Abstract
Osteoporosis is a condition featured by bone mass loss and bone tissue microarchitectural alterations due to impaired tissue homeostasis favoring excessive bone resorption versus deposition. The trigger of such an impairment and the downstream molecular pathways involved are yet to be clarified. The natural course of osteoporosis is particularly worrisome because, through a “silent” progression, it enhances bone fragility, increases the risk of fractures and is associated with increased risk of disability and mortality. To date, the assessment of bone mineral density by dual-energy X-ray absorptiometry, represents the non-invasive gold standard for the evaluation of bone mineralization and the diagnosis of osteoporosis. Although long known as a condition merely related to the hormonal-driven loss of bone homeostasis, emerging evidence supports the need of reframing osteoporosis in the context of structural and functional changes of the musculoskeletal system as a whole. Several age-related alterations of bone microenvironment and an altered bone-muscle crosstalk have been suggested to be relevant contributors to loss of bone strength and mass characterizing osteoporosis. The present work provides an overview of the current knowledge of the pathophysiology of osteoporosis obtained through advances in epigenetics, cell biology and osteoimmunology. In light of the increasingly recognized importance of bone-muscle interconnection, this review also discusses relevant pathways that may be dissected for identifying new therapeutic targets for age-related musculoskeletal degeneration.
Keywords: Bone loss, DXA, inflammation, muscle wasting, sarcopenia, aging, biomarkers, fractures.
Current Pharmaceutical Design
Title:Bone-Muscle Crosstalk: Unraveling New Therapeutic Targets for Osteoporosis
Volume: 23 Issue: 41
Author(s): Anna Picca, Riccardo Calvani*, Ester Manes-Gravina, Leonardo Spaziani, Francesco Landi, Roberto Bernabei and Emanuele Marzetti
Affiliation:
- Center for Geriatrics, Neurosciences, Ear Nose and Throat, and Orthopedics, Catholic University of the Sacred Heart, Teaching Hospital "Agostino Gemelli", Rome 00168,Italy
Keywords: Bone loss, DXA, inflammation, muscle wasting, sarcopenia, aging, biomarkers, fractures.
Abstract: Osteoporosis is a condition featured by bone mass loss and bone tissue microarchitectural alterations due to impaired tissue homeostasis favoring excessive bone resorption versus deposition. The trigger of such an impairment and the downstream molecular pathways involved are yet to be clarified. The natural course of osteoporosis is particularly worrisome because, through a “silent” progression, it enhances bone fragility, increases the risk of fractures and is associated with increased risk of disability and mortality. To date, the assessment of bone mineral density by dual-energy X-ray absorptiometry, represents the non-invasive gold standard for the evaluation of bone mineralization and the diagnosis of osteoporosis. Although long known as a condition merely related to the hormonal-driven loss of bone homeostasis, emerging evidence supports the need of reframing osteoporosis in the context of structural and functional changes of the musculoskeletal system as a whole. Several age-related alterations of bone microenvironment and an altered bone-muscle crosstalk have been suggested to be relevant contributors to loss of bone strength and mass characterizing osteoporosis. The present work provides an overview of the current knowledge of the pathophysiology of osteoporosis obtained through advances in epigenetics, cell biology and osteoimmunology. In light of the increasingly recognized importance of bone-muscle interconnection, this review also discusses relevant pathways that may be dissected for identifying new therapeutic targets for age-related musculoskeletal degeneration.
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Cite this article as:
Picca Anna , Calvani Riccardo*, Manes-Gravina Ester , Spaziani Leonardo, Landi Francesco , Bernabei Roberto and Marzetti Emanuele, Bone-Muscle Crosstalk: Unraveling New Therapeutic Targets for Osteoporosis, Current Pharmaceutical Design 2017; 23 (41) . https://dx.doi.org/10.2174/1381612823666170526112300
DOI https://dx.doi.org/10.2174/1381612823666170526112300 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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