1，25-二羟基维生素D3在牙齿和下颌骨形成及长骨骨形成中的不同作用
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摘要
为了明确内源性1,25-二羟基维生素D_3(1,25(OH)_2D_3)在小鼠下颌骨(包括牙齿和牙槽骨)和长骨骨小梁的形成和矿化过程中是否发挥不同的作用,我们使用6周龄1-α羟化酶基因敲除(1α(OH)ase~(-/-))小鼠,通过影像学、组织学、组织化学,免疫组织化学和RT-PCR、Western-Blot等方法检测了1,25(OH)_2D_3的缺失对牙齿和牙槽骨的形成和矿化的影响,并且比较分析了成骨细胞骨形成在下颌牙槽骨与长骨的差别。结果显示:与同窝的野生型(WT)小鼠相比,1α(OH)ase~(-/-)小鼠的牙齿和下颌骨的骨密度明显降低,未矿化的前期牙本质和未矿化的牙槽骨骨基质明显增加;1α(OH)ase~(-/-)小鼠的牙量、修复性牙本质的面积、Ⅰ型胶原和骨钙素(OCN)的阳性面积及mRNA表达水平、牙本质唾液酸蛋白(DSP)的阳性面积均明显减少;皮质骨厚度、牙槽骨体积和成骨细胞数量也均明显的减少,而长骨中骨小梁的容量、成骨细胞的数量和活性均明显增加;1α(OH)ase~(-/-)小鼠下颌牙槽骨的甲状旁腺素受体(PTHR)和胰岛素样生长因子-1(IGF-1)蛋白表达水平轻度减少,而长骨骨小梁中PTHR和IGF-1蛋白表达水平明显增加。上述结果表明:在小鼠下颌骨(包括牙齿和牙槽骨)和长骨骨小梁的骨形成中,内源性1,25(OH)_2D_3起着不同的作用;经IGF-1介导,PTH通过与PTHR结合对下颌骨(包括牙齿和牙槽骨)和长骨骨小梁骨形成起着不同的作用。本实验通过体内实验证明:与PTH相比,1,25(OH)_2D_3在牙本质的形成和牙槽骨的骨形成中发挥主导作用。
Elevated PTH in the secondary hyperparathyroidism of vitamin D deficiency is believed to be anabolic for long bones.We previously compared mice with targeted disruption of the gene encoding parathyroid hormone(PTH)(PTH~(-/-)mice)or the gene encoding 25 hydroxyvitamin D 1α-hydroxylase[1α(OH)ase][1α(OH)ase~(-/-)mice]with compound mutant PTH~(-/-)1α(OH)ase~(-/-)mice.We found that PTH plays a predominant role in appositional bone growth,whereas 1,25(OH)_2D_3 acts predominantly on endochondral bone formation in long bones.It is unknown,however, whether 1,25(OH)_2D_3 or PTH plays a role in dentin and dental alveolar bone formation in the mandibles as it does in long bones.To determine whether 1,25(OH)_2D plays a distinctive role in flat bones such as mandibles,we examined the effect of 1,25(OH)_2D_3 deficiency on dentin and dental alveolar bone formation and mineralization in the mandibles, and compared osteoblastic bone formation in the mandibles and tibiae in 1α(OH)ase~(-/-)mice.Compared to wild-type(WT)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 1α(OH)ase~(-/-)mice.The dental volume,reparative dentin volume and dentin sialoprotein immunopositive areas were reduced in 1α(OH)ase~(-/-) mice.The cortical thickness,dental alveolar bone volume and osteoblast numbers were all decreased significantly in the mandibles;in contrast,the osteoblast number and surface were increased in the trabecular bone of the tibiae in 1α(OH)ase~(-/-)mice consistent with their secondary hyperparathryoidism.The expression of parathyroid hormone receptor (PTHR)and insulin-like growth factor-1(IGF-1)was reduced slightly in mandibles,but enhanced in the long bones in the 1α(OH)ase~(-/-)mice. These results indicate that 1α,25(OH)_2D_3 plays distinct roles in dentin and dental alveolar bone formation in the mandibles relative to trabecular bone formation in long bones,and suggests that 1,25(OH)_2D_3 plays a more prominent anabolic role than does PTH in dentin and dental alveolar bone formation in mandibles.
Elevated PTH in the secondary hyperparathyroidism of vitamin D deficiency is believed to be anabolic for long bones.We previously compared mice with targeted disruption of the gene encoding parathyroid hormone(PTH)(PTH~(-/-)mice)or the gene encoding 25 hydroxyvitamin D 1α-hydroxylase[1α(OH)ase][1α(OH)ase~(-/-)mice]with compound mutant PTH~(-/-)1α(OH)ase~(-/-)mice.We found that PTH plays a predominant role in appositional bone growth,whereas 1,25(OH)_2D_3 acts predominantly on endochondral bone formation in long bones.It is unknown,however, whether 1,25(OH)_2D_3 or PTH plays a role in dentin and dental alveolar bone formation in the mandibles as it does in long bones.To determine whether 1,25(OH)_2D plays a distinctive role in flat bones such as mandibles,we examined the effect of 1,25(OH)_2D_3 deficiency on dentin and dental alveolar bone formation and mineralization in the mandibles, and compared osteoblastic bone formation in the mandibles and tibiae in 1α(OH)ase~(-/-)mice.Compared to wild-type(WT)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 1α(OH)ase~(-/-)mice.The dental volume,reparative dentin volume and dentin sialoprotein immunopositive areas were reduced in 1α(OH)ase~(-/-) mice.The cortical thickness,dental alveolar bone volume and osteoblast numbers were all decreased significantly in the mandibles;in contrast,the osteoblast number and surface were increased in the trabecular bone of the tibiae in 1α(OH)ase~(-/-)mice consistent with their secondary hyperparathryoidism.The expression of parathyroid hormone receptor (PTHR)and insulin-like growth factor-1(IGF-1)was reduced slightly in mandibles,but enhanced in the long bones in the 1α(OH)ase~(-/-)mice. These results indicate that 1α,25(OH)_2D_3 plays distinct roles in dentin and dental alveolar bone formation in the mandibles relative to trabecular bone formation in long bones,and suggests that 1,25(OH)_2D_3 plays a more prominent anabolic role than does PTH in dentin and dental alveolar bone formation in mandibles.
引文
1.Deeb KK,Trump DL,Johnson CS.Vitamin D signalling pathways in cancer:potential for anticancer therapeutics.Nat Rev Cancer 2007;7(9):684-700.
2.Holick MF,Schnoes HK,DeLuca HF,Suda T,Cousins RJ.Isolation and identification of 1,25-dihydroxycholecalciferol.A metabolite of vitamin D active in intestine.Biochemistry 1971;10(14):2799-804.
3.Lawson DE,Fraser DR,Kodicek E,Morris HR,Williams DH.Identification of 1,25-dihydroxycholecalciferol,a new kidney hormone controlling calcium metabolism.Nature 1971;230(5291):228-30.
4.Norman AW,Myrtle JF,Midgett RJ,Nowicki HG,Williams V,Popjak G.1,25-dihydroxycholecalciferol:identification of the proposed active form of vitamin D3 in the intestine.Science 1971;173(991):51-4.
5.Haussler MR,McCain TA.Basic and clinical concepts related to vitamin D metabolism and action (first of two parts).N Engl J Med 1977;297(18):974-83.
6.Liao J,Ozono K,Sone T,McDonnell DP,Pike JW.Vitamin D receptor interaction with specific DNA requires a nuclear protein and 1,25-dihydroxyvitamin D3.Proc Natl Acad Sci U S A 1990;87(24):9751-5.
7.Takeyama K,Kitanaka S,Sato T,Kobori M,Yanagisawa J,Kato S.25-Hydroxyvitamin D31alpha-hydroxylase and vitamin D synthesis.Science 1997;277(5333):1827-30.
8.Shinki T,Shimada H,Wakino S,et al.Cloning and expression of rat 25-hydroxyvitamin D3- 1alpha-hydroxylase cDNA.Proc Natl A cad Sci U S A 1997;94(24):12920-5.
9.Wada M,Furuya Y,Sakiyama J,et al.The calcimimetic compound NPS R-568 suppresses parathyroid cell proliferation in rats with renal insufficiency.Control of parathyroid cell growth via a calcium receptor.J Clin Invest 1997;100(12):2977-83.
10.Prader A,Illig R,Heierli E.[An unusual form of primary vitamin D-resistant rickets with hypocalcemia and autosomal-dominant hereditary transmission:hereditary pseudo-deficiency rickets.].Helv Paediatr Acta 1961;16:452-68.
11.Fraser D,Kooh SW,Kind HP,Holick MF,Tanaka Y,DeLuca HF.Pathogenesis of hereditary vitamin-D-dependent rickets.An inborn error of vitamin D metabolism involving defective conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D.N Engl J Med 1973;289(16):817-22.
12.Zambrano M,Nikitakis NG,Sanchez-Quevedo MC,Sauk JJ,Sedano H,Rivera H.Oral and dental manifestations of vitamin D-dependent rickets type I:report of a pediatric case.Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;95(6):705-9.
13.Panda DK,Miao D,Tremblay ML,et al.Targeted ablation of the 25-hydroxyvitamin D 1alpha -hydroxylase enzyme:evidence for skeletal,reproductive,and immune dysfunction.Proc Natl Acad Sci USA 2001;98(13):7498-503.
14.Dardenne O,Prud'homme J,Arabian A,Glorieux FH,St-Amaud R.Targeted inactivation of the 25-hydroxyvitamin D(3)-1(alpha)-hydroxylase gene(CYP27B1)creates an animal model of pseudovitamin D-deficiency rickets.Endocrinology 2001;142(7):3135-41.
15.Xue Y,Karaplis AC,Hendy GN,Goltzman D,Miao D.Genetic models show that parathyroid hormone and 1,25-dihydroxyvitamin D3 play distinct and synergistic roles in postnatal mineral ion homeostasis and skeletal development.Hum Mol Genet 2005;14(11):1515-28.
16. Panda DK, Miao D, Bolivar I, et al. Inactivation of the 25-hydroxyvitamin D lalpha-hydroxylase and vitamin D receptor demonstrates independent and interdependent effects of calcium and vitamin D on skeletal and mineral homeostasis. J Biol Chem 2004;279(16): 16754-66.
17. Ye L, MacDougall M, Zhang S, et al. Deletion of dentin matrix protein-1 leads to a partial failure of maturation of predentin into dentin, hypomineralization, and expanded cavities of pulp and root canal during postnatal tooth development. J Biol Chem 2004;279( 18): 19141-8.
18. Ritchie HH, Pinero GJ, Hou H, Butler WT. Molecular analysis of rat dentin sialoprotein. Connect Tissue Res 1995;33(1-3):73-9.
19. Makino S, Fukuda K, Miyoshi S, et al. Cardiomyocytes can be generated from marrow stromal cells in vitro. J Clin Invest 1999;103(5):697-705.
20. Holick MF, Shao Q, Liu WW, Chen TC. The vitamin D content of fortified milk and infant formula. N Engl J Med 1992;326(18):1178-81.
21. Holtrop ME, Cox KA, Carnes DL, Holick MF. Effects of serum calcium and phosphorus on skeletal mineralization in vitamin D-deficient rats. Am J Physiol 1986;251(2 Pt 1):E234-40.
22. Balsan S, Garabedian M, Larchet M, et al. Long-term nocturnal calcium infusions can cure rickets and promote normal mineralization in hereditary resistance to 1,25-dihydroxyvitamin D. J Clin Invest 1986;77(5):1661-7.
23. George A, Bannon L, Sabsay B, et al. The carboxyl-terminal domain of phosphophoryn contains unique extended triplet amino acid repeat sequences forming ordered carboxyl-phosphate interaction ridges that may be essential in the biomineralization process. J Biol Chem 1996;271(51):32869-73.
24. George A, Hao J. Role of phosphophoryn in dentin mineralization. Cells Tissues Organs 2005;181(3-4):232-40.
25. Kim JW, Simmer JP. Hereditary dentin defects. J Dent Res 2007;86(5):392-9.
26. Xue Y, Karaplis AC, Hendy GN, Goltzman D, Miao D. Exogenous 1,25-dihydroxyvitamin D3 exerts a skeletal anabolic effect and improves mineral ion homeostasis in mice that are homozygous for both the lalpha-hydroxylase and parathyroid hormone null alleles. Endocrinology 2006;147(10):480I-10.
27. Turnbull RS, Heersche JN, Tam CS, Howley TP. Parathyroid hormone stimulates dentin and bone apposition in the thyroparathyroidectomized rat in a dose-dependent fashion. Calcif Tissue Int 1983;35(4-5):586-90.
28. Miller SC, Hunziker J, Mecham M, Wronski TJ. Intermittent parathyroid hormone administration stimulates bone formation in the mandibles of aged ovariectomized rats. J Dent Res 1997;76(8): 1471-6.
29. Berdal A, Papagerakis P, Hotton D, Bailleul-Forestier I, Davideau JL. Ameloblasts and odontoblasts, target-cells for 1,25-dihydroxyvitamin D3: a review. Int J Dev Biol 1995;39(1):257-62.
30. Davideau JL, Lezot F, Kato S, Bailleul-Forestier I, Berdal A. Dental alveolar bone defects related to Vitamin D and calcium status. J Steroid Biochem Mol Biol 2004;89-90(1-5):615-8.
31. Hunziker J, Wronski TJ, Miller SC. Mandibular bone formation rates in aged ovariectomized rats treated with anti-resorptive agents alone and in combination with intermittent parathyroid hormone. J Dent Res 2000;79(6):1431-8.
32. Lee SK, Kim YS, Oh HS, Yang KH, Kim EC, Chi JG. Prenatal development of the human mandible. Anat Rec 2001 ;263(3):314-25.
33. Bikle DD, Sakata T, Leary C, et al. Insulin-like growth factor I is required for the anabolic actions of parathyroid hormone on mouse bone.J Bone Miner Res 2002;17(9):1570-8.
34.Wang Y,Nishida S,Boudignon BM,et al.IGF-I receptor is required for the anabolic actions of parathyroid hormone on bone.J Bone Miner Res 2007;22(9):1329-37.
35.Yamaguchi M,Ogata N,Shinoda Y,et al.Insulin receptor substrate-1 is required for bone anabolic function of parathyroid hormone in mice.Endocrinology 2005;146(6):2620-8.
1.Ruch JV.Odontoblast commitment and differentiation.Biochem Cell Biol 1998;76(6):923-38.
2.Mjor IA,Sveen OB,Heyeraas KJ.Pulp-dentin biology in restorative dentistry.Part 1:normal structure and physiology. Quintessence Int 2001;32(6):427-46.
3. Ruch JV, Lesot H, Begue-Kirn C. Odontoblast differentiation. Int J Dev Biol 1995;39(1):51-68.
4. Roemmich JN, Huerta MG, Sundaresan SM, Rogol AD. Alterations in body composition and fat distribution in growth hormone-deficient prepubertal children during growth hormone therapy. Metabolism 2001;50(5):537-47.
5. Sasagawa I. Mineralization patterns in elasmobranch fish. Microsc Res Tech 2002;59(5):396-407.
6. Linde A. Dentin mineralization and the role of odontoblasts in calcium transport. Connect Tissue Res 1995;3(1-3): 163-70.
7. Kim JW, Simmer JP. Hereditary dentin defects. J Dent Res 2007;86(5):392-9.
8. Plate U, Hohling HJ, Reimer L, et al. Analysis of the calcium distribution in predentine by EELS and of the early crystal formation in dentine by ESI and ESD. J Microsc 1992;166(Pt 3):329-41.
9. Yokoyama M, Trams EG. Effect of enzymes on blood group antigens. Nature 1962;194:1048-9.
10. Houlle P, Voegel JC, Schultz P, Steuer P, Cuisinier FJ. High resolution electron microscopy: structure and growth mechanisms of human dentin crystals. J Dent Res 1997;76(4):895-904.
11. Plate U, Hohling HJ. Morphological and structural studies of early mineral formation in enamel of rat incisors by electron spectroscopic imaging (ESI) and electron spectroscopic diffraction (ESD). Cell Tissue Res 1994;277(1): 151-8.
12. Sreenath T, Thyagarajan T, Hall B, et al. Dentin sialophosphoprotein knockout mouse teeth display widened predentin zone and develop defective dentin mineralization similar to human dentinogenesis imperfecta type III. J Biol Chem 2003;278(27):24874-80.
13. Ye L, MacDougall M, Zhang S, et al. Deletion of dentin matrix protein-1 leads to a partial failure of maturation of predentin into dentin, hypomineralization, and expanded cavities of pulp and root canal during postnatal tooth development. J Biol Chem 2004;279(18):19141-8.
14. Nakamura O, Gohda E, Ozawa M, et al. Immunohistochemical studies with a monoclonal antibody on the distribution of phosphophoryn in predentin and dentin. Calcif Tissue Int 1985;37(5):491-500.
15. Hohling HJ, Arnold S, Barckhaus RH, Plate U, Wiesmann HP. Structural relationship between the primary crystal formations and the matrix macromolecules in different hard tissues. Discussion of a general principle. Connect Tissue Res 1995;33(1-3): 171-8.
16. Boskey AL. The role of extracellular matrix components in dentin mineralization. Crit Rev Oral Biol Med 1991;2(3):369-87.
17. Butler WT. Dentin matrix proteins and dentinogenesis. Connect Tissue Res 1995;33(1-3):59-65.
18. D'Souza RN, Bronckers AL, Happonen RP, Doga DA, Farach-Carson MC, Butler WT. Developmental expression of a 53 KD dentin sialoprotein in rat tooth organs. J Histochem Cytochem 1992;40(3):359-66.
19. Camacho NP, Rimnac CM, Meyer RA, Jr., Doty S, Boskey AL. Effect of abnormal mineralization on the mechanical behavior of X-linked hypophosphatemic mice femora. Bone 1995;17(3):271-8.
20. George A, Sabsay B, Simonian PA, Veis A. Characterization of a novel dentin matrix acidic phosphoprotein. Implications for induction of biomineralization. J Biol Chem 1993;268(17): 12624-30.
21. Feng JQ, Huang H, Lu Y, et al. The Dentin matrix protein 1 (Dmp 1) is specifically expressed in mineralized, but not soft, tissues during development. J Dent Res 2003;82(10):776-80.
2.Holick MF,Schnoes HK,DeLuca HF,Suda T,Cousins RJ.Isolation and identification of 1,25-dihydroxycholecalciferol.A metabolite of vitamin D active in intestine.Biochemistry 1971;10(14):2799-804.
3.Lawson DE,Fraser DR,Kodicek E,Morris HR,Williams DH.Identification of 1,25-dihydroxycholecalciferol,a new kidney hormone controlling calcium metabolism.Nature 1971;230(5291):228-30.
4.Norman AW,Myrtle JF,Midgett RJ,Nowicki HG,Williams V,Popjak G.1,25-dihydroxycholecalciferol:identification of the proposed active form of vitamin D3 in the intestine.Science 1971;173(991):51-4.
5.Haussler MR,McCain TA.Basic and clinical concepts related to vitamin D metabolism and action (first of two parts).N Engl J Med 1977;297(18):974-83.
6.Liao J,Ozono K,Sone T,McDonnell DP,Pike JW.Vitamin D receptor interaction with specific DNA requires a nuclear protein and 1,25-dihydroxyvitamin D3.Proc Natl Acad Sci U S A 1990;87(24):9751-5.
7.Takeyama K,Kitanaka S,Sato T,Kobori M,Yanagisawa J,Kato S.25-Hydroxyvitamin D31alpha-hydroxylase and vitamin D synthesis.Science 1997;277(5333):1827-30.
8.Shinki T,Shimada H,Wakino S,et al.Cloning and expression of rat 25-hydroxyvitamin D3- 1alpha-hydroxylase cDNA.Proc Natl A cad Sci U S A 1997;94(24):12920-5.
9.Wada M,Furuya Y,Sakiyama J,et al.The calcimimetic compound NPS R-568 suppresses parathyroid cell proliferation in rats with renal insufficiency.Control of parathyroid cell growth via a calcium receptor.J Clin Invest 1997;100(12):2977-83.
10.Prader A,Illig R,Heierli E.[An unusual form of primary vitamin D-resistant rickets with hypocalcemia and autosomal-dominant hereditary transmission:hereditary pseudo-deficiency rickets.].Helv Paediatr Acta 1961;16:452-68.
11.Fraser D,Kooh SW,Kind HP,Holick MF,Tanaka Y,DeLuca HF.Pathogenesis of hereditary vitamin-D-dependent rickets.An inborn error of vitamin D metabolism involving defective conversion of 25-hydroxyvitamin D to 1 alpha,25-dihydroxyvitamin D.N Engl J Med 1973;289(16):817-22.
12.Zambrano M,Nikitakis NG,Sanchez-Quevedo MC,Sauk JJ,Sedano H,Rivera H.Oral and dental manifestations of vitamin D-dependent rickets type I:report of a pediatric case.Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2003;95(6):705-9.
13.Panda DK,Miao D,Tremblay ML,et al.Targeted ablation of the 25-hydroxyvitamin D 1alpha -hydroxylase enzyme:evidence for skeletal,reproductive,and immune dysfunction.Proc Natl Acad Sci USA 2001;98(13):7498-503.
14.Dardenne O,Prud'homme J,Arabian A,Glorieux FH,St-Amaud R.Targeted inactivation of the 25-hydroxyvitamin D(3)-1(alpha)-hydroxylase gene(CYP27B1)creates an animal model of pseudovitamin D-deficiency rickets.Endocrinology 2001;142(7):3135-41.
15.Xue Y,Karaplis AC,Hendy GN,Goltzman D,Miao D.Genetic models show that parathyroid hormone and 1,25-dihydroxyvitamin D3 play distinct and synergistic roles in postnatal mineral ion homeostasis and skeletal development.Hum Mol Genet 2005;14(11):1515-28.
16. Panda DK, Miao D, Bolivar I, et al. Inactivation of the 25-hydroxyvitamin D lalpha-hydroxylase and vitamin D receptor demonstrates independent and interdependent effects of calcium and vitamin D on skeletal and mineral homeostasis. J Biol Chem 2004;279(16): 16754-66.
17. Ye L, MacDougall M, Zhang S, et al. Deletion of dentin matrix protein-1 leads to a partial failure of maturation of predentin into dentin, hypomineralization, and expanded cavities of pulp and root canal during postnatal tooth development. J Biol Chem 2004;279( 18): 19141-8.
18. Ritchie HH, Pinero GJ, Hou H, Butler WT. Molecular analysis of rat dentin sialoprotein. Connect Tissue Res 1995;33(1-3):73-9.
19. Makino S, Fukuda K, Miyoshi S, et al. Cardiomyocytes can be generated from marrow stromal cells in vitro. J Clin Invest 1999;103(5):697-705.
20. Holick MF, Shao Q, Liu WW, Chen TC. The vitamin D content of fortified milk and infant formula. N Engl J Med 1992;326(18):1178-81.
21. Holtrop ME, Cox KA, Carnes DL, Holick MF. Effects of serum calcium and phosphorus on skeletal mineralization in vitamin D-deficient rats. Am J Physiol 1986;251(2 Pt 1):E234-40.
22. Balsan S, Garabedian M, Larchet M, et al. Long-term nocturnal calcium infusions can cure rickets and promote normal mineralization in hereditary resistance to 1,25-dihydroxyvitamin D. J Clin Invest 1986;77(5):1661-7.
23. George A, Bannon L, Sabsay B, et al. The carboxyl-terminal domain of phosphophoryn contains unique extended triplet amino acid repeat sequences forming ordered carboxyl-phosphate interaction ridges that may be essential in the biomineralization process. J Biol Chem 1996;271(51):32869-73.
24. George A, Hao J. Role of phosphophoryn in dentin mineralization. Cells Tissues Organs 2005;181(3-4):232-40.
25. Kim JW, Simmer JP. Hereditary dentin defects. J Dent Res 2007;86(5):392-9.
26. Xue Y, Karaplis AC, Hendy GN, Goltzman D, Miao D. Exogenous 1,25-dihydroxyvitamin D3 exerts a skeletal anabolic effect and improves mineral ion homeostasis in mice that are homozygous for both the lalpha-hydroxylase and parathyroid hormone null alleles. Endocrinology 2006;147(10):480I-10.
27. Turnbull RS, Heersche JN, Tam CS, Howley TP. Parathyroid hormone stimulates dentin and bone apposition in the thyroparathyroidectomized rat in a dose-dependent fashion. Calcif Tissue Int 1983;35(4-5):586-90.
28. Miller SC, Hunziker J, Mecham M, Wronski TJ. Intermittent parathyroid hormone administration stimulates bone formation in the mandibles of aged ovariectomized rats. J Dent Res 1997;76(8): 1471-6.
29. Berdal A, Papagerakis P, Hotton D, Bailleul-Forestier I, Davideau JL. Ameloblasts and odontoblasts, target-cells for 1,25-dihydroxyvitamin D3: a review. Int J Dev Biol 1995;39(1):257-62.
30. Davideau JL, Lezot F, Kato S, Bailleul-Forestier I, Berdal A. Dental alveolar bone defects related to Vitamin D and calcium status. J Steroid Biochem Mol Biol 2004;89-90(1-5):615-8.
31. Hunziker J, Wronski TJ, Miller SC. Mandibular bone formation rates in aged ovariectomized rats treated with anti-resorptive agents alone and in combination with intermittent parathyroid hormone. J Dent Res 2000;79(6):1431-8.
32. Lee SK, Kim YS, Oh HS, Yang KH, Kim EC, Chi JG. Prenatal development of the human mandible. Anat Rec 2001 ;263(3):314-25.
33. Bikle DD, Sakata T, Leary C, et al. Insulin-like growth factor I is required for the anabolic actions of parathyroid hormone on mouse bone.J Bone Miner Res 2002;17(9):1570-8.
34.Wang Y,Nishida S,Boudignon BM,et al.IGF-I receptor is required for the anabolic actions of parathyroid hormone on bone.J Bone Miner Res 2007;22(9):1329-37.
35.Yamaguchi M,Ogata N,Shinoda Y,et al.Insulin receptor substrate-1 is required for bone anabolic function of parathyroid hormone in mice.Endocrinology 2005;146(6):2620-8.
1.Ruch JV.Odontoblast commitment and differentiation.Biochem Cell Biol 1998;76(6):923-38.
2.Mjor IA,Sveen OB,Heyeraas KJ.Pulp-dentin biology in restorative dentistry.Part 1:normal structure and physiology. Quintessence Int 2001;32(6):427-46.
3. Ruch JV, Lesot H, Begue-Kirn C. Odontoblast differentiation. Int J Dev Biol 1995;39(1):51-68.
4. Roemmich JN, Huerta MG, Sundaresan SM, Rogol AD. Alterations in body composition and fat distribution in growth hormone-deficient prepubertal children during growth hormone therapy. Metabolism 2001;50(5):537-47.
5. Sasagawa I. Mineralization patterns in elasmobranch fish. Microsc Res Tech 2002;59(5):396-407.
6. Linde A. Dentin mineralization and the role of odontoblasts in calcium transport. Connect Tissue Res 1995;3(1-3): 163-70.
7. Kim JW, Simmer JP. Hereditary dentin defects. J Dent Res 2007;86(5):392-9.
8. Plate U, Hohling HJ, Reimer L, et al. Analysis of the calcium distribution in predentine by EELS and of the early crystal formation in dentine by ESI and ESD. J Microsc 1992;166(Pt 3):329-41.
9. Yokoyama M, Trams EG. Effect of enzymes on blood group antigens. Nature 1962;194:1048-9.
10. Houlle P, Voegel JC, Schultz P, Steuer P, Cuisinier FJ. High resolution electron microscopy: structure and growth mechanisms of human dentin crystals. J Dent Res 1997;76(4):895-904.
11. Plate U, Hohling HJ. Morphological and structural studies of early mineral formation in enamel of rat incisors by electron spectroscopic imaging (ESI) and electron spectroscopic diffraction (ESD). Cell Tissue Res 1994;277(1): 151-8.
12. Sreenath T, Thyagarajan T, Hall B, et al. Dentin sialophosphoprotein knockout mouse teeth display widened predentin zone and develop defective dentin mineralization similar to human dentinogenesis imperfecta type III. J Biol Chem 2003;278(27):24874-80.
13. Ye L, MacDougall M, Zhang S, et al. Deletion of dentin matrix protein-1 leads to a partial failure of maturation of predentin into dentin, hypomineralization, and expanded cavities of pulp and root canal during postnatal tooth development. J Biol Chem 2004;279(18):19141-8.
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