@article{oai:mdu.repo.nii.ac.jp:00000559,
 author = {中村, 美どり and 松浦, 幸子 and 宮沢, 裕夫 and 宇田川, 信之},
 issue = {1},
 journal = {松本歯学},
 month = {Apr},
 note = {application/pdf, Deficiency of osteoprotegerin (OPG), a soluble decoy receptor for the receptor activator of NF-kB ligand (RANKL), in mice induces osteoporosis caused by enhanced bone resorption, but also accelerates bone formation. We examined whether bone formation is coupled with bone resorption in OPG-deficient (OPG^<-/->) mice delete using risedronate, an inhibitor of bone resorption. Histomorphometric analysis showed that bone formation-related parameters (e.g., mineral apposition rate and osteoblast surface/bone surface) in OPG^<-/-> mice sharply decreased with suppression of bone resorption by daily injection of risedronate for 30 days. OPG^<-/-> mice exhibited high serum alkaline phosphatase activity and osteocalcin concentration, both of which were decreased to the levels of wild-type mice by the risedronate injection. Serum levels of RANKL were markedly elevated in the OPG^<-/-> mice, but were unaffected by risedronate. These results suggest that bone formation is coupled with bone resorption at local sites in OPG^<-/-> mice, and that serum RANKL levels do not reflect this coupling.},
 pages = {9--19},
 title = {破骨細胞の神秘},
 volume = {30},
 year = {2004}
}