Monoclonal antibodies to molecular targets important for bone formation and bone 
resorption are being investigated for treatment of postmenopausal osteoporosis. 
Postmenopausal osteoporosis is characterized by increased bone turnover, with 
bone resorption typically exceeding bone formation. These pathophysiological 
changes cause decreased bone mineral density and disruption of bone 
microarchitecture which lead to low-trauma fractures. Sclerostin is a 
glycoprotein inhibitor of osteoblast Wnt signaling produced by osteocytes that 
has been recognized as a new target for therapeutic intervention in patients 
with osteoporosis. Sclerostin was first recognized when disorders with 
inactivating mutations of the sclerostin gene SOST were found to be associated 
with high bone mass. These observations suggested that inhibitors of sclerostin 
might be used to increase bone mineral density. Romosozumab (AMG 785) is the 
first humanized anti-sclerostin monoclonal antibody that has been demonstrated 
to increase bone formation. This investigational monoclonal antibody, and 
blosozumab, another investigational anti-sclerostin antibody, have osteoanabolic 
properties with the potential to improve clinical outcomes in patients with 
osteoporosis. Similar to preclinical animal studies with sclerostin antibodies, 
initial clinical studies have shown that romosozumab increases bone formation 
and BMD. Further evaluation of the efficacy and safety of this agent in a large 
phase III controlled study is awaited. Phase I clinical trial data have recently 
been published with blosozumab. These novel interventions appear to be promising 
agents for the treatment of osteoporosis.