New cellular models for tracking the odontoblast phenotype

Priam, Fabienne; Ronco, V.; Locker, Morgane; Bourd, Katia; Bonnefoix, Mireille; Duchêne, T.; Bitard, Juliette; Wurtz, Tilmann; Kellermann, Odile; Goldberg, Michel; Poliard, Anne

doi:10.1016/j.archoralbio.2004.10.007

Cited by 56 publications

(65 citation statements)

References 28 publications

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“…Pulp cultures contain heterogeneous cell types (odontoprogenitors, osteoprogenitors, and a small number of stem cells) and (Priam et al 2005) that lacks mineralization potential, and these values were subtracted from respective XO measurements. Expression of all genes except Dspp was normalized to that in VHtreated cultures at day 7, which is arbitrarily set to 1 and is indicated by the dashed line.…”

Section: Effects Of Fgf2 On Facs-sorted 23-gfp + and 23-gfp − Populmentioning

confidence: 99%

Enhanced Dentinogenesis of Pulp Progenitors by Early Exposure to FGF2

et al. 2015

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Members of the fibroblast growth factor (FGF) family play essential and important roles in primary and reparative dentinogenesis. Although there appears to be a general agreement on the effects of FGF signaling on the proliferation of pulp cells, there are conflicting results regarding its effects on odontoblast differentiation. We recently examined the effects of continuous exposure of dental pulp cells to FGF2 and showed that the effects of FGF2 on differentiation of progenitor cells into odontoblasts were stage specific and dependent on the stage of cell maturity. The purpose of this study was to gain further insight into cellular and molecular mechanisms regulating the stimulatory effects of FGF2 on odontoblast differentiation. To do so, we examined the effects of early and limited exposure of pulp cells from a series of green fluorescent protein (GFP) reporter transgenic mice that display stage-specific activation of transgenes during odontoblast differentiation to FGF2. Our results showed that early and limited exposure of pulp cells to FGF2 did not have significant effects on the extent of mineralization but induced significant increases in the expression of Dmp1 and Dspp and the number of DMP1-GFP + and DSPP-Cerulean + odontoblasts. Our results also showed that the stimulatory effects of FGF2 on odontoblast differentiation were mediated through FGFR/MEK/Erk1/2 signaling, increases in Bmp2, and activation of the BMP/BMPR signaling pathway. These observations show that early and limited exposure of pulp cells to FGF2 alone promotes odontoblast differentiation and provides critical insight for applications of FGF2 in dentin regeneration.

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Section: Effects Of Fgf2 On Facs-sorted 23-gfp + and 23-gfp − Populmentioning

confidence: 99%

Enhanced Dentinogenesis of Pulp Progenitors by Early Exposure to FGF2

et al. 2015

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“…Cell Culture-Preodontoblast cell line was kindly provided by Dr. A. Poliard, France (29). The cells were cultured in Dulbecco's modified Eagle's medium (Invitrogen), supplemented with 10% fetal bovine serum, penicillin G (100 IU/ml), and streptomycin (100 mg/ml), and incubated at 37°C and 5% CO 2 in air.…”

Section: Double Fluorochrome Labeling Of the Teeth-mentioning

confidence: 99%

A Novel Role of Periostin in Postnatal Tooth Formation and Mineralization

Zhang

Sun

et al. 2011

Journal of Biological Chemistry

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Periostin plays multiple functions during development. Our previous work showed a critical role of this disulfide-linked cell adhesion protein in maintenance of periodontium integrity in response to occlusal load. In this study, we attempted to address whether this mechanical response molecule played a direct role in postnatal tooth development. Our key findings are 1) periostin is expressed in preodontoblasts, and odontoblasts; and the periostin-null incisor displayed a massive increase in dentin formation after mastication; 2) periostin is also expressed in the ameloblast cells, and an enamel defect is identified in both the adult-null incisor and molar; 3) deletion of periostin leads to changes in expression profiles of many non-collagenous protein such as DSPP, DMP1, BSP, and OPN in incisor dentin; 4) the removal of a biting force leads to reduction of mineralization, which is partially prevented in periostin-null mice; and 6) both in vitro and in vivo data revealed a direct regulation of periostin by TGF-␤1 in dentin formation. In conclusion, periostin plays a novel direct role in controlling postnatal tooth formation, which is required for the integrity of both enamel and dentin.It is well known that mechanical loading stimulates new bone formation, whereas unloading or disuse of bone (e.g. longtime bed rest, spaceflight, or cast immobilization) accelerates bone resorption. This adaptation is critical for bone modeling and remodeling (1). The anabolic degree to which the bone responds to physical activity has being associated with the intensity and loading magnitude of the exercise. Under normal conditions, strenuous exercise such as weightlifting yields thicker and denser bone compared with jogging and swimming; the latter two types of exercise are less forceful and produce less mechanical stimulus (2). A well-designed study by Tatsumi et al. (3) demonstrated that osteocytes are the key sensor controlling both bone formation and bone resorption in the unloading animal model. The accumulated evidence supports a recommendation by the National Osteoporosis Foundation: regular weight-bearing and muscle strengthening exercise is an effective countermeasure to fight against osteoporosis, a silent bone loss in the elderly population worldwide.The development and maintenance of the dental and periodontal structures are also directly influenced by mechanical stimuli (4). This stimulation can be the result of normal occlusal function or orthodontic treatment. It is well documented that during orthodontic treatment, tension on the side from which a tooth moves away results in the formation of new bone (i.e. osteogenic), while compression on the opposite site leads to bone resorption. This relationship seems contrary to the situation in the long bone where the loaded site is osteogenic and the unloaded site is resorptive (5). One of the interpretations regarding this difference between the alveolar bone and long bone is that the periodontal ligament (PDL), 3 a soft tissue located between the teeth and alveolar bone,...

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“…Clones-Immortalized pulp cell colonies were obtained from tooth germs of day 18-mouse embryos transgenic for an adenovirus SV40 recombinant plasmid [9]. All the cells isolated from these mice express the large T antigen of SV40.…”

Section: Immortalized Progenitorsmentioning

confidence: 99%

“…Five of these clones were further analyzed. They express nestin, RP59, Pax9, Msx 1 and 2, Dlx 2 and 9, Lhx6 and 7, DSP, DPP, DMP-1, amelogenin, enamelysin (MMP-20) and alkaline phosphatase, and therefore display the characteristics expected for odontoblast progenitors [9,10].…”

Section: Immortalized Progenitorsmentioning

confidence: 99%

Matricellular molecules and odontoblast progenitors as tools for dentin repair and regeneration

et al. 2007

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This review summarizes the in vivo experiments carried out by our group after implantation of bioactive molecules (matricellular molecules) into the exposed pulp of the first maxillary molar of the rat or the mandibular incisor of rats and mice. We describe the cascade of recruitment, proliferation and terminal differentiation of cells involved in the formation of reparative dentin. Cloned immortalized odontoblast progenitors were also implanted in the incisors and in vitro studies aimed at revealing the signaling pathways leading from undifferentiated progenitors to fully differentiated polarized cells. Together, these experimental approaches pave the way for controlled dentin regenerative processes and repair. NIH Public Access

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New cellular models for tracking the odontoblast phenotype

Cited by 56 publications

References 28 publications

Enhanced Dentinogenesis of Pulp Progenitors by Early Exposure to FGF2

Enhanced Dentinogenesis of Pulp Progenitors by Early Exposure to FGF2

A Novel Role of Periostin in Postnatal Tooth Formation and Mineralization

Matricellular molecules and odontoblast progenitors as tools for dentin repair and regeneration

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