The leucine-rich amelogenin peptide alters the amelogenin null enamel phenotype.

INTRODUCTION: The amelogenin proteins secreted by ameloblasts during dental enamel development are required for normal enamel structure. Amelx null (KO) mice have hypoplastic, disorganized enamel similar to that of human patients with mutations in the AMELX gene, and provide a model system for studies of the enamel defect amelogenesis imperfecta. Because many amelogenin proteins are present in developing enamel due to RNA alternative splicing and proteolytic processing, understanding the function of individual amelogenins has been challenging. PURPOSE: Our objective was to better understand the role of LRAP, a 59 amino acid leucine-rich amelogenin peptide, in the development of enamel. APPROACH: Teeth from transgenic mice that express LRAP under control of the Amelx regulatory regions were analyzed for mechanical properties, and transgenic males were mated with female KO mice. Male offspring with a null background that were transgene positive or transgene negative were compared to determine phenotypic differences using microcomputed tomography (microCT) and scanning electron microscopy (SEM). RESULTS: Nanoindentation revealed no differences between LRAP transgenic and wild-type murine enamel. Using microCT, LRAPKO enamel volume and density measurements were similar to those from KO mice. However, in etched samples examined by SEM, the organization of the enamel rod pattern was altered by the presence of the LRAP transgene. CONCLUSIONS: The presence of LRAP leads to changes in enamel appearance compared to enamel from KO mice. Expression of a combination of amelogenin transgenes in KO mice may lead to rescue of the individual characteristics of normal enamel.

Dehydration-induced shrinkage of dentin as a potential cause of vertical root fractures.

Vertical root fractures (VRF) of endodontically treated teeth constitute a severe clinical condition frequently requiring removal of the affected tooth. Numerous attempts have been made to find the cause for VRF without reaching definitive conclusions. As changes in moisture content have been reported to appear as a consequence of root canal therapy, it is the goal of this paper to evaluate associated volume changes as a possible cause for VRF. Considering disk shaped horizontal cross sections of endodontically treated teeth with a moisture content of dentin decreasing from the root surface towards the root canal, both relative circumferential and relative radial stresses resulting from volume changes of dentin were calculated. It could be shown that the presence of a root canal itself increases radial and circumferential stresses acting on root dentin by a factor of two. Reduction in moisture content of dentin at the wall of the root canal results in shrinkage of the tooth structure and tensile stress. On the outer surface of the root, compressive stresses occur. Thus, VRF would start at the canal wall and propagate to the root surface. The theory presented appears to be consistent with previous reports on stress development as a consequence of dehydration of dentin and finite element analysis on root fractures. It may be concluded that dehydration of dentin induces cracks at the walls of a root canal which subsequently grow as a result of cyclic loading or traumatic overload.