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NaF induces early differentiation of murine bone marrow cells along the granulocytic pathway but not the monocytic, or preosteoclastic pathway in vitro

SummaryThe stimulatory effects of sodium fluoride (NaF) on bone formation have been explained solely, by its activation of osteoblasts. However, whether and how NaF acts on the osteoclast linearge is poorly understood. We previously found that NaF differentiates HL-60 cells to granulocytic cells. To further test this action, we have employed here primary cultures of progenitor cells derived from murine bone marrow. NaF at subtoxic concentations (<0.5 mM) significantly up-regulated activities of several intracellular enzymes (lactate dehydrogenase, β-glucuronidase, acid phosphatase), cellular reduction of nitroblue tetrazolium, and nitric oxide (NO) production; which are all accepted as general differentiation markers. NaF (<0.5 mM) also up-regulated granulocyte-specific markers (chloroacetate esterase, cell surface antigens[Mac-1, Gr-1]) but not any of the monocyte-specific markers (nonspecific esterase, cell surface antigens [F4/80, MOMA-2]). Although other general differentiation markers (phagocytosis, adhesion, appearance, nuclear:cytoplasmic ratio) were not appreciably influenced by NaF, essentially in support of our prevous data from HL-60 cells, the present findings suggest that NaF induces early differentiation of bone marrow hemopoietic progenitor cells along the granulocytic pathway but not the monoicytic pathway that is linked to osteoclast formation. Therefore, in addition to its potent stimulatory effects on osteoblastic bone formation, NaF applied to patients with osteoporosis could be expected to indirectly reduce osteoclastic bone resorption.