Fluoride at non-toxic dose affects odontoblast gene expression in vitro

Wurtz, Tilmann; Houari, Sophia; Mauro, Nicole; MacDougall, Mary; Peters, Heiko; Berdal, Ariane

doi:10.1016/j.tox.2008.04.013

Cited by 45 publications

(34 citation statements)

References 56 publications

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“…These findings clearly indicate that NaF, but not serum starvation, contributes to apoptosis in MDPC-23 cells. In the mouse odontoblast cell line MO6-G3 treated with 0.5-3 mM NaF for 96 hrs at 33°C in the presence of 20% FBS, morphological analysis did not show signs of apoptotic transformation (Wurtz et al, 2008). The differences in experimental conditions might influence the occurrence of apoptosis in odontoblasts.…”

Section: Discussionmentioning

confidence: 89%

NaF Activates MAPKs and Induces Apoptosis in Odontoblast-like Cells

et al. 2009

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The cytotoxic effects of fluoride on odontoblasts are not clear. In this study, we examined whether NaF induces apoptosis in MDPC-23 odontoblast-like cells and the involvement of mitogen-activated protein kinase (MAPK) signaling pathways in NaF-induced apoptosis. MDPC-23 cells incubated with 5 mM NaF for 24 hrs exhibited caspase-3 activation, cleavage of poly(ADP-ribose) polymerase, DNA fragmentation, and an increase in cytoplasmic nucleosomes. Prior to the induction of apoptosis, all MAPKs examined were phosphorylated, but in a different manner. In contrast to the sustained phosphorylation of c-Jun NH(2)-terminal kinase (JNK) and p38, NaF exposure induced a biphasic phosphorylation of extracellular signal-regulated protein kinase (ERK). NaF-induced apoptosis was markedly suppressed by treatment with the JNK inhibitor, SP600125, and mildly suppressed by the MAPK/ERK kinase inhibitor, U0126. Inhibition of p38 activity did not protect cells from apoptosis. Thus, exposure to NaF induces apoptosis in odontoblast-like cells, depending on JNK and, less significantly, ERK pathways.

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Section: Discussionmentioning

confidence: 89%

NaF Activates MAPKs and Induces Apoptosis in Odontoblast-like Cells

et al. 2009

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“…The penetration of fluoride ions into the Ti structure could potentially play a role as a fluoride reserve for stimulating osteoblast gene expression [17] and improving the bone-to-implant contact [16]. Moreover, since fluoride is toxic at high dosage [35] it is also important to investigate its safety limit. It is also important to include the importance of the surface topography when discussing the number of cell attached on the surfaces.…”

Section: Elementsmentioning

confidence: 99%

The effect of hydrofluoric acid treatment of titanium surface on nanostructural and chemical changes and the growth of MC3T3-E1 cells

et al. 2009

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“…In a bone mineralizing culture system derived from rat femur washes, the influence of fluoride on MMP expression was investigated at the onset of mineralization: incubation with 10 -7 (1.9 μg/l) and 10 -5 (190 μg/l) M fluoride resulted in a decreased expression of a 45-kDa MMP (probably MMP-1), in an increased expression of MMP-3, and in the appearance of a band at 110 kDa (MMP-9) [38]. In mouse MO6-G3 cultured odontoblasts incubated for 5 days with 1 mM sodium fluoride (19 mg/l fluoride), no sign of apoptosis was found, but several RNAs, such as those encoding the extracellular matrix proteins asporin and fibromodulin and the cell membrane-associated proteins periostin and IMT2A were greatly reduced [39].…”

Section: Effects Of Fluoride On Bonementioning

confidence: 99%

Fluoride Effects: The Two Faces of Janus

Gazzano

Bergandi²,

Riganti³

et al. 2010

CMC

103

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The behavior of fluoride ions in the human organism is a classic example of double-edged sword. On the one hand the daily supplementation with fluoride is undoubtedly an important preventing factor in protecting teeth from caries, and, as an important mitogenic stimulus for osteoblasts, it may enhance mineral deposition in bone, but on the other hand fluoride, above a threshold concentration, has been demonstrated to be toxic. We present here a brief review of fluoride metabolism and exposure, its use in caries prevention and its effects on bone, followed by an updating about the main hypotheses concerning its mechanism of action and toxicity. The effects of fluoride have been related mainly to its ability to evoke the activation of G proteins and the inhibition of phosphotyrosine phosphatases, leading to an intracellular increase of tyrosine phosphorylation and activation of the mitogen-activated protein kinase pathway, and its capacity to cause generation of reactive oxygen species. We present also a unifying hypothesis accounting for these apparently different effects, although the available experimental models and conditions are highly variable in the literature. A lot of experiments still need to be performed to clarify the positive and negative effects of fluoride. Finding the mechanisms accounting for fluoride toxicity is an important point: indeed, the use of fluoride has been proposed in the preparation of new biomaterials to be inserted in the bone, in order to improve their stable and safe integration.

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Fluoride at non-toxic dose affects odontoblast gene expression in vitro

Cited by 45 publications

References 56 publications

NaF Activates MAPKs and Induces Apoptosis in Odontoblast-like Cells

NaF Activates MAPKs and Induces Apoptosis in Odontoblast-like Cells

The effect of hydrofluoric acid treatment of titanium surface on nanostructural and chemical changes and the growth of MC3T3-E1 cells

Fluoride Effects: The Two Faces of Janus

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