Myeloma bone disease

Natalie S. Callander, G. David Roodman

Research output: Contribution to journalArticle

122 Citations (Scopus)

Abstract

Bone destruction is a hallmark of myeloma, with 70% to 80% of patients manifesting bone involvement. Destruction is mediated through normal osteoclasts (OCLs), which respond to local osteoclast-activating factors (OAFs) produced by myeloma cells or by other cells in the local microenvironment. OAFs implicated in myeloma bone disease include tumor necrosis factor-beta (TNFβ), RANK ligand (RANKL), interleukin-1 (IL-1), parathyroid hormone-related protein (PTHrP), hepatocyte growth factor (HGH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFα), and macrophage inflammatory protein-1-alpha (MIP-1α). To date, the leading candidates for OAFs are MIP-1α and RANKL. Adhesive interactions between marrow stromal cells and myeloma cells induce marrow stromal cells to secrete IL-6, a potent myeloma growth/survival factor that may contribute to the bone disease. Evaluation of myeloma bone disease includes plain radiographs, and newer methods, such as magnetic resonance imaging (MRI), positron emission tomography (PET) scans, technetium-99m-sestamibi (Mibi) scanning, and dual-energy x-ray absorptiometry (DEXA) scanning, may provide more complete information. In addition, biochemical markers of bone resorption are being evaluated, although the limited availability of these assays and lack of extensive testing in patients make their routine use premature. Treatment of myeloma bone disease includes radiation therapy, vertebroplasty, surgery, and bisphosphonates. New developments on the pathogenesis and treatment of myeloma bone disease present great opportunities to combat bone disease.

Original languageEnglish (US)
Pages (from-to)276-285
Number of pages10
JournalSeminars in Hematology
Volume38
Issue number3
StatePublished - 2001
Externally publishedYes

Fingerprint

Bone Diseases
RANK Ligand
Chemokine CCL3
Stromal Cells
Interleukin-6
Bone Marrow
Vertebroplasty
Technetium Tc 99m Sestamibi
Parathyroid Hormone-Related Protein
Bone and Bones
Lymphotoxin-alpha
Hepatocyte Growth Factor
Diphosphonates
Osteoclasts
Bone Resorption
Interleukin-1
Adhesives
Positron-Emission Tomography
Intercellular Signaling Peptides and Proteins
Radiotherapy

ASJC Scopus subject areas

  • Hematology

Cite this

Callander, N. S., & Roodman, G. D. (2001). Myeloma bone disease. Seminars in Hematology, 38(3), 276-285.

Myeloma bone disease. / Callander, Natalie S.; Roodman, G. David.

In: Seminars in Hematology, Vol. 38, No. 3, 2001, p. 276-285.

Research output: Contribution to journalArticle

Callander, NS & Roodman, GD 2001, 'Myeloma bone disease', Seminars in Hematology, vol. 38, no. 3, pp. 276-285.
Callander NS, Roodman GD. Myeloma bone disease. Seminars in Hematology. 2001;38(3):276-285.
Callander, Natalie S. ; Roodman, G. David. / Myeloma bone disease. In: Seminars in Hematology. 2001 ; Vol. 38, No. 3. pp. 276-285.
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