ArticleJBMR plus2026
Bone anabolic effects of tibial loading in combination with dual sclerostin and Dkk1 antibodies in aged mice.
Article in JBMR plus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Aging is associated with decreased bone formation and bone mass and increased fracture risk. Wnt pathway activation by mechanical loading is a potent strategy to improve bone mass; however, load-induced bone formation is diminished with aging. Neutralizing antibody (Ab) therapies targeting Wnt pathway inhibitors sclerostin (Scl) and Dickkopf-related protein 1 (Dkk1) have proven successful in preclinical and clinical osteoporotic conditions. We asked whether treatment combining Scl-Ab and Dkk1-Ab can increase load-induced bone formation in a preclinical model of osteoporosis. Aged (22-mo) C57BL/6N female mice underwent combination Scl-Ab plus Dkk1-Ab therapy (15 mg/kg each; s.c.; 2×/wk; saline control) for 2 wk, concomitant with tibial loading (-2200 me, 1200 cycles/d, 5 d/wk). Based on serial micro-CT, dual-antibody treatment had a significant, positive effect on bone morphology, independent of loading. For example, from day 0 to day 15 cancellous BV/TV increased by 50% and cortical area by 25% in non-loaded limbs of antibody-treated mice, while vehicle-treated mice had no change. However, antibody treatment did not enhance the effects of tibial loading on bone morphology, which was not significant. On the other hand, antibody treatment and loading each increased periosteal bone formation indices and together had a synergistic effect. For example, periosteal BFR/BS was 10-fold higher in loaded limbs of antibody- vs vehicle-treated mice. Gene expression analysis showed that antibody treatment and loading synergistically upregulated
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