Interní Med. 2012; 14(8-9): 309-311
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/β-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.
Published: September 20, 2012 Show citation