| Theme | Menopausal derangement in bone metabolism | |
|---|---|---|
| Title | Coupling factor in OPG-deficient mice | |
| Publish Date | 2004/04 | |
| Author | Midori Nakamura | Departments of Pediatric Dentistry, Matsumoto Dental University |
| Author | Nobuyuki Udagawa | Biochemistry, and, Institute for Oral Science, Matsumoto Dental University |
| Author | Hiroo Miyazawa | Departments of Pediatric Dentistry, Matsumoto Dental University / Division of Oral Health Promotion, Institute for Oral Science, Matsumoto Dental University |
| [ Summary ] | Deficiency of osteoprotegerin (OPG), a soluble decoy receptor for 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, 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 OPG-/- mice, but were unaffected by risedronate. The ectopic bone formation induced by bone morphogenetic protein-2 implantation into OPG-/- mice was not accelerated even in a high turnover rate of bone, but attenuation of mineral density from the ectopic bone was more pronounced than in wild-type mice. 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. | |