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This article is part of the supplement: Basic science, rationale, background and future of denosumab: a RANK ligand inhibitor

Review

Role of RANKL inhibition in osteoporosis

Michael McClung

Author affiliations

Oregon Osteoporosis Center, NE Hoyt Street, Portland, Oregon 97213, USA

Citation and License

Arthritis Research & Therapy 2007, 9(Suppl 1):S3  doi:10.1186/ar2167

Published: 29 June 2007

Abstract

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.