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Title: Antiresorptive and anabolic agents in the prevention and reversal of bone fragility.
Austin Authors: Seeman, Ego ;Martin, T J
Affiliation: Department of Medicine and St Vincent's Institute, University of Melbourne, Melbourne, Victoria, Australia
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
Mary MacKillop Institute of Health Research, Australian Catholic University, Melbourne, Victoria, Australia
Department of Endocrinology, Austin Health, Heidelberg, Victoria, Australia
Issue Date: Apr-2019
Date: 2019-02-12
Publication information: Nature reviews. Rheumatology 2019; 15(4): 225-236
Abstract: Bone volume, microstructure and its material composition are maintained by bone remodelling, a cellular activity carried out by bone multicellular units (BMUs). BMUs are focally transient teams of osteoclasts and osteoblasts that respectively resorb a volume of old bone and then deposit an equal volume of new bone at the same location. Around the time of menopause, bone remodelling becomes unbalanced and rapid, and an increased number of BMUs deposit less bone than they resorb, resulting in bone loss, a reduction in bone volume and microstructural deterioration. Cortices become porous and thin, and trabeculae become thin, perforated and disconnected, causing bone fragility. Antiresorptive agents reduce fracture risk by reducing the rate of bone remodelling so that fewer BMUs are available to remodel bone. Bone fragility is not abolished by these drugs because existing microstructural deterioration is not reversed, unsuppressed remodelling continues producing microstructural deterioration and unremodelled bone that becomes more mineralized can become brittle. Anabolic agents reduce fracture risk by stimulating new bone formation, which partly restores bone volume and microstructure. To guide fracture prevention, this Review provides an overview of the structural basis of bone fragility, the mechanisms of remodelling and how anabolic and antiresorptive agents target remodelling defects.
DOI: 10.1038/s41584-019-0172-3
ORCID: 0000-0002-9692-048X
Journal: Nature reviews. Rheumatology
PubMed URL: 30755735
Type: Journal Article
Appears in Collections:Journal articles

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