Longitudinal analysis of mesenchymal progenitors and bone quality in the stem cell antigen-1-null osteoporotic mouse.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

We performed a longitudinal analysis of bone quality in Sca-1-null mice. A tight temporal, site-specific association between Sca-1-deficient BMD deficiency and reduced mesenchymal progenitor frequency was observed. Defects in trabecular microarchitecture and mineralization were, at least partially, responsible for the age-related reduction in toughness of Sca-1(-/-) bones. We previously showed that stem cell antigen 1 (Sca-1)-null mice undergo normal bone development but exhibit significantly decreased bone mass characteristic of age-dependent osteoporosis. The objective of this study was to characterize the initiation and progression of the Sca-1 mutant skeletal phenotype at the cellular, structural, material, and mechanical levels. Sca-1-null and control mice were analyzed at 3, 5, 7, and 9 mo of age. In vitro osteoclastogenesis of bone marrow and spleen-derived progenitor populations was assessed. Bone marrow-derived mesenchymal progenitor frequency, along with osteogenic and adipogenic differentiation potential, was analyzed in vitro. Static histomorphometry of the sixth lumbar vertebrae was performed. Whole body, femoral, and vertebral BMD were assessed using DXA. Lumbar vertebrae were analyzed using microCT, back-scattered electron imaging, and compression tests. Three-point bending and femoral neck fracture tests were performed on excised femurs. Sca-1-null mice displaye

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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