Pathogenesis of myeloma bone disease
Abstract
Bone disease in multiple myeloma (MM) is characterized by lytic bone lesions, which can cause severe bone pain, pathologic fractures and hypercalcemia. However, the lytic bone disease in MM differs from that in other cancer patients who have lytic bone metastases. Although increased osteoclastic bone destruction is involved in MM and other tumors involving bone, in contrast to other tumors, once the MM tumor burden exceeds 50% in a local area, osteoblast activity is either suppressed or absent. The basis for this severe imbalance between increased osteoclastic bone resorption and decreased bone formation has been a topic of intensive investigation over the last several years and will be reviewed in this article.
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Both bone modeling and remodeling necessitate the manufacture of collagen and other matrix proteins by osteoblasts, thereby consuming a substantial quantity of ATP.
“In fact, both the modeling and remodeling processes necessitate the manufacture of collagen and other matrix proteins by osteoblasts (OBs), thereby consuming a substantial quantity of energy in the form of adenosine triphosphate (ATP) [44, 45].”
From Mesenchymal stromal cells in bone marrow niche of patients with multiple myeloma: a double-edged sword (2025) · cites this paper as [45]
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Multiple myeloma: 2024 update on diagnosis, risk-stratification, and management
Rajkumar, S. V. (2024) · American Journal of Hematology · doi:10.1002/ajh.27422 · Cited by 534 · see citing works
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p38 MAPK in Myeloma Cells Regulates Osteoclast and Osteoblast Activity and Induces Bone Destruction
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Thymidine phosphorylase exerts complex effects on bone resorption and formation in myeloma
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“In fact, both the modeling and remodeling processes necessitate the manufacture of collagen and other matrix proteins by osteoblasts (OBs), thereby consuming a substantial quantity of energy in the form of adenosine triphosphate (ATP) [44, 45].”
The Metabolic Features of Osteoblasts: Implications for Multiple Myeloma (MM) Bone Disease
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- Authors
- Roodman, G. D.
- Affiliations
- University of Pittsburgh (US)
- Corresponding author
- Roodman, G D
- Venue
- Leukemia
- Published
- 2008-11-27
- Volume
- 23
- Issue
- 3
- Pages
- 435-441
- ISSN
- 0887-6924 (ISSN-L)
- 1476-5551
- OpenAlex
- W2122038117
- Cited by
- 398
- References
- 3
- Citations by year
- 2026: 10 · 2025: 19 · 2024: 9 · 2023: 11 · 2022: 23 · 2021: 33 · 2020: 36 · 2019: 11 · 2018: 30 · 2017: 29 · 2016: 28 · 2015: 25 · 2014: 28 · 2013: 20 · 2012: 30
- FWCI
- 2.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Leukemia (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Hematology › Multiple Myeloma Research and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Oncology › Bone health and treatments
- Keywords
- multiple myeloma, myeloma bone disease, osteolytic lesions, osteoclast resorption, osteoblast activity, bone formation, hypercalcemia, pathological fracture, bone pain, tumor-induced osteolysis
- MeSH terms
- Bortezomib, Denosumab, Antibodies, Monoclonal, Antineoplastic Agents, Boronic Acids, Cell Adhesion, Fractures, Spontaneous, Glucocorticoids, Humans, Hypercalcemia, Immunologic Factors, Interleukins, Multiple Myeloma, Neoplasm Proteins, Osteoblasts, Osteoclasts, Osteolysis, Pyrazines, Cytokines, Stromal Cells, Wnt Proteins, RANK Ligand, Antibodies, Monoclonal, Humanized
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