IMMUNOLOCALIZATION OF VITAMIN-D-RECEPTOR AND CALBINDIN-D28K IN HUMAN TOOTH GERM

The role of vitamin D in ameloblasts and odontoblasts has been studied experimentally in rodents. Dental dysplasias have also been reported in clinical studies of children with rickets, Vitamin D acts via a nuc lear receptor which binds the major metabolite, 1,25-dihydroxyvitamin D-3, and positively or negatively controls the expression of specific genes. The most extensively studied markers of 1,25-dihydroxyvitamin D -3 action are calbindin-D9k, calbindin-D28k, and osteocalcin. Therefor e, to study in more detail the potential role of 1,25-dihydroxyvitamin D-3 in human dental development, 1,25-dihydroxyvitamin D-3 receptor ( VDR) was localized by immunofluorescence in forming teeth (8-26 wk of gestation). Calbindin-D28k was also mapped by immunoperoxidase in ante natal and postnatal forming and formed teeth. VDR were detected in bot h dental epithelium and mesenchyme of bud, cap, and bell stages of too th germs. Nuclei of overtly differentiated ameloblasts and odontoblast s were also immunostained. Calbindin-D28k was present in differentiate d ameloblasts and odontoblasts. The presence of VDR and calbindin-D28k in ameloblasts and odontoblasts suggests that 1,25-dihydroxyvitamin D -3 may contribute to the regulation of enamel and dentin formation, as classically reported for bone formation. Finally, the early appearanc e of VDR supports the concept that 1,25-dihydroxyvitamin D-3 may also control forward stages of tooth crown development in humans.