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Dentonin, a MEPE Fragment, Initiates Pulp-healing Response to Injury

¹ Laboratoire de Réparation et Remodelage des Tissus Orofaciaux, EA 2496, Groupe Matrices Extracellulaires et Biominéralisation, Faculté de Chirurgie Dentaire, Université Paris 5, 1, rue Maurice Arnoux, 92120 Montrouge, France;
² Acologix Inc., 3960 Point Eden Way, Hayward, CA 94545, USA; and
³ Department of Orofacial Sciences, University of California at San Francisco, P.O. Box 0422, San Francisco, CA 94143-0422, USA

View larger version (115K): [in this window] [in a new window]   Figure 1. At 8 days, the pulps implanted with Dentonin-loaded agarose beads (b) show a slight to moderate inflammation in the area beneath the cavity (a,c). Cells accumulated around agarose beads used as carriers (arrow) (b). Matrix formation was already seen in some pulps, either around dentin debris (d) (a), or as dendritic bone-like structures (asterisk) (c). However, there is no detectable formation of a reparative dentinal bridge at the exposure site. Anti-Dentonin stains the surfaces of Dentonin-coated agarose beads (arrow) (d). PCNA-positive proliferating cells are seen within the pulp and accumulated around the beads (b) (arrow) (e). Positively labeled RP59 are also detected in the pulp and around the agarose beads used as Dentonin carriers (b) (f). A few cells, located at the surfaces of the Dentonin-soaked beads, are labeled positively for osteopontin (OPN), suggesting an early differentiation into osteoblasts (g). Bar = 100 µm.

View larger version (107K): [in this window] [in a new window]   Figure 2. At 15 days, a cavity (c) is seen at the exposure area, partially filled by gingival overgrowth (g). After Dentonin implantation, inflammation was generally completely resolved (a). The formation of a reparative dentinal bridge (asterisk) has already started (a,b). In a few teeth, moderate inflammation is seen, together with the beginning of the repair process (asterisk) (c). Fifteen days after Dentonin implantation, x-ray microanalysis shows evidence of calcium (Ca) and phosphate (P) (d) distribution, and highlights the formation of a mineralized structure inside the pulp (asterisk). Positive anti-Dentonin staining (arrow) can still be observed around the Dentonin-coated agarose beads (e). There is a decrease in PCNA-positive cells (arrow) around Dentonin-coated agarose beads (b), compared with the staining at 8 days. Labeled cells are located near, but are not closely associated with, the surfaces of the beads (f). At this time interval, the shapes of the Dentonin-coated beads are less regular, with a few indentations, or flattening in some beads (e,f). Positive labeling can be seen for DSP in the odontoblasts, but is missing in the area where pulp repair was in progress. d = dentin (g). Positive cells for RP59 were located at the surfaces of the beads, but the overall staining was decreased compared with the staining seen at day 8 (h). In contrast, the staining for osteopontin (OPN) was enhanced at day 15, forming thick rings around the surfaces of the Dentonin-loaded beads (b) (i). Bar = 100 µm.

View larger version (111K): [in this window] [in a new window]   Figure 3. At 30 days, most Dentonin-implanted pulps display reparative dentin at different stages of formation (asterisk), near the beads (b) and partially filling (a) or totally filling the exposure site, and embedding the beads (b) and dentin debris pushed into the pulp during the perforation (b). In some teeth, the formation of reparative dentin has been initiated, with residual inflammation (c). In other teeth, reparative mineralization led to the closure of the pulp chamber (arrow) and to the formation of a dentinal bridge (asterisk), partially sealing the cavity (c), as shown by x-ray microanalysis for calcium (Ca) and phosphate (P) (d,e). Bar = 100 µm.

Journal of Dental Research, Vol. 86, No. 8, 780-785 (2007)
DOI: 10.1177/154405910708600818


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