Disturbed Enamel Biomineralization in col1-caPPR Mouse Incisor

Abstract

During the mineralization process of enamel, gene expression controls the activities of ameloblasts, the secretion and assembly of an extracellular protein matrix, affecting the final structure and functions. In this study, the enamel in the maxillary and mandibular incisors of wild-type and transgenic (col1-caPPR) mice, in which a constitutively active PTH/PTHrP receptor (PPR) was targeted to osteoblastic cells, was observed by scanning electron microscopy (SEM), Fourier transform infrared microscopy (FTIRM), and nanoindentation. The SEM studies showed that several different patterns of aberrations in crystal arrangement, disturbed prism organization without decussation, as well as abnormal enamel distribution were encountered in transgenic enamel. FTIRM analysis revealed poorer crystallinity/maturity after mutation. Nanoindentation measurement disclosed that transgenic enamel had 24.6% lower hardness and 12.3% lower elastic modulus. We attributed the inferior properties to the loosely packing crystals and abnormal prism organization. Furthermore, the col1-caPPR mouse model was substantiated to be useful to study how genes modulate the biomineralization process.