PTH Stimulates Bone Formation in Mice Deficient in Lrp5

摘要: Lrp5 deficiency decreases bone formation and results in low mass. This study evaluated the anabolic response to intermittent PTH treatment Lrp5-deficient mice. Our indicate that is not essential for stimulatory effect of on cancellous cortical formation. Introduction: Low-density lipoprotein receptor–related protein 5 (Lrp5), a co-receptor canonical Wnt signaling, increases osteoblast proliferation, differentiation, function. The purpose this was use mice evaluate potential role gene mediating effects PTH. Materials Methods: Adult wildtype (WT, 23 male 25 female) knockout (KO, 27 26 were treated subcutaneously with either vehicle or 80 μg/kg human PTH(1-34) alternate days 6 weeks. Femoral BMC BMD determined using DXA. Lumbar vertebrae processed quantitative histomorphometry. Bone architecture by μCT. Data analyzed multiway ANOVA. Results: Cancellous mass decreased deficiency. Compared WT mice, volume distal femur lumbar vertebra KO 54% 38% lower, respectively (p < 0.0001), whereas femoral thickness 11% lower 0.0001). decrease associated 45% surface 0.0001) comparable rate Osteoclast surface, an index resorption, 24% compared 0.007). Treatment weeks resulted 59% increase 19% osteoclast = 0.053) both genotypes, but did augment genotype. Femur higher PTH-treated comparison vehicle-treated regardless genotype. Conclusions: Whereas disruption because formation, does seem be formation.