Osteoblast cells proliferation

Several excellent reviews on the biological role of fluoride have been published recently [79,175-176]. The main effect of fluoride is related to osteoblast cell proliferation. 

Regarding angular cartilage, histologically, there were no developmental features of mandiblar angle, with some osteoblastic cell proliferation and a little bone matrices with mesencymal cell proliferation, in E14. Mouse mandiblar angle development started as a... 

From these experiments we observed that the thin films of Sucrose are an appropriate environment for osteoblast cells proliferation. The difference between the osteoblast cells attached to Sucrose in sample SI medium relative to control osteoblast culture is not obvious. This fact proves that Sucrose thin films are an appropriate medium to be used together with polysaccharides and iron oxides in biological active medium. 

Bioactivity is determined by the ability of a material to invoke a crystallized carbonated apatite layer from a physiological fluid. Silica incorporation in HAp promotes early crystallization and a higher rate of osteoblastic cell proliferation on sintered materials. This response has not been isolated from the effects of different Ca/P ratio, surface area, and presence of other calcium phosphate phases (Best et al. 1997). Such comparative information on the influence of different substituent elements on the bioactivity still remains to be developed. In assessing the cell growth on apatites, it is... 

Kumar, D., Gittings, J. P, Turner, I. G., Bowen, C. R., Bastida-Hidalgo, A., and Cartmell, S. H. (2010). Polarization of hydroxyapatite Influence on osteoblast cell proliferation. Acta Bio-materialia 6(4), 1549-1554. 

During bone formation, a series of sequential changes occur in cells in the osteoblast lineage, including osteoblast chemotaxis, proliferation and differentiation, which in turn is followed by formation of mineralised bone and cessation of osteoblast activity. The osteoblast changes are preceded by osteoclast apoptosis, which may be dependent on active TGF- 3 released from the resorbed bone. This is followed by chemotactic attraction of osteoblasts or their precursors to the sites of the resorption defect. Chemotactic attraction of osteoblast precursors is likely mediated by local factors produced during the resorption process. 

Lee et al., 2001 Murine osteoblastic MC3T3 cells Genistein at physiological concentrations stimulates cell proliferation and prevents oxidative damage. 

Kim, L., Rao, A.V., and Rao, L.G. 2003. Lycopene II-effect on osteoblasts The carotenoid lycopene stimulates cell proliferation and alkaline phosphatase activity of SaOS-2 cells. J Med Food 6 79-86. 

Once stem cells are committed to the osteoblast lineage, proliferating osteoprogenitors become preosteoblasts, cell growth declines, and there is a progressive expression of differentiation markers by osteoblasts (Stein et al. 1996). Osteoblastic differentiation is characterized by the sequential expression of alkaline phosphatase (ALP), an early marker of osteoblastic phenotype, followed by the synthesis and deposition of collagen type I, bone matrix proteins, and glycosaminoglycans and an increased expression of os-... 

Composites made with carbon nanostructures have demonstrated their high performance as biomaterials, basically applied in the field of tissue regeneration with excellent results. For example, P.R. Supronowicz et al. demonstrated that nanocomposites fabricated with polylactic acid and CNTs can be used to expose cells to electrical stimulation, thus promoting osteoblast functions that are responsible for the chemical composition of the organic and inorganic phases of bone [277]. MacDonald et al. prepared composites containing a collagen matrix CNTs and found that CNTs do not affect the cell viability or cell proliferation [278]. 

Finally, the modified surfaces have been tested in cell culture with human osteoblasts. Although cell adhesion was found to be roughly equivalent on treated and raw surfaces, cell proliferation greatly improved after 10 days on the fluoridated surface [159]. In addition, the fluoridation treatment considerably reduced the degradation of the coating. 

Fig. 11. Modes of action of fluorine on osteoblastic cells, (a) Tyrosine phosphatase hypothesis in osteoblastic cells, fluoride ion directly inhibits tyrosine phosphatase. Inhibition of this enzyme enhances the tyrosine phosphorylation of signalling molecules induced by receptor tyrosine kinase, which leads to activation of the extracellular signal-regulated kinase (ERK) through the Ras pathway and enhanced cell proliferation, (b) G-protein hypothesis in osteoblast-like cells, fluoride ions form a complex with aluminum, probably fluoroaluminate, which interacts with guanosine 5 -diphosphate (GDP) to form guanosine 5 -triphosphate (GTP)-like molecule. Activation of the G, protein stimulates the tyrosine phosphorylation of signalling molecules by a yet unknown tyrosine kinase (Tyr Kin) and activation of the ERK kinase through the Ras pathway leads to enhanced cell proliferation. (Reproduced by permission of Elsevier from Ref. [175] ...

The data concerning the effect of fluoride-containing apatites on cell adhesion, proliferation and expression seem rather disparate, probably because of the variation of other surface characteristics and the use of different cell strains. No real negative effect of fluoride-containing substrates has been reported so far and the osteoblast cells seem to behave similarly [184,185] or better [183,186,187] on fluoridated apatites than on HA surfaces. Some reports mention weaker attachment and proliferation, compensated for by improved collagen matrix production [188]. The shape of cells appeared different on fluoridated apatites than on HA. Other authors have found an improvement in cell attachment [183] which has been attributed to the change in surface charge of FA compared to HA. 

They also reported that lycopene had a stimulatory effect on ALP activity, a marker of osteoblastic differentiation in more mature cells, but depending on the time of addition, it had an inhibitory or no effect on younger SaOS-Dex cells (Figure 14). These findings constituted the first report on the effect of lycopene on human osteoblasts. In another study by Park et al. (1997), the effect of lycopene on MC3T3 cells (the osteoblastic cells of mice) was contrary to the findings of Kim et al. (2003). Park demonstrated that lycopene had an inhibitory effect on cell proliferation. Both studies, however, reported that ALP activity was stimulated. The discrepancy in the effect of lycopene on cell proliferation could be a result of species differences or experimental conditions. More studies are required to clarify the role of lycopene in osteoblasts. 

FIG. 13 Effect of lycopene on the proliferation of SaOS-2 cells. Compared with respective vehicle control of the same dilution a = p < 0.05, b = p < 0.001, c=p < 0.005 (Kim et al., 2003). (Lycopene II - Effect on osteoblasts The carotenoid lycopene stimulates cell proliferations and alkaline phosphotase activity of SaOS-2 cells. Reprinted from Journal of Medicinal Food. 2003 6, pp. 79-86 by permission of Mary Ann Liebert, Inc., Publishers.)... 

Hulley, P. A., F. Gordon, and F.S. Hough. 1998. Inhibition of mitogen-activated protein kinase activity and proliferation of an early osteoblast cell line (MBA 15.4) by dexamethasone Role of protein phosphatases. Endocrinology 139 2423-31. 

Three distinct periods of osteoblast differentiation at the genetic level have been identified during in vitro examination of developing osteoblasts after initial adhesion to a surface (1) cell proliferation and extracellular matrix synthesis, (2) extracellular matrix development and maturation, and (3) extracellular matrix mineralization (Stein and Lian, 1993). A schematic of the time course of osteoblast function and synthesis of extracellular matrix proteins on a newly implanted biomaterial is shown in Fig. 6. 

In osteoblasts, keratinocytes, and colonocytes, andpossibly other cells, calcitriol acts via cell surface receptors linked to phospholipase C, resulting in release of diacylglycerol and inositol trisphosphate (Section 14.4.1), followed by opening of intracellular calcium channels and activation of protein kinase C and mitogen-activated protein (MAP) kinases. The effect of this is inhibition of cell proliferation and induction of differentiation. A variety of analogs of calcitriol that do not bind to the nuclear receptor do bind to, and activate, the cell surface receptor, including l,25-dihydroxy-7-dehydrocholesterol and 1,25-dihydroxylumisterol. The rapid nongenomic responses to vitamin D can be demonstrated in knockout mice that lack the vitamin D nuclear receptor (Farach-Carson and Ridall, 1998 Nemere and Farach-Carson, 1998). 

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