The cellular and extracellular distribution of osteocalcin and dentin phosphoprotein in teeth of vitamin D-deficient rats.

Experimental and clinical data indicate that dentin mineralization is vitamin D-dependent. This calcium-regulating steroid controls protein synthesis, for instance that of osteocalcin in osteoblasts. This protein also elaborated by odontoblasts was used as a molecular marker for vitamin D action on odontoblasts. Since the most characteristic protein synthesized by odontoblasts is the dentin phosphoprotein which is thought to regulate hydroxyapatite growth, its cellular and extracellular distribution was also studied. Tooth formation in the molars and incisors of successive generations of vitamin D-deficient animals (-D) and in controls (+D) was compared by microadiography, toluidine blue histochemistry, and immunocytochemistry. In -D samples, the presence of dentin phosphoprotein in odontoblasts indicated that their differentiation occurred despite major morphological disturbances at the cusp tips. In contralateral teeth, osteocalcin was depleted in odontoblasts and dentin, suggesting an inhibition of protein synthesis induced by vitamin D-deficiency. In the extracellular matrix of +D animals, phosphoprotein distribution was associated with dentin, especially within actively forming calcospherites at the mineralization front. In contrast, in -D dentin, the mineralization defects corresponded to irregular absence of histochemically detectable phosphoprotein. This protein indeed appeared either absent or uniformly sparse in -D dentin by immunocytochemistry. These data suggest that vitamin D acts directly on odontogenic cells at various synthetic (osteocalcin) or secretory (phosphoprotein) levels indicating that odontoblasts are target-cells for vitamin D. Therefore, this hormone could contribute to the regulation of extracellular mineralization during dentinogenesis, via different mechanisms in the processing of matrix protein.