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1 ibody has been approved for the treatment of postmenopausal osteoporosis.
2 tment of osteoclast-related diseases such as postmenopausal osteoporosis.
3  as reported in patients with high-turnover, postmenopausal osteoporosis.
4 olume and osteoid and osteoblast surfaces in postmenopausal osteoporosis.
5 arkers in an ovariectomized rodent model for postmenopausal osteoporosis.
6  contribute to bone loss in diseases such as postmenopausal osteoporosis.
7 approved for the prevention and treatment of postmenopausal osteoporosis.
8 ntary therapeutic efficacy of PTHrP(1-36) in postmenopausal osteoporosis.
9 characterized by increased bone loss such as postmenopausal osteoporosis.
10 ramatic increases in bone mass in women with postmenopausal osteoporosis.
11 vely repress bone loss in an animal model of postmenopausal osteoporosis.
12 ed rats, an established preclinical model of postmenopausal osteoporosis.
13 relevant role, into a comprehensive model of postmenopausal osteoporosis.
14 targets for various bone diseases, including postmenopausal osteoporosis.
15 he overall community prevalence of anemia or postmenopausal osteoporosis.
16 ans to control bone loss in diseases such as postmenopausal osteoporosis.
17 ly used for both prevention and treatment of postmenopausal osteoporosis.
18 py should be considered in the management of postmenopausal osteoporosis.
19 of human age-related osteopenic diseases and postmenopausal osteoporosis.
20 en evaluated in the treatment of established postmenopausal osteoporosis.
21 d in the treatment of women with established postmenopausal osteoporosis.
22 aluation for the prevention and treatment of postmenopausal osteoporosis.
23 have potential as a therapeutic strategy for postmenopausal osteoporosis.
24 ting that alpha(v)beta3 blockade may prevent postmenopausal osteoporosis.
25  important implications for the treatment of postmenopausal osteoporosis.
26 aluation for the prevention and treatment of postmenopausal osteoporosis.
27  bone protective effects in the treatment of postmenopausal osteoporosis.
28 ul and novel therapeutic approach to prevent postmenopausal osteoporosis.
29 rrow stromal cells (hBMSC) and is altered in postmenopausal osteoporosis.
30 morphologic structure, and mineralization in postmenopausal osteoporosis.
31  in clinically relevant skeletal benefits in postmenopausal osteoporosis.
32 rgical ovariectomy (Ovx) as a mouse model of postmenopausal osteoporosis.
33 ans should follow guidelines established for postmenopausal osteoporosis.
34  bone loss in the ovariectomy mouse model of postmenopausal osteoporosis.
35 ring the 5' end of PTHLH was associated with postmenopausal osteoporosis.
36                                              Postmenopausal osteoporosis, a global public health prob
37        Vertebral fractures are a hallmark of postmenopausal osteoporosis and an important end point i
38 es in reduced bone mass, similar to cases of postmenopausal osteoporosis and cancerous osteolysis.
39 hibits beneficial effects in mouse models of postmenopausal osteoporosis and multiple sclerosis in vi
40 sing therapeutic agent for the management of postmenopausal osteoporosis and rheumatoid arthritis.
41 and safety of denosumab for the treatment of postmenopausal osteoporosis and rheumatoid arthritis.
42 f therapeutic relevance for diseases such as postmenopausal osteoporosis and rheumatoid arthritis.
43                                              Postmenopausal osteoporosis and rheumatoid joint destruc
44 density, reduces fracture risk in women with postmenopausal osteoporosis, and inhibits structural dam
45                        Bone diseases such as postmenopausal osteoporosis are primarily caused by exce
46 be effective for prevention and treatment of postmenopausal osteoporosis, but whether combination ant
47 and rs17013181, were associated with BMD and postmenopausal osteoporosis by the two-stage strategy, a
48 ns such as primary ovarian insufficiency and postmenopausal osteoporosis, disrupts the delicate balan
49     We, therefore, propose that bone loss in postmenopausal osteoporosis does not only result from a
50                          Key Clinical Points Postmenopausal Osteoporosis Fractures and osteoporosis a
51 steoclast formation and resorption occurs in postmenopausal osteoporosis, inflammatory arthritis, and
52  optimal duration of treatment of women with postmenopausal osteoporosis is uncertain.
53 ent of bone remodeling and angiogenesis in a postmenopausal osteoporosis mouse model.
54 ization, and osteoid density are affected in postmenopausal osteoporosis (OP) and to examine associat
55 onsible for the enhanced bone destruction in postmenopausal osteoporosis, Paget's disease, bone metas
56                                              Postmenopausal osteoporosis (PMO) is a risk factor for p
57                                              Postmenopausal osteoporosis (PMO) is characterized by an
58                          Many strategies for postmenopausal osteoporosis screening are effective and
59                         For the treatment of postmenopausal osteoporosis, several drug classes with d
60 nd plays a major role in the pathogenesis of postmenopausal osteoporosis, structural damage in rheuma
61 e now undergoing menopause, a major cause of postmenopausal osteoporosis that also increases fracture
62 ematical framework of drug interventions for postmenopausal osteoporosis that unifies fundamental mec
63                                              Postmenopausal osteoporosis, the most common bone diseas
64  on bone mineral density (BMD) in women with postmenopausal osteoporosis transitioning from bisphosph
65 eview will focus on three new treatments for postmenopausal osteoporosis which have either been recen
66 olled women (aged >/=55 to </=90 years) with postmenopausal osteoporosis who had taken an oral bispho
67                                 Treatment of postmenopausal osteoporosis with parathyroid hormone (1-