Abstract
The bone loss after menopause contributes to increased bone resorption (due to estrogen deficiency and vitamin D deficiency in the elderly) and decreasing with age reduced activity of osteoblasts and bone formation. The agents that suppress bone resorption can stabilize bone mass, but do not stimulate bone formation and do not prevent loss of bone quality due to aging.
In contrast, agents that target the osteoblast can increase bone formation and bone mass. Novel antiresorptive agents focus attention on effective and revesible effect on osteoclastogenesis and osteoclast aktivity (they include denosumab, an antibody for receptor activator of nuclear factor kappa B ligand) or on selective suppression of osteoclast aktivity without attenuation of osteoblast aktivity (cathepsin K inhibitors, such as odanacatib, and Src kinase inhibitors).
Novel anabolic therapies for osteoporosis may include the use of factors with direct anabolic properties for bone or the neutralization of growth factor antagonists. The Wnt/Beta-catenin signaling pathway has a central role in osteoblastic cell differentiation.
Antibodies to Wnt antagonists, such as sclerostin, are still far in the development and has been going phase II study in humans. Anabolic therapies have the potencial to enhance bone mass, but their long-term safety must be proven.