Treatment options for postmenopausal osteoporosis

Correspondence: Garry M Walsh Division of Applied Medicine, School of Medicine and Dentistry, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, United Kingdom To serve our readership better, future editions of Therapeutics and Clinical Risk Management will once again feature the Editor’s comments and views on some of the articles published in that issue of the journal. Bone is a complex tissue that, in addition to protecting vital organs and giving mechanical support for muscles and joints, provides a mineral reservoir essential for calcium homeostasis, together with the microenvironment essential for hematopoiesis. Osteoporosis is the most common metabolic bone disease, with up to a third of postmenopausal women suffering from this increasingly important public health problem. Key characteristics include low bone mineral density with microarchitectural deterioration of bone tissue leading to increased susceptibility to fragility fractures. Bone remodeling is vital for a healthy skeleton through removal of damaged tissue by the reabsorptive action of osteoclasts, with osteoblasts accounting for generation of new bone matrix. In recent years, our knowledge of the molecular pathways involved in bone formation and resorption has greatly improved, and it is now appreciated that the interplay between osteoclasts and osteoblasts is controlled by a complex array of hormones, cytokines, and growth factors. This has led to the development of new drugs to treat osteoporosis and these have been classified according to their mode of action on this remodeling process. For example, antiresorptive drugs include bisphosphonates and raloxifene, while anabolic drugs such as teriparatide or parathyroid hormone enhance remodelling. Bone resorption is regulated by a transmembranous and soluble protein highly expressed by osteoclasts known as receptor activator of nuclear factor-κB (RANK), a member of the tumor necrosis factor receptor superfamily essential for osteoclastogenesis. Denosumab is a fully humanized monoclonal antibody specific for RANK-ligand. Binding of the latter by denosumab prevents its interaction with RANK, thereby leading to a reduction in osteoclast activity and consequently bone resorption. The place of denosumab in the treatment of osteoporosis, particularly in the context of postmenopausal women, has been comprehensively reviewed in the current issue of the journal. Treatment with denosumab was characterized by rapid, sustained, and reversible reduction in bone turnover markers, a marked increase in bone mineral density at all sites, and a marked decrease in the risk of vertebral, hip, and nonvertebral fractures in women with postmenopausal osteoporosis. The safety and long-term treatment issues associated with denosumab use in osteoporosis was also reviewed by Anastasilakis et al in the same issue. These authors point out that although to date the majority of Dovepress