In conclusion our data indicate that – during medium-term follow-up (3 years) and using self-reported clinical risk factors – more complex tools as FRAX® did not perform better in the fracture risk prediction compared with simpler tools such as OST, ORAI, OSIRIS and SCORE or even age alone in a screening scenario where BMD was not measured. These findings suggest that simpler tools based on fewer risk factors, which would be easier to use in clinical practice

by the GP or the patient herself, could just as well as FRAX® be used to identify women with increased risk of fracture and therefore should be referred to a DXA scan. This study is a part of the Risk-stratified Osteoporosis Strategy Evaluation study (ROSE study) which is supported by INTERREG 4A (JNR 08/4177), the Region of Southern Denmark (JNR 08/8133 and JNR 11/5761) and Odense University Hospital. The funding agencies had no direct role in the conduct of the study; collection, management, analysis R428 clinical trial and interpretation of the data; and preparation, review or final approval of the manuscript. Conflicts of interest None. “
“Parathyroid hormone (PTH) is the major regulator of calcium homeostasis through its actions on bone and kidney. PTH is critical for bone remodeling, exerting both anabolic and catabolic effects on bone in vivo by activating the PTH1 receptor, Olaparib datasheet a G-protein coupled receptor, on osteoblast (OB) lineage cells [1] and [2]. Intermittent PTH was the first anabolic agent approved

for osteoporosis therapy 3-mercaptopyruvate sulfurtransferase in the USA [1] and [3]. For reasons still not completely understood, daily injections of PTH increase bone formation more than resorption, thereby increasing bone mass, while continuous infusion increases bone resorption more than formation, resulting in bone loss [4], [5] and [6]. Despite the anabolic effects of PTH in vivo and the demonstration that PTH can stimulate OB precursors or mesenchymal stem cells (MSCs) to differentiate into OBs [2] and [7], it has been difficult to demonstrate

osteogenic effects of PTH in vitro. A number of in vitro studies have reported that PTH present continuously in culture inhibits OB differentiation [8], [9], [10] and [11]. These observations suggest that the bone loss associated with continuous PTH is not simply the result of increased resorption but may also involve suppressed differentiation of bone-forming cells. PTH is also a potent inducer of cyclooxygenase-2 (COX-2) and prostaglandin (PG) production, especially PGE2, in OB lineage cells [12] and [13]. PGs are locally produced lipids that have receptors on both OB and osteoclast (OC) lineage cells [14] and [15]. PGE2 is abundantly expressed in bone and can have important roles in skeletal metabolism. Although originally identified as a resorption agonist, PGE2 also increases bone formation in vivo [16] and OB differentiation in vitro [14] and [15]. Multiple regulators of bone metabolism induce COX-2, the major enzyme responsible for PG production.