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Disorders of Bone Remodeling
Open accessAbstract
The skeleton provides mechanical support for stature and locomotion, protects vital organs, and controls mineral homeostasis. A healthy skeleton must be maintained by constant bone modeling to carry out these crucial functions throughout life. Bone remodeling involves the removal of old or damaged bone by osteoclasts (bone resorption) and the subsequent replacement of new bone formed by osteoblasts (bone formation). Normal bone remodeling requires a tight coupling of bone resorption to bone formation to guarantee no alteration in bone mass or quality after each remodeling cycle. However, this important physiological process can be derailed by a variety of factors, including menopause-associated hormonal changes, age-related factors, changes in physical activity, drugs, and secondary diseases, which lead to the development of various bone disorders in both women and men. We review the major diseases of bone remodeling, emphasizing our current understanding of the underlying pathophysiological mechanisms.
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“OPG, a soluble receptor also produced by osteoblasts that acts as a decoy receptor and neutralizes RANKL, prevents RANKL from interacting with RANK and consequently inhibits osteoclast proliferation, activity, and survival [73, 74].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [73]
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“Once RANKL binds to its natural receptor, expressed by osteoclast precursor cells, it stimulates osteoclast precursor differentiation to active mature osteoclasts and accelerates bone resorption [73].”
From The Effect of Tobacco Smoking on Bone Mass: An Overview of Pathophysiologic Mechanisms (2018) · cites this paper as [73]
In the citing paper
“Abnormal increase in osteoclast formation and activity leads to some bone diseases such as osteoporosis, where resorption exceeds formation causing decreased bone density and increased bone fractures [105].”
From Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells (2015) · cites this paper as [105]
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“In patients with chronic liver disease, the balance between osteoclasts and osteoblasts is affected by liver disease, resulting in BRU imbalance [46,50].”
From Bone diseases in patients with chronic liver disease (2019) · cites this paper as [46]
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The role of osteocytes in bone mechanotransduction
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Teriparatide or Alendronate in Glucocorticoid-Induced Osteoporosis
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Osteoclast Apoptosis: The Role of Fasin Vivoandin Vitro
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The Type I/Type II Model for Involutional Osteoporosis
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Osteoclasts Secrete the Chemotactic Cytokine Mim-1
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Self-citationChapter 6. The Composition of Bone
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NFATc1: A Novel Anabolic Therapeutic Target for Osteoporosis
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Calmodulin—an often‐ignored signal in osteoclasts
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“This idea is supported by genetic studies in humans and mice as well as by pharmacological studies [105, 171].”
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Kim, J., Lin, C., Stavre, Z., Greenblatt, M. B., & Shim, J. (2020) · Cells · doi:10.3390/cells9092073 · Cited by 1,254
“bone resorption is tightly regulated without a major alteration in a net bone mass or mechanical strength under homeostatic conditions [2].”
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Domazetovic, V (2017) · Clinical Cases in Mineral and Bone Metabolism · doi:10.11138/ccmbm/2017.14.1.209 · Cited by 758
“In fact, bone is a dynamic tissue that continuously renews itself throughout life by the coordinated action of three major types of bone cells: osteoclasts, osteoblasts and osteocytes (28, 29).”
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“This field has been previously extensively reviewed by Feng and McDonald, and therefore this review will focus specifically on osteoporosis.(140) Osteoporosis is the most common metabolic bone disorder and resultant fragility fractures are associated with increased morbidity and mortality; its European prevalence is 2…”
MethodType H blood vessels in bone modeling and remodeling
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“In bone modeling, bone formation occurs independently of bone resorption, whereas bone resorption and formation are coupled during bone remodeling to maintain skeletal homeostasis [3-5].”
Background
Metadata
- Authors
- Feng, X., & McDonald, J. M.
- Affiliations
- University of Alabama at Birmingham (US)
- ORCID
- Feng, Xu
- Venue
- Annual Review of Pathology: Mechanisms of Disease
- Publisher
- Annual Reviews
- Published
- 2011-02-28
- Volume
- 6
- Issue
- 1
- Pages
- 121-145
- ISSN
- 1553-4006 (ISSN-L)
- 1553-4014
- PMC
- PMC3571087
- OpenAlex
- W2166266977
- Cited by
- 1,272
- References
- 171
- Citations by year
- 2026: 59 · 2025: 109 · 2024: 102 · 2023: 124 · 2022: 135 · 2021: 142 · 2020: 107 · 2019: 117 · 2018: 86 · 2017: 68 · 2016: 59 · 2015: 47 · 2014: 36 · 2013: 37 · 2012: 29
- FWCI
- 3.28
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Annual Review of Pathology Mechanisms of Disease (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (R01CA109119)
- National Institute of Neurological Disorders and Stroke (R21NS061677, NS061677)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (5P30 AR0406031, R01AR047830, AR 47830, R01AR050235)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Health Sciences › Medicine › Oncology › Bone health and treatments
- Keywords
- bone remodeling, bone resorption, bone formation, osteoclasts, osteoblasts, bone disease, menopause, hormonal changes, age-related bone loss, physical activity, drug-induced bone loss, mineral homeostasis, pathophysiology
- MeSH terms
- Animals, Bone Diseases, Humans, Bone Remodeling
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