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      Monoclonal antibodies for treating osteoporosis

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          Most cited references 72

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          WNT signaling in bone homeostasis and disease: from human mutations to treatments.

          Low bone mass and strength lead to fragility fractures, for example, in elderly individuals affected by osteoporosis or children with osteogenesis imperfecta. A decade ago, rare human mutations affecting bone negatively (osteoporosis-pseudoglioma syndrome) or positively (high-bone mass phenotype, sclerosteosis and Van Buchem disease) have been identified and found to all reside in components of the canonical WNT signaling machinery. Mouse genetics confirmed the importance of canonical Wnt signaling in the regulation of bone homeostasis, with activation of the pathway leading to increased, and inhibition leading to decreased, bone mass and strength. The importance of WNT signaling for bone has also been highlighted since then in the general population in numerous genome-wide association studies. The pathway is now the target for therapeutic intervention to restore bone strength in millions of patients at risk for fracture. This paper reviews our current understanding of the mechanisms by which WNT signalng regulates bone homeostasis.
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            Pathogenesis of osteoporosis: concepts, conflicts, and prospects.

            Osteoporosis is a disorder in which loss of bone strength leads to fragility fractures. This review examines the fundamental pathogenetic mechanisms underlying this disorder, which include: (a) failure to achieve a skeleton of optimal strength during growth and development; (b) excessive bone resorption resulting in loss of bone mass and disruption of architecture; and (c) failure to replace lost bone due to defects in bone formation. Estrogen deficiency is known to play a critical role in the development of osteoporosis, while calcium and vitamin D deficiencies and secondary hyperparathyroidism also contribute. There are multiple mechanisms underlying the regulation of bone remodeling, and these involve not only the osteoblastic and osteoclastic cell lineages but also other marrow cells, in addition to the interaction of systemic hormones, local cytokines, growth factors, and transcription factors. Polymorphisms of a large number of genes have been associated with differences in bone mass and fragility. It is now possible to diagnose osteoporosis, assess fracture risk, and reduce that risk with antiresorptive or other available therapies. However, new and more effective approaches are likely to emerge from a better understanding of the regulators of bone cell function.
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              Romosozumab in postmenopausal women with low bone mineral density.

              Sclerostin is an osteocyte-derived inhibitor of osteoblast activity. The monoclonal antibody romosozumab binds to sclerostin and increases bone formation.
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                Author and article information

                Journal
                Expert Opinion on Biological Therapy
                Expert Opinion on Biological Therapy
                Informa UK Limited
                1471-2598
                1744-7682
                December 28 2017
                November 07 2017
                February 2018
                : 18
                : 2
                : 149-157
                Affiliations
                [1 ] Department of Biomedical Sciences and Human Oncology, Pediatric Section, University ‘A. Moro’ of Bari, Bari, Italy
                [2 ] Neonatal Intensive Care Unit, Di Venere Hospital, Bari, Italy
                [3 ] Department of Emergency and Organ Transplantation, Section of Human Anatomy and Histology, University ‘A. Moro’ of Bari, Bari, Italy
                [4 ] Department of Basic Medical Sciences, Neurosciences and Sense Organs, Section of Human Anatomy and Histology, University ‘A. Moro’ of Bari, Bari, Italy
                Article
                10.1080/14712598.2018.1401607
                © 2018

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