Pathophysiology of multiple myeloma bone disease
Suzanne Lentzsch1, Lori A Ehrlich, G David Roodman
1Division of Hematology/Oncology, Department of Medicine, University of Pittsburgh, and Division of Hematology/Oncology, Veterans Administration Pittsburgh Healthcare System, Research and Development, PA 15232, USA. lentzschs@upmc.edu
Hematology/Oncology Clinics of North America
|November 13, 2007
Summary
Multiple myeloma causes bone destruction by increasing osteoclast activity and suppressing osteoblast function, leading to osteolytic lesions. Understanding these mechanisms may reveal new treatments for myeloma bone disease.
Area of Science:
- Oncology
- Bone Biology
- Pathophysiology
Background:
- Multiple myeloma is a plasma cell cancer.
- It frequently causes osteolytic bone lesions.
- Bone destruction results from imbalanced osteoclast and osteoblast activity.
Purpose of the Study:
- To review the pathophysiology of bone remodeling imbalance in multiple myeloma.
- To discuss potential new therapeutic strategies for bone disease in multiple myeloma.
Main Methods:
- Review of current literature on multiple myeloma and bone pathophysiology.
- Analysis of biological mechanisms driving bone destruction in myeloma.
Main Results:
- Multiple myeloma cells induce increased osteoclast activity.
- Myeloma cells suppress osteoblast differentiation and activity.
- This leads to impaired bone formation and osteolytic lesions.
Conclusions:
- The mechanisms of imbalanced bone remodeling in multiple myeloma are becoming clearer.
- New therapeutic strategies targeting bone disease in multiple myeloma are being developed.
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