Expression of odontogenic ameloblast‐associated and amelotin proteins in the junctional epithelium

Nishio, Clarice; Wazen, Rima; Moffatt, Pierre; Nanci, Antonio

doi:10.1111/prd.12031

Cited by 32 publications

(33 citation statements)

References 47 publications

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“…Immunogold labeling characterized by transmission electron microscopy showed that early in the maturation stage AMTN penetrates into the enamel surface and seems to concentrate in the less-mineralized crypts left behind as the ameloblasts retracted their Tomes’ processes at the end of the secretory stage [20]. By late maturation AMTN localizes specifically to the ameloblast-enamel interface and then disappears beneath the late, reduced enamel epithelium [20], only to reappear at the cell-enamel interface beneath the junctional epithelium following tooth eruption [29,30] where it is believed to facilitate adherence of the junctional epithelium to the tooth surface [31]. AMTN interacts with itself and with ODAM [32] and colocalizes with ODAM in the basal lamina beneath maturation stage ameloblasts and junctional epithelium.…”

Section: Introductionmentioning

confidence: 99%

Maturation stage enamel malformations in Amtn and Klk4 null mice

et al. 2016

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Amelotin (AMTN) and kallikrein-4 (KLK4) are secreted proteins specialized for enamel biomineralization. We characterized enamel from wild-type, Amtn−/−, Klk4−/−, Amtn+/−Klk4+/− and Amtn−/−Klk4−/− mice to gain insights into AMTN and KLK4 functions during amelogenesis. All of the null mice were healthy and fertile. The mandibular incisors in Amtn−/−, Klk4−/− and Amtn−/−Klk4−/− mice were chalky-white and chipped. No abnormalities except in enamel were observed, and no significant differences were detected in enamel thickness or volume, or in rod decussation. Micro-computed tomography (µCT) maximum intensity projections localized the onset of enamel maturation in wild-type incisors distal to the first molar, but mesial to this position in Amtn−/−, Klk4−/− and Amtn−/−Klk4−/− mice, demonstrating a delay in enamel maturation in Amtn−/− incisors. Micro-CT detected significantly reduced enamel mineral density (2.5 and 2.4 gHA/cm3) in the Klk4−/− and Amtn−/−Klk4−/− mice respectively, compared with wild-type enamel (3.1 gHA/cm3). Backscatter scanning electron microscopy showed that mineral density progressively diminished with enamel depth in the Klk4−/− and Amtn−/−Klk4−/− mice. Knoop hardness of Amtn−/− outer enamel was significantly reduced relative to the wild-type and was not as hard as the middle or inner enamel. Klk4−/− enamel hardness was significantly reduced at all levels, but the outer enamel was significantly harder than the inner and middle enamel. Thus the hardness patterns of the Amtn−/− and Klk4−/− mice were distinctly different, while the Amtn−/−Klk4−/− outer enamel was not as hard as in the Amtn−/− and Klk4−/− mice. We conclude that AMTN and KLK4 function independently, but are both necessary for proper enamel maturation.

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Section: Introductionmentioning

confidence: 99%

Maturation stage enamel malformations in Amtn and Klk4 null mice

et al. 2016

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“…As noted by Nishio et al. , the epithelium of the dento–gingival junction probably plays a central role in maintaining periodontal health. Working out the protective role played by specific molecules in junctional and crevicular epithelia would seem to be a productive approach for developing new antidestructive therapeutics.…”

Section: Normal Periodontium and Homeostasismentioning

confidence: 86%

“…Accordingly, an improved understanding of the molecules that mediate epithelial attachment to teeth could provide new insights into pathogenic mechanisms in periodontitis and may yield high-value targets for prevention and therapeutic intervention. Consistent with this notion, Nishio et al (19) have explored cell-adhesion molecules that mediate attachment of gingival epithelium to the tooth surface, focussing on the expression of odontogenic and ameloblast-associated molecules, such as amelotin, in the junctional epithelium. Here they consider the structure and the function of the junctional epithelium and how the pattern of expression of these molecules impacts the formation and regeneration of the junctional epithelium in wound healing.…”

Section: Normal Periodontium and Homeostasismentioning

confidence: 99%

Information generation and processing systems that regulate periodontal structure and function

Bartold¹,

McCulloch²

2013

Periodontology 2000

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The periodontium is a very dynamic organ that responds rapidly to mechanical and chemical stimuli. It is very complex in that it is composed of two hard tissues (cementum and bone) and two soft connective tissues (periodontal ligament and gingiva). Together these tissues are defined by the molecules expressed by the resident periodontal cells in each compartment and this determines not only the structure and function of the periodontium but also how it responds to infection and inflammation. The biological activity of these molecules is tightly regulated in time and space to preserve tissue homeostasis, influence inflammatory responses and participate in tissue regeneration. In this issue of Periodontology 2000 we explore new experimental approaches and data sets which help to understand the molecules and cells that regulate tissue form and structure in health, disease and regeneration.

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“…AMTN protein is continuously detected at the ameloblast-enamel interface from the maturation through the reduced enamel epithelium to the JE in mice (Somogyi-Ganss et al, 2012) and rats (Moffatt et al, 2006b; Nishio et al, 2013). The localization of AMTN in the JE is restricted to the cell/mineral interface, while ODAM is localized in a pericellular fashion in the JE.…”

Section: Roles In the Junctional Epitheliummentioning

confidence: 99%

Maturation and beyond: proteins in the developmental continuum from enamel epithelium to junctional epithelium

Ganß

Abbarin

2014

Front. Physiol.

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Enamel, covering the surface of teeth, is the hardest substance in mammals. It is designed to last a lifetime in spite of severe environmental challenges. Enamel is formed in a biomineralization process that is essentially divided into secretory and maturation stages. While the molecular events of enamel formation during the secretory stage have been elucidated to some extent, the mechanisms of enamel maturation are less defined, and little is known about the molecules present beyond the maturation stage. Several genes, all located within the secreted calcium-binding phosphoprotein (SCPP) gene cluster, were recently shown to be expressed during the developmental continuum from maturation stage ameloblasts to junctional epithelium (JE). This review introduces four such genes and their protein products, and presents our current state of knowledge on their roles, primarily in enamel formation and JE biology. The discovery of these proteins, and a more detailed analysis of their biological functions, will likely contribute to a more thorough understanding of the molecular mechanisms of enamel maturation and dentogingival attachment.

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Expression of odontogenic ameloblast‐associated and amelotin proteins in the junctional epithelium

Cited by 32 publications

References 47 publications

Maturation stage enamel malformations in Amtn and Klk4 null mice

Maturation stage enamel malformations in Amtn and Klk4 null mice

Information generation and processing systems that regulate periodontal structure and function

Maturation and beyond: proteins in the developmental continuum from enamel epithelium to junctional epithelium

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