Similarities Between Disuse and Age-Induced Bone Loss.
AGING
BONE DISORDERS AND DISEASES-OSTEOPOROSIS
CELLS OF BONE-OSTEOCYTES
MOLECULAR PATHWAYS-REMODELING
PRECLINICAL STUDIES
SENESCENCE
Journal
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
ISSN: 1523-4681
Titre abrégé: J Bone Miner Res
Pays: United States
ID NLM: 8610640
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
revised:
17
06
2022
received:
22
11
2021
accepted:
24
06
2022
pubmed:
2
7
2022
medline:
11
8
2022
entrez:
1
7
2022
Statut:
ppublish
Résumé
Disuse and aging are known risk factors associated with low bone mass and quality deterioration, resulting in increased fracture risk. Indeed, current and emerging evidence implicate a large number of shared skeletal manifestations between disuse and aging scenarios. This review provides a detailed overview of current preclinical models of musculoskeletal disuse and the clinical scenarios they seek to recapitulate. We also explore and summarize the major similarities between bone loss after extreme disuse and advanced aging at multiple length scales, including at the organ/tissue, cellular, and molecular level. Specifically, shared structural and material alterations of bone loss are presented between disuse and aging, including preferential loss of bone at cancellous sites, cortical thinning, and loss of bone strength due to enhanced fragility. At the cellular level bone loss is accompanied, during disuse and aging, by increased bone resorption, decreased formation, and enhanced adipogenesis due to altered gap junction intercellular communication, WNT/β-catenin and RANKL/OPG signaling. Major differences between extreme short-term disuse and aging are discussed, including anatomical specificity, differences in bone turnover rates, periosteal modeling, and the influence of subject sex and genetic variability. The examination also identifies potential shared mechanisms underlying bone loss in aging and disuse that warrant further study such as collagen cross-linking, advanced glycation end products/receptor for advanced glycation end products (AGE-RAGE) signaling, reactive oxygen species (ROS) and nuclear factor κB (NF-κB) signaling, cellular senescence, and altered lacunar-canalicular connectivity (mechanosensation). Understanding the shared structural alterations, changes in bone cell function, and molecular mechanisms common to both extreme disuse and aging are paramount to discovering therapies to combat both age-related and disuse-induced osteoporosis. © 2022 American Society for Bone and Mineral Research (ASBMR).
Identifiants
pubmed: 35773785
doi: 10.1002/jbmr.4643
pmc: PMC9378610
mid: NIHMS1820610
doi:
Types de publication
Journal Article
Review
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1417-1434Subventions
Organisme : NASA
ID : 80NSSC18K1473
Pays : United States
Organisme : National Space Biomedical Research Institute Grant
ID : MA02802
Organisme : NICHD NIH HHS
ID : R01 HD102909
Pays : United States
Organisme : NIAAA NIH HHS
ID : R37 AA018282
Pays : United States
Organisme : NIAMS NIH HHS
ID : R01 AR068132
Pays : United States
Organisme : Translational Research Institute for Space Health
ID : NNX16AO69A
Informations de copyright
© 2022 American Society for Bone and Mineral Research (ASBMR).
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