Zebrafish scales consist of bone-forming osteoblasts, bone-resorbing 
osteoclasts, and calcified bone matrix. To elucidate the underlying molecular 
mechanism of the effects induced by dynamic and static acceleration, we 
investigated the scale osteoblast- and osteoclast-specific marker gene 
expression involving osteoblast-osteoclast communication molecules. Osteoblasts 
express RANKL, which binds to the osteoclast surface receptor, RANK, and 
stimulates bone resorption. OPG, on the other hand, is secreted by osteoblast as 
a decoy receptor for RANKL, prevents RANKL from binding to RANK and thus 
prevents bone resorption. Therefore, the RANK-RANKL-OPG pathway contributes to 
the regulation of osteoclastogenesis by osteoblasts. Semaphorin 4D, in contrast, 
is expressed on osteoclasts, and binding to its receptor Plexin-B1 on 
osteoblasts results in suppression of bone formation. In the present study, we 
found that both dynamic and static acceleration at 3.0×g decreased RANKL/OPG 
ratio and increased osteoblast-specific functional mRNA such as alkaline 
phosphatase, while static acceleration increased and dynamic acceleration 
decreased osteoclast-specific mRNA such as cathepsin K. Static acceleration 
increased semaphorin 4D mRNA expression, while dynamic acceleration had no 
effect. The results of the present study indicated that osteoclasts have 
predominant control over bone metabolism via semaphorin 4D expression induced by 
static acceleration at 3.0×g.