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      Osteosarcopenia: epidemiology, diagnosis, and treatment—facts and numbers

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          Abstract

          Background

          Osteosarcopenia, the presence of osteopenia/osteoporosis and sarcopenia, is an emerging geriatric giant, which poses a serious global health burden.

          Methods and results

          The prevalence of osteosarcopenia ranges in community‐dwelling older adults [5 37% (≥65 years)] with the highest rates observed in those with fractures (low‐trauma fracture: ~46%; hip fracture: 17.1 96.3%). Among 2353 community‐dwelling adults, risk factors associated with osteosarcopenia include older age [men: 14.3% (60 64 years) to 59.4% (≥75 years); women: 20.3% (60 64 years) to 48.3% (≥75 years), P < 0.05], physical inactivity [inverse relationship: 0.64, 95% confidence interval (CI) 0.46–0.88 (sexes combined)], low body mass index (inverse relationship: men: 0.84, 95% CI 0.81–0.88; women: 0.77, 95% CI 0.74–0.80), and higher fat mass (men: 1.46, 95% CI 1.11–1.92; women: 2.25, 95% CI 1.71–2.95). Among 148 geriatric inpatients, osteosarcopenic individuals demonstrate poorer nutritional status (mini‐nutritional assessment scores: 8.50 ± 2.52 points, P < 0.001) vs. osteoporosis or sarcopenia alone, while among 253 older Australians, osteosarcopenia is associated with impaired balance and functional capacity [odds ratios (ORs): 2.56 7.19; P < 0.05] vs. non‐osteosarcopenia. Osteosarcopenia also associates with falls (ORs: 2.83 3.63; P < 0.05), fractures (ORs: 3.86 4.38; P < 0.05), and earlier death [hazard ratio (1‐year follow‐up): 1.84, 95% CI; 0.69 4.92, P = 0.023] vs. non‐osteosarcopenia.

          Conclusions

          This syndrome is expected to grow in age‐related and disease‐related states, a likely consequence of immunosenescence coinciding with increased sedentarism, obesity, and fat infiltration of muscle and bone. Evidence suggests the pathophysiology of osteosarcopenia includes genetic polymorphisms, reduced mechanical loading, and impaired endocrine functioning, as well as altered crosstalk between muscle, bone, and fat cells. Clinicians should screen for osteosarcopenia via imaging methods (i.e. dual‐energy X‐ray absorptiometry) to quantify muscle and bone mass, in addition to assessing muscle strength (i.e. grip strength) and functional capacity (i.e. gait speed). A comprehensive geriatric assessment, including medical history and risk factors, must also be undertaken. Treatment of this syndrome should include osteoporotic drugs [bone anabolics/antiresorptives (i.e. teriparatide, denosumab, bisphosphates)] where indicated, and progressive resistance and balance exercises (at least 2‐3 times/week). To maximize musculoskeletal health, nutritional recommendations [protein (1.2 1.5 g/kg/day), vitamin D (800–1000 IU/day), calcium (1300 mg/day), and creatine (3 5 g/day)] must also be met. It is anticipated that diagnosis and treatment for osteosarcopenia will become part of routine healthcare in the future. However, further work is required to identify biomarkers, which, in turn, may increase diagnosis, risk stratification, and targeted treatments to improve health outcomes.

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          Most cited references32

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          Ethical guidelines for publishing in the Journal of Cachexia, Sarcopenia and Muscle : update 2019

          Abstract This article details an updated version of the principles of ethical authorship and publishing in the Journal of Cachexia, Sarcopenia and Muscle (JCSM) and its two daughter journals JCSM Rapid Communication and JCSM Clinical Reports. We request of all author sending to the journal a paper for consideration that at the time of submission to JCSM, the corresponding author, on behalf of all co‐authors, needs to certify adherence to these principles. The principles are as follows: all authors listed on a manuscript considered for publication have approved its submission and (if accepted) approve publication in JCSM as provided; each named author has made a material and independent contribution to the work submitted for publication; no person who has a right to be recognized as author has been omitted from the list of authors on the submitted manuscript; the submitted work is original and is neither under consideration elsewhere nor that it has been published previously in whole or in part other than in abstract form; all authors certify that the submitted work is original and does not contain excessive overlap with prior or contemporaneous publication elsewhere, and where the publication reports on cohorts, trials, or data that have been reported on before the facts need to be acknowledged and these other publications must be referenced; all original research work has been approved by the relevant bodies such as institutional review boards or ethics committees; all relevant conflicts of interest, financial or otherwise, that may affect the authors' ability to present data objectively, and relevant sources of funding of the research in question have been duly declared in the manuscript; the manuscript in its published form will be maintained on the servers of JCSM as a valid publication only as long as all statements in the guidelines on ethical publishing remain true. If any of the aforementioned statements ceases to be true, the authors have a duty to notify as soon as possible the Editors of JCSM, JCSM Rapid Communication, and JCSM Clinical Reports, respectively, so that the available information regarding the published article can be updated and/or the manuscript can be withdrawn.
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            Osteosarcopenia: where bone, muscle, and fat collide.

            As the world's population ages, the prevalence of chronic diseases increases. Sarcopenia and osteoporosis are two conditions that are associated with aging, with similar risk factors that include genetics, endocrine function, and mechanical factors. Additionally, bone and muscle closely interact with each other not only anatomically, but also chemically and metabolically. Fat infiltration, a phenomenon observed in age-related bone and muscle loss, is highly prevalent and more severe in sarcopenic and osteoporotic subjects. Clinically, when individuals suffer a combination of both disorders, negative outcomes such as falls, fractures, loss of function, frailty, and mortality increase, thus generating significant personal and socio-economic costs. Therefore, it is suggested that when bone mineral density loss is synchronic with decreased muscle mass, strength, and function, it should be interpreted as a single diagnosis of osteosarcopenia, which may be preventable and treatable. Simple interventions such as resistance training, adequate protein and calcium dietary intake, associated with maintenance of appropriate levels of vitamin D, have a dual positive effect on bone and muscle, reducing falls, fractures, and, consequently, disability. It is essential that fracture prevention approaches-including postfracture management-involve assessment and treatment of both osteoporosis and sarcopenia. This is of particular importance as in older persons the combination of osteopenia/osteoporosis and sarcopenia has been proposed as a subset of frailer individuals at higher risk of institutionalization, falls, and fractures. This review summarizes osteosarcopenia epidemiology, pathophysiology, diagnosis, outcomes, and management strategies.
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              RANKL inhibition improves muscle strength and insulin sensitivity and restores bone mass

              Receptor activator of Nfkb ligand (RANKL) activates, while osteoprotegerin (OPG) inhibits, osteoclastogenesis. In turn a neutralizing Ab against RANKL, denosumab improves bone strength in osteoporosis. OPG also improves muscle strength in mouse models of Duchenne's muscular dystrophy (mdx) and denervation-induce atrophy, but its role and mechanisms of action on muscle weakness in other conditions remains to be investigated. We investigated the effects of RANKL inhibitors on muscle in osteoporotic women and mice that either overexpress RANKL (HuRANKL-Tg+), or lack Pparb and concomitantly develop sarcopenia (Pparb-/-). In women, denosumab over 3 years improved appendicular lean mass and handgrip strength compared to no treatment, whereas bisphosphonate did not. HuRANKL-Tg+ mice displayed lower limb force and maximal speed, while their leg muscle mass was diminished, with a lower number of type I and II fibers. Both OPG and denosumab increased limb force proportionally to the increase in muscle mass. They markedly improved muscle insulin sensitivity and glucose uptake, and decrease anti-myogenic and inflammatory gene expression in muscle, such as myostatin and protein tyrosine phosphatase receptor-γ. Similarly, in Pparb-/-, OPG increased muscle volume and force, while also normalizing their insulin signaling and higher expression of inflammatory genes in skeletal muscle. In conclusions, RANKL deteriorates, while its inhibitor improves, muscle strength and insulin sensitivity in osteoporotic mice and humans. Hence denosumab could represent a novel therapeutic approach for sarcopenia.
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                Author and article information

                Contributors
                gustavo.duque@unimelb.edu.au
                Journal
                J Cachexia Sarcopenia Muscle
                J Cachexia Sarcopenia Muscle
                10.1007/13539.2190-6009
                JCSM
                Journal of Cachexia, Sarcopenia and Muscle
                John Wiley and Sons Inc. (Hoboken )
                2190-5991
                2190-6009
                22 March 2020
                June 2020
                : 11
                : 3 ( doiID: 10.1002/jcsm.v11.3 )
                : 609-618
                Affiliations
                [ 1 ] Department of Medicine, Western Health, Melbourne Medical School University of Melbourne Melbourne Australia
                [ 2 ] Australian Institute for Musculoskeletal Science (AIMSS) University of Melbourne and Western Health Melbourne Australia
                Author notes
                [*] [* ]Correspondence to: Prof. Gustavo Duque, MD, PhD, FRACP, FGSA, Australian Institute for Musculoskeletal Science (AIMSS), University of Melbourne and Western Health, 176 Furlong Road, St. Albans, VIC, Australia 3121. Tel: +61 3 8395 8121, Email: gustavo.duque@ 123456unimelb.edu.au
                Author information
                https://orcid.org/0000-0002-0176-776X
                https://orcid.org/0000-0003-3463-6827
                https://orcid.org/0000-0001-8126-0637
                Article
                JCSM12567 JCSM-D-19-00583
                10.1002/jcsm.12567
                7296259
                32202056
                f8904568-476b-42ad-aa6c-6db191240681
                © 2020 The Authors. Journal of Cachexia, Sarcopenia and Muscle published by John Wiley & Sons Ltd on behalf of Society on Sarcopenia, Cachexia and Wasting Disorders

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Page count
                Figures: 3, Tables: 1, Pages: 10, Words: 4164
                Categories
                Editorial
                Editorial
                Custom metadata
                2.0
                June 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.4 mode:remove_FC converted:16.06.2020

                Orthopedics
                osteosarcopenia,bone,muscle,falls,fractures,mortality
                Orthopedics
                osteosarcopenia, bone, muscle, falls, fractures, mortality

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