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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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In the citing paper
“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]
In the citing paper
“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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“Bone homoeostasis depends on 2 opposing processes, resorption and synthesis, which requires strict temporal control to maintain the bone mass and structural quality (Feng and McDonald, 2011).”
BackgroundInfluentialNutraceuticals for better management of osteoporosis: An overview
Rajput, R., Wairkar, S., & Gaud, R. S. (2018) · Journal of Functional Foods · doi:10.1016/j.jff.2018.06.013 · Cited by 43
Zhang, Z., Jiang, W., Hu, M., Gao, R., & Zhou, X. (2021) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2021.05.098 · Cited by 41
Loss of p53 compensates osteopenia in murine Mysml deficiency
Haffner‐Luntzer, M., Kovtun, A., Fischer, V., Prystaz, K., Hainzl, A., Kroeger, C. M., Krikki, I., Brinker, T. J., Ignatius, A. A., & Gatzka, M. (2017) · The FASEB Journal · doi:10.1096/fj.201700871r · Cited by 41
“Because an isolated defect of osteoclasts would usually lead to osteopetrosis (32), we speculated that, in accordance with other reports (33), likely combined dysfunctions of osteoclasts and osteoblasts cause osteopenia and skeletalmalformations inMysm1-deficientmice.”
ResultTao, Z.-S., Li, T., & Wei, S. (2022) · Molecular Medicine · doi:10.1186/s10020-022-00503-7 · Cited by 40
“Numerous promising pharmacotherapies have been examined as possible treatments for postmenopausal osteoporosis (Feng and McDonald 2011).”
BackgroundAssociation between Dysbiosis in the Gut Microbiota of Primary Osteoporosis Patients and Bone Loss
Waldbaum, J., Xhumari, J., Akinsuyi, O., Arjmandi, B. H., Anton, S. D., & Roesch, L. F. W. (2023) · Aging and Disease · doi:10.14336/ad.2023.0425 · Cited by 44
“To maintain a healthy skeleton and avoid alteration in bone mass and quality, these mechanisms must be coupled and regulated so that there is no net gain or loss of tissue [46].”
BackgroundNoninvasive Raman spectroscopy of rat tibiae: approach to in vivo assessment of bone quality
Okagbare, P. I., Morris, M. D., Begun, D. L., Goldstein, S. A., & Tecklenburg, M. (2012) · Journal of Biomedical Optics · doi:10.1117/1.jbo.17.9.090502 · Cited by 40
Sequential Delivery of Dual Growth Factors from Injectable Chitosan-Based Composite Hydrogels
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“The utility of a single factor may enhance bone healing by inducing osteogenesis and angiogenesis [15].”
BackgroundNam, B., Park, H., Lee, Y. L., Oh, Y., Park, J., Kim, S. Y., Weon, S., Choi, S. H., Yang, J. H., Jo, S., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21249771 · Cited by 41
“Considering that the misregulation of the TGFβ1 signaling pathways is frequently associated with various human diseases [19], and several diseases or pathologic conditions can lead to secondary osteoporosis or abnormal bone formation [2], we might provide a better understanding of the link between them, as well as new…”
BackgroundPERK signaling pathway in bone metabolism: Friend or foe?
Guo, J., Ren, R., Sun, K., He, J., & Shao, J. (2021) · Cell Proliferation · doi:10.1111/cpr.13011 · Cited by 40
A Multidisciplinary Journey towards Bone Tissue Engineering
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“Calcitonin also presents analgesic properties that further help treat patients with bone pain [31].”
BackgroundThe Role of NPY in the Regulation of Bone Metabolism
Chen, Q., & Zhang, Y. (2022) · Frontiers in Endocrinology · doi:10.3389/fendo.2022.833485 · Cited by 40
“Bone remodeling involves mineralized bone removal by osteoclasts followed by bone matrix formation through osteoblasts that subsequently become mineralized (16).”
BackgroundNiu, N., Xiang, J., Yang, Q., Wang, L., Wei, Z., Chen, L., Yang, L. C., & Zou, W. (2017) · Cell Discovery · doi:10.1038/celldisc.2016.50 · Cited by 39
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“The mechanism of bone remodeling is to maintain the skeleton and replacement of damaged bone [15].”
BackgroundNoce, M. L., Mele, L. L., Laino, L., Iolascon, G., Pieretti, G., Papaccio, G., Desiderio, V., Tirino, V., & Paino, F. (2019) · Cells · doi:10.3390/cells8030217 · Cited by 39
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Phromnoi, K., Suttajit, M., Saenjum, C., & Limtrakul, P. (2021) · Antioxidants · doi:10.3390/antiox10020307 · Cited by 39
“Impaired osteogenesis and excessive osteoclastogenesis can cause disorders such as Paget’s disease, rheumatoid arthritis, metastatic cancers, and osteoporosis [1].”
BackgroundThe KDM4B–CCAR1–MED1 axis is a critical regulator of osteoclast differentiation and bone homeostasis
Yi, S.-J., Jang, Y.-J., Kim, H., Lee, K., Lee, H.-R., Kim, Y., Kim, J., Hwang, S. Y., Song, J. S., Okada, H., et al. (2021) · Bone Research · doi:10.1038/s41413-021-00145-1 · Cited by 39
“NT (1-660) CT (661-1 146) SAP Coiled-coil (792-819)”
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“In addition, it has been reported that BMSCs could modulate osteoclast activation, differentiation, and function by secreting cytokines such as receptor activator of NF-κB ligand (RANKL), osteoprotegerin (OPG), and macrophage colony-stimulating factor (M-CSF) during osteoblast differentiation, thus influencing osteocl…”
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“The dysregulation of OB– OC coupling is one of the most common causes of osteopenia/ osteoporosis or other metabolic bone diseases (1).”
BackgroundLipidomics Profiling of Patients with Low Bone Mineral Density (LBMD)
Aleidi, S. M., Al‐Ansari, M. M., Alnehmi, E. A., Malkawi, A. K., Alodaib, A. N., Alshaker, M., Benabdelkamel, H., & Rahman, A. M. A. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms231912017 · Cited by 38
Histone demethylase JMJD3 is required for osteoblast differentiation in mice
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Cell Sources for Human In vitro Bone Models
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Targeting STING: From antiviral immunity to treat osteoporosis
Gao, Z., Gao, Z., Zhang, H., Hou, S., Zhou, Y., & Liu, X. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2022.1095577 · Cited by 38
“Disruption of bone homeostasis is the frequent pathophysiological mechanism of bone metabolic diseases (49).”
BackgroundLoh, H.-Y., Norman, B. P., Lai, K., Cheng, W.-H., Rahman, N. M. A. N. A., Alitheen, N. B., & Osman, M. A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24076423 · Cited by 40
Osteoporosis: interferon-gamma-mediated bone remodeling in osteoimmunology
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“Throughout this stage, OC formation and bone resorption persist, while recruited MSCs gradually undergo differentiation into OBs (21).”
InfluentialDevelopments in Dental Implant Surface Modification
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“Abnormal bone remodeling is mainly caused by imbalance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation (Feng and McDonald, 2011).”
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“Bone remodeling is a physiological condition regulated by osteoblasts replacing new bone formations and osteoclasts removing old or damaged bone [1].”
InfluentialmTORC1 Activation in Osteoclasts Prevents Bone Loss in a Mouse Model of Osteoporosis
Hiraiwa, M., Ozaki, K., Yamada, T., Iezaki, T., Park, G., Fukasawa, K., Horie, T., Kamada, H., Tokumura, K., Motono, M., et al. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00684 · Cited by 37
“An imbalance in the sophisticated regulation of osteoclasts and osteoblasts leads to pathogenesis as well as the etiology of certain metabolic bone diseases such as osteoporosis, osteopetrosis, and rheumatoid arthritis (Feng and McDonald, 2011).”
BackgroundOsteoblast-osteoclast co-cultures: A systematic review and map of available literature
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“In diseases such as osteoporosis and osteopetrosis this equilibrium is disturbed, leading to pathological changes in bone mass that adversely affect the bone’s mechanical functionality [1].”
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Osteogenesis and osteoclastogenesis on a chip: Engineering a self-assembling 3D coculture
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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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