Disease relevance of Dental Papilla

• Immortalization of bovine dental papilla cells with simian virus 40 large t antigen [1].
• The observed crown size reduction could result from the same factors that cause cleft palate and/or hypodontia, or from a lack of sulfation in the developing dental papilla [2].

High impact information on Dental Papilla

• In situ hybridization demonstrated that the HGF gene was expressed only in the cells of the dental papilla of the tooth germ in vivo [3].
• Msx2 expression greatly overlaps both histone H4 and Colla1 expression in ovoid preodontoblasts and dental papilla cells [4].
• Recombinant human GDF11 induced the expression of dentin sialoprotein (Dsp), a differentiation marker for odontoblasts, in mouse dental papilla mesenchyme in organ culture [5].
• Dkk2 was seen in the dental papilla, whereas Dkk3 was specifically expressed in the putative epithelial signaling centers, the primary and secondary enamel knots [6].
• By the age of 1 week, the dental papilla was widened, with disorganization of the odontoblastic layer and decreased dentin matrix [7].

Anatomical context of Dental Papilla

• Enamelysin transcripts have previously been observed in the enamel organ and dental papillae of the developing tooth [8].
• Here, we show that the sources of the enamelysin transcripts are the ameloblasts of the enamel organ and the odontoblasts of the dental papilla [8].
• EDTA-isolated dental papillae remained covered by the basal lamina for 15 to 18 h [9].
• EDTA-treatment removed the basal lamina from the basal surface of the epithelium, but left it associated with the dental papillae [9].
• Both splice forms of FGFR3 were expressed in dental papilla mesenchyme [10].

Associations of Dental Papilla with chemical compounds

• EDTA- or trypsin-isolated dental papillae were grown for three to 24 h at the top of a plasma clot [9].
• A chondroitin sulfate epitope in mammalian dental pulp and its developmental expression in mouse dental papilla [11].
• During root formation, the follicular cells lost NCAM first from the level of the cervical root and later from the coronal part, while an additional NCAM positive area appeared deep in the dental papilla [12].
• After the onset of cusp formation, strong staining was also observed over the occlusal region of the dental papilla while the cervical region of the dental papilla remained 2B6-negative [13].
• In the region with poorly-developed aperiodic fibrils, the separation occurred at the junction between the inner enamel epithelial BM and the dental papilla, and the aperiodic fibrils were exposed, showing the typical picture of dithiothreitol separation [14].

Gene context of Dental Papilla

• In situ hybridization analysis showed developmentally regulated expression during tooth formation for Fgf-3 and Fgf-10 that was mainly restricted to the dental papilla mesenchymal cells [15].
• At the late bud stage, however, Robo1 transcripts were evident in the primary enamel knot, and at the cap stage a pronounced expression was noted in the middle of the tooth germ covering the primary enamel knot and dental papilla mesenchyme [16].
• NT-3 mRNA was observed in the dental papilla and in the area of the cervical loop [17].
• NGF mRNA labeling was weak and confined predominantly to the dental papilla [17].
• At E14, Fgf10 and Fgf3 were coexpressed in the dental papilla [18].

Analytical, diagnostic and therapeutic context of Dental Papilla

• Fibronectin was, however, detected intracellularly, and metabolic labeling and immunoprecipitation studies indicated that the dental papilla cells continued to synthesize fibronectin in culture [19].
• Autoradiography confirmed the preferential interaction of fibronectin with the dental papilla [20].

References