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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0247v1 203/2/203    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Liu, H. Articles by Miao, D. PubMed PubMed Citation Articles by Liu, H. Articles by Miao, D.

¹ Institute of Dental Research, Stomatological College
² The Research Center for Bone and Stem Cells, Nanjing Medical University, Nanjing, Jiangsu 210029, People's Republic of China
³ Department of Medicine, McGill University Health Centre, McGill University, Montreal, Quebec, Canada H3A 1A1

(Correspondence should be addressed to D Miao who is now at Institute of Dental Research, Nanjing Medical University; Email: dsmiao{at}njmu.edu.cn)

To assess the roles of 1,25-dihydroxyvitamin D (1,25(OH)₂D) and parathyroid hormone (PTH) in hard tissue formation in oro-facial tissues, we examined the effect of either 1,25(OH)₂D or PTH deficiency on dentin and dental alveolar bone formation and mineralization in the mandibles, and osteoblastic bone formation in long bones of 1-hydroxylase knockout (1(OH)ase^–/–) mice. Compared with wild-type mice, the mineral density was decreased in the teeth and mandibles, and unmineralized dentin (predentin and biglycan immunopositive dentin) and unmineralized bone matrix in the dental alveolar bone were increased in 1(OH)ase^–/– mice. The dental volume, reparative dentin volume, and dentin sialoprotein immunopositive areas were reduced in 1(OH)ase^–/– mice. The cortical thickness, dental alveolar bone volume, and osteoblast number were all decreased significantly in the mandibles; in contrast, the osteoblast number and surface were increased in the trabecular bone of the tibiae in 1(OH)ase^–/– mice consistent with their secondary hyperparathyroidism. The expression of PTH receptor and IGF1 was reduced slightly in mandibles, but enhanced significantly in the long bones in the 1(OH)ase^–/– mice. To control for the role of secondary hyperparathyroidism, we also examined teeth and mandibles in 6-week-old PTH^–/– mice. In these animals, dental and bone volumes in mandibles were not altered when compared with their wild-type littermates. These results suggest that 1,25(OH)₂D₃ plays an anabolic role in both dentin and dental alveolar bone as it does in long bones, whereas PTH acts predominantly in long bones rather than mandibular bone.