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Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts.

Fukumoto S, Kiba T, Hall B, Iehara N, Nakamura T, Longenecker G, Krebsbach PH, Nanci A, Kulkarni AB, Yamada Y - J. Cell Biol. (2004)

Bottom Line: Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin.We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation.Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

View Article: PubMed Central - PubMed

Affiliation: Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.

ABSTRACT
Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin- mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

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Defects in enamel formation of ameloblastin- mice. (A) Faxitron analysis of the craniofacial region of 8-wk-old heterozygote and homozygote mice. Boxed areas were enlarged in B, 1–3. (B) High magnification of incisor tips (1), bottom incisors and alveolar bone space (2), and bottom molars (3). Round incisor tips, wider incisor-alveolar bone space, and a flat occlusal plane are observed in mutant mice. Arrows indicate incisor tips, incisor-alveolar bone space, and occlusal planes. inc, incisor; alv, alveolar bone. (C) CT-scan analysis of top first molar of heterozygous and homozygous mice. E, enamel; D, dentin; P, pulp. (D) SEM analysis of incisor. E, enamel; D, dentin; p, pulp, dE, defective enamel.
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fig2: Defects in enamel formation of ameloblastin- mice. (A) Faxitron analysis of the craniofacial region of 8-wk-old heterozygote and homozygote mice. Boxed areas were enlarged in B, 1–3. (B) High magnification of incisor tips (1), bottom incisors and alveolar bone space (2), and bottom molars (3). Round incisor tips, wider incisor-alveolar bone space, and a flat occlusal plane are observed in mutant mice. Arrows indicate incisor tips, incisor-alveolar bone space, and occlusal planes. inc, incisor; alv, alveolar bone. (C) CT-scan analysis of top first molar of heterozygous and homozygous mice. E, enamel; D, dentin; P, pulp. (D) SEM analysis of incisor. E, enamel; D, dentin; p, pulp, dE, defective enamel.

Mentions: The Ambn- mice were fertile, and the newborns appeared normal. However, as early as 3 wk old, incisors from Ambn−/− mice displayed a chalky white color, indicating hypoplastic or hypocalcified enamel (Fig. 1 E). Stereomicroscopic analysis of molars and incisors of 3-wk-old heterozygous mice showed translucent enamel, whereas Ambn−/− molars and incisors lacked enamel (unpublished data). Microradiographic imaging showed normal development of the craniofacial bone and the outward appearance of tooth (Fig. 2 A). It was reported that ameloblastin is transiently expressed in Hertwig's root sheath (Fong et al., 1996; Bosshardt and Nanci, 1998; Simmons et al., 1998). However, root formation in the mutant mice was not different from wild-type and Ambn+/− mice (unpublished data). Both maxillary and mandibular incisor tips of Ambn−/− mice were rounded, and the occlusal plane of the molar was flattened (arrow) because of attrition after tooth eruption (Fig. 2 B). Interestingly, the space between tooth and alveolar bone (arrows) was wider in Ambn−/− mice than in Ambn+/− mice. In this space, invasion of calcified tissue was observed (Fig. 2 B).


Ameloblastin is a cell adhesion molecule required for maintaining the differentiation state of ameloblasts.

Fukumoto S, Kiba T, Hall B, Iehara N, Nakamura T, Longenecker G, Krebsbach PH, Nanci A, Kulkarni AB, Yamada Y - J. Cell Biol. (2004)

Defects in enamel formation of ameloblastin- mice. (A) Faxitron analysis of the craniofacial region of 8-wk-old heterozygote and homozygote mice. Boxed areas were enlarged in B, 1–3. (B) High magnification of incisor tips (1), bottom incisors and alveolar bone space (2), and bottom molars (3). Round incisor tips, wider incisor-alveolar bone space, and a flat occlusal plane are observed in mutant mice. Arrows indicate incisor tips, incisor-alveolar bone space, and occlusal planes. inc, incisor; alv, alveolar bone. (C) CT-scan analysis of top first molar of heterozygous and homozygous mice. E, enamel; D, dentin; P, pulp. (D) SEM analysis of incisor. E, enamel; D, dentin; p, pulp, dE, defective enamel.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2172447&req=5

fig2: Defects in enamel formation of ameloblastin- mice. (A) Faxitron analysis of the craniofacial region of 8-wk-old heterozygote and homozygote mice. Boxed areas were enlarged in B, 1–3. (B) High magnification of incisor tips (1), bottom incisors and alveolar bone space (2), and bottom molars (3). Round incisor tips, wider incisor-alveolar bone space, and a flat occlusal plane are observed in mutant mice. Arrows indicate incisor tips, incisor-alveolar bone space, and occlusal planes. inc, incisor; alv, alveolar bone. (C) CT-scan analysis of top first molar of heterozygous and homozygous mice. E, enamel; D, dentin; P, pulp. (D) SEM analysis of incisor. E, enamel; D, dentin; p, pulp, dE, defective enamel.
Mentions: The Ambn- mice were fertile, and the newborns appeared normal. However, as early as 3 wk old, incisors from Ambn−/− mice displayed a chalky white color, indicating hypoplastic or hypocalcified enamel (Fig. 1 E). Stereomicroscopic analysis of molars and incisors of 3-wk-old heterozygous mice showed translucent enamel, whereas Ambn−/− molars and incisors lacked enamel (unpublished data). Microradiographic imaging showed normal development of the craniofacial bone and the outward appearance of tooth (Fig. 2 A). It was reported that ameloblastin is transiently expressed in Hertwig's root sheath (Fong et al., 1996; Bosshardt and Nanci, 1998; Simmons et al., 1998). However, root formation in the mutant mice was not different from wild-type and Ambn+/− mice (unpublished data). Both maxillary and mandibular incisor tips of Ambn−/− mice were rounded, and the occlusal plane of the molar was flattened (arrow) because of attrition after tooth eruption (Fig. 2 B). Interestingly, the space between tooth and alveolar bone (arrows) was wider in Ambn−/− mice than in Ambn+/− mice. In this space, invasion of calcified tissue was observed (Fig. 2 B).

Bottom Line: Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin.We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation.Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

View Article: PubMed Central - PubMed

Affiliation: Craniofacial Developmental Biology and Regeneration Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA.

ABSTRACT
Tooth morphogenesis results from reciprocal interactions between oral epithelium and ectomesenchyme culminating in the formation of mineralized tissues, enamel, and dentin. During this process, epithelial cells differentiate into enamel-secreting ameloblasts. Ameloblastin, an enamel matrix protein, is expressed by differentiating ameloblasts. Here, we report the creation of ameloblastin- mice, which developed severe enamel hypoplasia. In mutant tooth, the dental epithelium differentiated into enamel-secreting ameloblasts, but the cells were detached from the matrix and subsequently lost cell polarity, resumed proliferation, and formed multicell layers. Expression of Msx2, p27, and p75 were deregulated in mutant ameloblasts, the phenotypes of which were reversed to undifferentiated epithelium. We found that recombinant ameloblastin adhered specifically to ameloblasts and inhibited cell proliferation. The mutant mice developed an odontogenic tumor of dental epithelium origin. Thus, ameloblastin is a cell adhesion molecule essential for amelogenesis, and it plays a role in maintaining the differentiation state of secretory stage ameloblasts by binding to ameloblasts and inhibiting proliferation.

Show MeSH
Related in: MedlinePlus