Skeletal mass is regulated by the coordinated action of bone forming osteoblasts and bone
resorbing osteoclasts. Accelerated rates of bone resorption relative to bone formation lead to net bone loss
and the development of osteoporosis, a devastating disease that predisposes the skeleton to fractures. Bone
fractures are associated with significant morbidity and in the case of hip fractures, high mortality. Gentian violet
(GV), a cationic triphenylmethane dye, has long been used as an antifungal and antibacterial agent and is
presently under investigation as a potential chemotherapeutic and antiangiogenic agent. However, effects on
bone cells have not been previously reported and the mechanisms of action of GV, are poorly understood. In
this study we show that GV suppresses receptor activator of NF-κB ligand (RANKL)-induced differentiation of
RAW264.7 osteoclast precursors into mature osteoclasts, but paradoxically stimulates the differentiation of
MC3T3 cells into mineralizing osteoblasts. These actions stem from the capacity of GV to suppress activation
of the nuclear factor kappa B (NF-κB) signal transduction pathway that is required for osteoclastogenesis, but
inhibitory to osteoblast differentiation and activity. Our data reveal that GV is an inhibitor of NF-κB activation
and may hold promise for modulation of bone turnover to promote a balance between bone formation and
bone resorption, favorable to gain of bone mass.
Keywords: Bone formation, gentian violet, NF-κB, osteoblast, osteoclast, osteoporosis.
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