Bone Abstracts

Osteoclast presents a central role in several inflammatory diseases that are associated to bone destruction. This condition results from increased osteoclastic bone resorption and/or decreased bone formation. Fluoride (F) is widely consumed in the drinking water due to its anticariogenic effect and has been shown to modulate in vivo bone metabolism in a strain-specific dependent manner. It enhances bone formation in 129P3/J mice but not in A/J mice. However, its effect on osteoclastogenesis and the strain dependency remain uncertain. Therefore, the objective of this study was to evaluate the effects of F on formation and function of bone marrow macrophage-derived osteoclasts in a strain-specific manner. Thus, bone marrow cells from A/J and 129P3/J were cultivated in α-MEM medium containing M-CSF and RANKL in presence or absence of different concentrations of F for 7 days. The number of osteoclasts was evaluated by tartrate-resistant acid phosphatase (TRAP) staining and their functional responses were evaluated by the tartrate-resistant acid phosphatase (TRAP), metaloproteinase (MMP)-2 and -9 and resorptive activities. In A/J-derived cells, F varying from 10⁻³ to 10⁻⁷ M significantly increased TRAP activity compared to untreated cells (P< 0.05). However, no significant alterations were observed in F-treated 129P3/J cells compared to untreated cells. Moreover, control A/J and 129P3/J present similar TRAP activity, suggesting that the strain-specific response was associated to F effect. While the MMP-2 did not change, the activity of osteoclast-produced MMP-9 increased about 30% by 10⁻³ M F in A/J but did not alter in 129P3/J cells. Moreover, 129P3/J-derived osteoclast demonstrated slightly effect on the resorptive function after F treatment whereas osteoclast from A/J mice was significantly altered. Therefore, F enhances osteoclast formation and function in A/J-derived cells but not in 129P3/J- derived cells. The data provide knowledgement of cell-type contribution in the well-known effect of F on the bone metabolism.