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Bone response to fluoride exposure is influenced by genetics.

Kobayashi CA, Leite AL, Peres-Buzalaf C, Carvalho JG, Whitford GM, Everett ET, Siqueira WL, Buzalaf MA - PLoS ONE (2014)

Bottom Line: Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined.Also, F exposure was associated with dose-specific and strain-specific alterations in expression of proteins involved in osteogenesis and osteoclastogenesis.In conclusion, our findings confirm a genetic influence in bone response to F exposure and point to several proteins that may act as targets for the differential F responses in this tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, SP, Brazil.

ABSTRACT
Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined. A label-free proteomics approach was employed to identify and evaluate changes in bone protein expression in two mouse strains having different susceptibilities to develop dental fluorosis and to alter bone quality. In vivo bone formation and histomorphometry after F intake were also evaluated and related to the proteome. Resistant 129P3/J and susceptible A/J mice were assigned to three groups given low-F food and water containing 0, 10 or 50 ppmF for 8 weeks. Plasma was evaluated for alkaline phosphatase activity. Femurs, tibiae and lumbar vertebrae were evaluated using micro-CT analysis and mineral apposition rate (MAR) was measured in cortical bone. For quantitative proteomic analysis, bone proteins were extracted and analyzed using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS), followed by label-free semi-quantitative differential expression analysis. Alterations in several bone proteins were found among the F treatment groups within each mouse strain and between the strains for each F treatment group (ratio ≥1.5 or ≤0.5; p<0.05). Although F treatment had no significant effects on BMD or bone histomorphometry in either strain, MAR was higher in the 50 ppmF 129P3/J mice than in the 50 ppmF A/J mice treated with 50 ppmF showing that F increased bone formation in a strain-specific manner. Also, F exposure was associated with dose-specific and strain-specific alterations in expression of proteins involved in osteogenesis and osteoclastogenesis. In conclusion, our findings confirm a genetic influence in bone response to F exposure and point to several proteins that may act as targets for the differential F responses in this tissue.

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Mineral apposition rate (MAR) of femur from A/J and 129P3/J mice after F exposure.(A) Upper squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of 129P3/J mice. Lower squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of A/J mice. Concentrations of F are indicated. (B) Values are mean ± SD of the measurement distances between the labels, n = 8/group. * Represents significant differences between strains for each group (p<0.05); #p<0.01 and ##p<0.001 represent significant differences of control and 10 ppmF-treated 129P3/J versus 50 ppmF-treated 129P3/J mice, respectively.
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pone-0114343-g003: Mineral apposition rate (MAR) of femur from A/J and 129P3/J mice after F exposure.(A) Upper squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of 129P3/J mice. Lower squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of A/J mice. Concentrations of F are indicated. (B) Values are mean ± SD of the measurement distances between the labels, n = 8/group. * Represents significant differences between strains for each group (p<0.05); #p<0.01 and ##p<0.001 represent significant differences of control and 10 ppmF-treated 129P3/J versus 50 ppmF-treated 129P3/J mice, respectively.

Mentions: Slight dose-dependent increases in the rate of new bone deposition were observed for both strains but they were significant only in the 50 ppmF-treated 129P3/J group when compared to the control and 10 ppmF groups (p<0.01 and p<0.05, respectively) (Fig. 3A,B). Comparing both strains, the MAR data were significantly higher in 50 ppmF-treated 129P3/J than the respective A/J (p<0.05) (Fig. 3A,B).


Bone response to fluoride exposure is influenced by genetics.

Kobayashi CA, Leite AL, Peres-Buzalaf C, Carvalho JG, Whitford GM, Everett ET, Siqueira WL, Buzalaf MA - PLoS ONE (2014)

Mineral apposition rate (MAR) of femur from A/J and 129P3/J mice after F exposure.(A) Upper squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of 129P3/J mice. Lower squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of A/J mice. Concentrations of F are indicated. (B) Values are mean ± SD of the measurement distances between the labels, n = 8/group. * Represents significant differences between strains for each group (p<0.05); #p<0.01 and ##p<0.001 represent significant differences of control and 10 ppmF-treated 129P3/J versus 50 ppmF-treated 129P3/J mice, respectively.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4263599&req=5

pone-0114343-g003: Mineral apposition rate (MAR) of femur from A/J and 129P3/J mice after F exposure.(A) Upper squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of 129P3/J mice. Lower squares: Representative images showing calcein (green) and alizarin complexone (red) labeled mid-diaphyseal cross-sections of A/J mice. Concentrations of F are indicated. (B) Values are mean ± SD of the measurement distances between the labels, n = 8/group. * Represents significant differences between strains for each group (p<0.05); #p<0.01 and ##p<0.001 represent significant differences of control and 10 ppmF-treated 129P3/J versus 50 ppmF-treated 129P3/J mice, respectively.
Mentions: Slight dose-dependent increases in the rate of new bone deposition were observed for both strains but they were significant only in the 50 ppmF-treated 129P3/J group when compared to the control and 10 ppmF groups (p<0.01 and p<0.05, respectively) (Fig. 3A,B). Comparing both strains, the MAR data were significantly higher in 50 ppmF-treated 129P3/J than the respective A/J (p<0.05) (Fig. 3A,B).

Bottom Line: Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined.Also, F exposure was associated with dose-specific and strain-specific alterations in expression of proteins involved in osteogenesis and osteoclastogenesis.In conclusion, our findings confirm a genetic influence in bone response to F exposure and point to several proteins that may act as targets for the differential F responses in this tissue.

View Article: PubMed Central - PubMed

Affiliation: Department of Biological Sciences, Bauru School of Dentistry, University of São Paulo, Bauru, SP, Brazil.

ABSTRACT
Genetic factors influence the effects of fluoride (F) on amelogenesis and bone homeostasis but the underlying molecular mechanisms remain undefined. A label-free proteomics approach was employed to identify and evaluate changes in bone protein expression in two mouse strains having different susceptibilities to develop dental fluorosis and to alter bone quality. In vivo bone formation and histomorphometry after F intake were also evaluated and related to the proteome. Resistant 129P3/J and susceptible A/J mice were assigned to three groups given low-F food and water containing 0, 10 or 50 ppmF for 8 weeks. Plasma was evaluated for alkaline phosphatase activity. Femurs, tibiae and lumbar vertebrae were evaluated using micro-CT analysis and mineral apposition rate (MAR) was measured in cortical bone. For quantitative proteomic analysis, bone proteins were extracted and analyzed using liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS), followed by label-free semi-quantitative differential expression analysis. Alterations in several bone proteins were found among the F treatment groups within each mouse strain and between the strains for each F treatment group (ratio ≥1.5 or ≤0.5; p<0.05). Although F treatment had no significant effects on BMD or bone histomorphometry in either strain, MAR was higher in the 50 ppmF 129P3/J mice than in the 50 ppmF A/J mice treated with 50 ppmF showing that F increased bone formation in a strain-specific manner. Also, F exposure was associated with dose-specific and strain-specific alterations in expression of proteins involved in osteogenesis and osteoclastogenesis. In conclusion, our findings confirm a genetic influence in bone response to F exposure and point to several proteins that may act as targets for the differential F responses in this tissue.

Show MeSH
Related in: MedlinePlus