Bone Abstracts

It is known that body weight is positively correlated with increased bone mineral density and decreased fracture risk. Adiponectin is expressed in bone forming cells, and administration of adiponectin has been demonstrated to stimulated osteoblast proliferation. The overall role of adiponectin in bone metabolism remains unrevealed as both stimulated and inhibiting effects on osteoclastogenesis have been reported. We aimed at describing the relationship between adiponectin and mechanical properties of bone, and characterize possible autocrine and paracrine effects of adiponectin on osteoblast and osteoclast.

There were no significant relationship between plasma adiponectin levels and bone biomechanical data in rats. In contrast, the relative expression of adiponectin mRNA in femur correlated positively to ultimate bending moment, ultimate energy absorption and deflection, however, negative to bending stiffness. Recombinant adiponectin (80 ng/ml) induced spongier and more fragile spheres of three-dimensional bone formation models produced in rotating co-cultures of human osteoblasts and osteoclasts.

Adiponectin mRNA are expressed in human monocytes and the expression decreased upon stimulation with RANKL and MC-CSF and differentiation to osteoclasts. We found recombinant adiponectin (0.08–10 μg/ml) to stimulate human osteoclast differentiation and activity, whereas no effect was observed on osteoblast differentiation and the expression of markers involved in osseoid mineralization (alkaline phosphatase, collagen type 2, osteocalcin and CD44) in mesenchymal stem cells. Beside acutely up-regulating adiponectin mRNA expression, adiponectin also stimulated leptin expression and secretion.

Adiponectin has effects on the elasticity and flexibility of the bones, by regulating recruitment and differentiated endpoint of cells involved in bone remodelling.