Inhibition of RANKL a key mediator of osteoclast formation – new opportunities in osteoporosis treatment

Tomasz Blicharski; Ireneusz Sowa; Maciej Strzemski; Wojciech Szwerc; Adam Majewski

Authors

Tomasz Blicharski Department of Orthopaedics and Rehabilitation, Medical University of Lublin, Poland Author https://orcid.org/0000-0001-9747-8817
Ireneusz Sowa Department of Analytical Chemistry Medical University of Lublin, Poland Author https://orcid.org/0000-0001-9346-6325
Maciej Strzemski Department of Analytical Chemistry Medical University of Lublin, Poland Author https://orcid.org/0000-0002-0039-4455
Wojciech Szwerc Department of Analytical Chemistry Medical University of Lublin, Poland Author https://orcid.org/0000-0003-3491-6319
Adam Majewski Department of Rehabilitation, Physiotherapy and Balneology Medical University of Lublin, Poland Author

Keywords:

human monoclonal antibody, osteoporosis, RANKL, osteoclast

Abstract

The perspective of clinical use fully human monoclonal antibody that inhibits bone resorption by neutralizing RANKL holds enormous promise for the treatment of large number of bone loss diseases. Denosumab is a novel antibody that binds to RANKL and inhibits bone resorption. Administered subcutaneously every 6 months reduces bone turnover associated with a significant increase in DXA BMD in postmenopausal women with osteoporosis. Denodumab increases BMD in all skeletal sites and reduces new radiologic vertebral fractures, with cumulative evidence of 2.3% in the denosumab group, versus 7.2% in placebo group- a relative decrease of 68%. Denosumab reduced the risk of hip fracture with cumulative evidence of 0.7% in denosumab group, versus 1.2% in the placebo group- arelative decreaseof 40%. Denosumab also reduced the risk of nonvertebral fractures with cumulative evidence of 6.5% in denosumab group, versus 8.0% in the placebo group- a relative decrease of 20% [11]. These results demonstrate that human monoclonal antibody reduces the risk of fractures in osteoporotic patients and can be used as first choice treatment.

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Inhibition of RANKL a key mediator of osteoclast formation – new opportunities in osteoporosis treatment

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