowed to proceed for a period of 2 hours at 37°C with gentle agitation. Enamel specimens were then washed with distilled water and immersed into a demineralization solution containing 1% citric acid, pH 2.3 for 15 minutes. This solution was used to measure the amount of calcium and phosphate released from enamel and the mineral loss from enamel sections was evaluated by microradiography. Results: All histatin coated specimens showed a statistically significant higher protection than those not coated with histatins. Natural histatin 1 and phosphorylated histatin 3 were significantly more effective in protecting the enamel against demineralization than histatin 3, histatin 5 and the unphosphorylated histatin 1. Conclusion: The present investigation indicates that all three major histatins exhibit a protective function in reducing acid induced enamel demineralization. Furthermore, the presence of a covalently linked phosphate group (at residue 2) is able to augment this important biological function. Supported by NIH/NIDCR Grants DE05672, DE07652, DE15163, DE16699 and DE17788.