Vertebral compression fractures in multiple myeloma. Part I. Distribution and appearance at MR imaging.

Lecouvet, Frédéric; Berg, Bruno C. Vande; Maldague, Baudouin; Michaux, Lucienne; Laterre, Emile-Christian; Michaux, Jean‐Louis; Ferrant, Augustin

doi:10.1148/radiology.204.1.9205246

Cited by 145 publications

(74 citation statements)

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“…In accordance with the literature [22,23], the most common site of fracture in our analysis was the spine (59%), especially in the lower thoracic or lumbar vertebral bodies. Other common sites of fracture included the femur, pelvis, trunk and humerus.…”

Section: Discussionsupporting

confidence: 91%

Surgical therapy of skeletal complications in multiple myeloma

Utzschneider

Schmidt

Weber

et al. 2010

International Orthopaedics (SICOT)

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Patients with multiple myeloma are often treated surgically as though they have bone metastases. Due to major differences in oncological therapy and comparatively long survival times these patients should be considered separately. Seventy-five multiple myeloma patients were treated surgically (83 interventions) for skeletal complications of the disease. Location and dissemination, symptoms, method of surgery, complications, recurrence and survival time were evaluated retrospectively. Most of the lesions were in the axial skeleton or the proximal extremities apart from one distal lesion of the fibula, and most surgery was performed in the spine (35 patients). The mean follow-up of patients was 5.4 years (range 1-25 years). Survival proved to be very favourable (37% at five years). Patients with a single bone lesion, a negative bone marrow biopsy, no paraproteinaemia in serum or a Salmon-Durie-stage I had a better survival probability. Surgical treatment in patients with multiple myeloma was mostly limited to a palliative approach but survival time was better (37% at five years) than in patients with metastatic bone disease which has to be considered in their surgical treatment.

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Section: Discussionsupporting

confidence: 91%

Surgical therapy of skeletal complications in multiple myeloma

Utzschneider

Schmidt

Weber

et al. 2010

International Orthopaedics (SICOT)

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“…In addition, their site distribution is similar to that of compression VFs in patients with osteoporosis. On imaging multiple myeloma's appearance may be misleading, simulating an osteoporotic compression VF in about 67% of the cases and the fractures may present different state of evolution with 38% of the patients having only benign appearing VFs (68) …”

Section: Vfs Due To Malignant Diseasesmentioning

confidence: 99%

Identifying osteoporotic vertebral endplate and cortex fractures

Wáng

Santiago

Deng

et al. 2017

Quant. Imaging Med. Surg.

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“…About 86 000 new cases of myeloma are diagnosed globally each year, 1 and 95% of patients develop bone disease, which leads to a 16-fold increase in the risk of skeletal fractures, most commonly in the vertebrae. [1][2][3][4][5][6] The bone disease results from tumor cell production of paracrine factors that increase osteoclast-mediated bone resorption and suppress bone formation by osteoblasts. 7,8 Inhibiting the osteoclastic bone resorption component prevents development of myeloma bone disease.…”

Section: Introductionmentioning

confidence: 99%

Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma

McDonald

Reagan

Youlten

et al. 2017

Blood

163

161

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Multiple myeloma (MM) is a plasma cell cancer that develops in the skeleton causing profound bone destruction and fractures. The bone disease is mediated by increased osteoclastic bone resorption and suppressed bone formation. Bisphosphonates used for treatment inhibit bone resorption and prevent bone loss but fail to influence bone formation and do not replace lost bone, so patients continue to fracture. Stimulating bone formation to increase bone mass and fracture resistance is a priority; however, targeting tumor-derived modulators of bone formation has had limited success. Sclerostin is an osteocyte-specific Wnt antagonist that inhibits bone formation. We hypothesized that inhibiting sclerostin would prevent development of bone disease and increase resistance to fracture in MM. Sclerostin was expressed in osteocytes from bones from naive and myeloma-bearing mice. In contrast, sclerostin was not expressed by plasma cells from 630 patients with myeloma or 54 myeloma cell lines. Mice injected with 5TGM1-eGFP, 5T2MM, or MM1.S myeloma cells demonstrated significant bone loss, which was associated with a decrease in fracture resistance in the vertebrae. Treatment with anti-sclerostin antibody increased osteoblast numbers and bone formation rate but did not inhibit bone resorption or reduce tumor burden. Treatment with anti-sclerostin antibody prevented myeloma-induced bone loss, reduced osteolytic bone lesions, and increased fracture resistance. Treatment with anti-sclerostin antibody and zoledronic acid combined increased bone mass and fracture resistance when compared with treatment with zoledronic acid alone. This study defines a therapeutic strategy superior to the current standard of care that will reduce fractures for patients with MM

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Vertebral compression fractures in multiple myeloma. Part I. Distribution and appearance at MR imaging.

Cited by 145 publications

References 0 publications

Surgical therapy of skeletal complications in multiple myeloma

Surgical therapy of skeletal complications in multiple myeloma

Identifying osteoporotic vertebral endplate and cortex fractures

Inhibiting the osteocyte-specific protein sclerostin increases bone mass and fracture resistance in multiple myeloma

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