Role of RANKL inhibition in osteoporosis 英文参考文献.docVIP

Available online /content/9/S1/S3 Review Role of RANKL inhibition in osteoporosis Michael McClung Oregon Osteoporosis Center, NE Hoyt Street, Portland, Oregon 97213, USA Corresponding author: Michael McClung, mmcclung@ Published: 29 June 2007 Arthritis Research Therapy 2007, 9(Suppl 1):S3 (doi:10.1186/ar2167) This article is online at /content/9/S1/S3 ? 2007 BioMed Central Ltd Abstract about 20% [3]. One-third of hip fractures occur in men. A healthy 50-year-old woman has a 40% to 50% chance of When the rate of bone resorption exceeds that of bone formation, destruction of bone tissue occurs, resulting in a fragile skeleton. The clinical consequences, namely osteoporosis and fragility fractures, are common and costly problems. Treatments that normalize the balance of bone turnover by inhibiting bone resorption preserve bone mass and reduce fracture risk. The discovery of receptor activator of nuclear factor-κB ligand (RANKL) as a pivotal regulator of osteoclast activity provides a new therapeutic target. Early studies have demonstrated that denosumab, an investigational, highly specific anti-RANKL antibody, rapidly and substantially reduces bone resorption. Pharmacokinetics of the antibody allow dosing by subcutaneous injection at an interval of 6 months. Inhibiting RANKL appears to be a promising new treatment for osteoporosis and related disorders. More information about the effectiveness of denosumab in reducing fracture risk, its tolerability and safety, and the response to discontinuing therapy will be provided by ongoing clinical studies. experiencing an osteoporosis-related fracture over the remainder of her lifetime, whereas approximately 20% of men will experience fragility fractures. Caring for patients with these fractures is expensive; the annual direct care expenditure on caring for patients with oste