Osteoporosis is characterised by a progressive loss of bone mass and 
microarchitecture which leads to increased fracture risk. Some of the drugs 
available to date have shown reductions in vertebral and non-vertebral fracture 
risk. However, in the ageing population of industrialised countries, still more 
fractures happen today than are avoided, which highlights the large medical need 
for new treatment options, models, and strategies. Recent insights into bone 
biology, have led to a better understanding of bone cell functions and crosstalk 
between osteoblasts, osteoclasts, and osteocytes at the molecular level. In the 
future, the armamentarium against osteoporotic fractures will likely be enriched 
by (1.) new bone anabolic substances such as antibodies directed against the 
endogenous inhibitors of bone formation sclerostin and dickkopf-1, PTH and PTHrp 
analogues, and possibly calcilytics; (2.) new inhibitors of bone resorption such 
as cathepsin K inhibitors which may suppress osteoclast function without 
impairing osteoclast viability and thus maintain bone formation by preserving 
the osteoclast-osteoblast crosstalk, and denosumab, an already widely available 
antibody against RANKL which inhibits osteoclast formation, function, and 
survival; and (3.) new therapeutic strategies based on an extended understanding 
of the pathophysiology of osteoporosis which may include sequential therapies 
with two or more bone active substances aimed at optimising the management of 
bone capital acquired during adolescence and maintained during adulthood in 
terms of both quantity and quality. Finally, one of the future challenges will 
be to identify those patients and patient populations expected to benefit the 
most from a given drug therapy or regimen. The WHO fracture risk assessment tool 
FRAX® and improved access to bone mineral density measurements by DXA will play 
a key role in this regard.