Different from bone: Tooth formation and enameloid mineralization are not affected by reduced dietary phosphorus intake

Vertebrates rely on phosphorus intake for skeletal mineralization. In humans, hypomineralized teeth associated with rickets, hypophosphatemia, hypophosphatasia, or idiopathic molar-incisor-hypomineralization pose significant problems. Here tooth development in wild-type zebrafish and in osteocalcin GFP reporter-line zebrafish is examined under conditions of low, regular, and high dietary phosphorus (P) intake. Mineralization of tooth and jaw bone matrices was analyzed by Alizarin red S staining, synchrotron X-ray tomography, Von Kossa staining of histological sections, Raman micro-spectroscopy, nanoindentation, phosphate transporter gene expression detection, and additional histological techniques.

Tooth development, enameloid and dentin formation, and bone matrix deposition proceed uninterrupted in zebrafish fed a low phosphorus diet. However, P-deficiency impairs bone matrix mineralization, dentin mineralization is delayed, and enameloid mineralization remains unaffected. Raman spectroscopy on erupted teeth reveals no changes in dentin mineral composition. The vectorial Na-P co-transporter slc34a2b is expressed in ameloblasts, which agrees with the cells' known contribution to enameloid mineralization.

It is hypothesized that active phosphate transport by ameloblasts possibly also contributes to the mineralization of dentin. The observed uncoupling of bone and tooth mineralization aligns with findings in other teleost species under natural conditions, and with laboratory studies on zebrafish and mammals that impair bone mineralization.