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Cancer-associated bone disease

  • Position Paper
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Abstract

Bone is commonly affected in cancer. Cancer-induced bone disease results from the primary disease, or from therapies against the primary condition, causing bone fragility. Bone-modifying agents, such as bisphosphonates and denosumab, are efficacious in preventing and delaying cancer-related bone disease. With evidence-based care pathways, guidelines assist physicians in clinical decision-making. Of the 57 million deaths in 2008 worldwide, almost two thirds were due to non-communicable diseases, led by cardiovascular diseases and cancers. Bone is a commonly affected organ in cancer, and although the incidence of metastatic bone disease is not well defined, it is estimated that around half of patients who die from cancer in the USA each year have bone involvement. Furthermore, cancer-induced bone disease can result from the primary disease itself, either due to circulating bone resorbing substances or metastatic bone disease, such as commonly occurs with breast, lung and prostate cancer, or from therapies administered to treat the primary condition thus causing bone loss and fractures. Treatment-induced osteoporosis may occur in the setting of glucocorticoid therapy or oestrogen deprivation therapy, chemotherapy-induced ovarian failure and androgen deprivation therapy. Tumour skeletal-related events include pathologic fractures, spinal cord compression, surgery and radiotherapy to bone and may or may not include hypercalcaemia of malignancy while skeletal complication refers to pain and other symptoms. Some evidence demonstrates the efficacy of various interventions including bone-modifying agents, such as bisphosphonates and denosumab, in preventing or delaying cancer-related bone disease. The latter includes treatment of patients with metastatic skeletal lesions in general, adjuvant treatment of breast and prostate cancer in particular, and the prevention of cancer-associated bone disease. This has led to the development of guidelines by several societies and working groups to assist physicians in clinical decision making, providing them with evidence-based care pathways to prevent skeletal-related events and bone loss. The goal of this paper is to put forth an IOF position paper addressing bone diseases and cancer and summarizing the position papers of other organizations.

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Abbreviations

ABCSG:

Austrian Breast & Colorectal Cancer Study Group

ADT:

Androgen deprivation therapy

AI:

Aromatase inhibitor

ALP:

Alkaline phosphatase

ASCO:

American Society of Clinical Oncology

ATAC:

Arimidex, Tamoxifen Alone or in Combination

AZURE:

Adjuvant Zoledronic Acid to Reduce Recurrence

BTM:

Bone turnover marker

BMD:

Bone mineral density

CI:

Confidence interval

CMF:

Cyclophosphamide–methotrexate–5 fluorouracil

CT:

Computed tomography

CTX:

Cross-linked terminal telopeptide

DKK1:

Dickkopf-related protein

DXA:

Dual-energy X-ray absorptiometry

ER:

Estrogen receptor

ET:

Endothelin

ESCEO:

European Society for Clinical and Economical Aspects of Osteoporosis and Osteoarthritis

FAC:

5-Fluorouracil–doxorubicin–cyclophosphamide

FDG:

Fluorodeoxyglucose

FGF:

Fibroblast growth factor

FRAX:

WHO fracture risk assessment tool

GnRH:

Gonadotropin-releasing hormone

HR:

Hazard ratio

IGF:

Insulin-like growth factor

IES:

Intergroup Exemestane Study

IL:

Interleukin

IV:

Intravenous

MRI:

Magnetic resonance imaging

NCCN:

National Comprehensive Cancer Network

NTX:

N-terminal telopeptide

ONJ:

Osteonecrosis of the jaw

OPG:

Osteoprotegerin

PDGF-BB:

Platelet-derived growth factor-BB

PET:

Positron emission tomography

PSA:

Prostate-specific antigen

PTHrP:

Parathyroid hormone-related protein

RANK:

Receptor activator of nuclear factor kappa-B

RANKL:

Receptor activator of nuclear factor kappa-B ligand

RCT:

Randomized controlled trial

RR:

Relative risk

SABRE:

Study of Anastrozole with the Bisphosphonate Risedronate

SERM:

Selective oestrogen receptor modulator

sFRP:

Secreted frizzled-related protein

SRE:

Skeletal-related event

TGF-β:

Transforming growth factor-beta

TNF-α:

Tumour necrosis factor-alpha

TRAcP:

Tartrate-resistant acid phosphatase

TSH:

Thyroid-stimulating hormone

VEGF:

Vascular endothelial growth factor

VFA:

Vertebral fracture assessment

WHO:

World Health Organization

Z-Fast and ZO-Fast:

Zometa-Femara Adjuvant Synergy Trials

αCTX:

Alpha cross-linked telopeptides type

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Acknowledgments

The authors thank Ms Aida Farha, Medical Information Specialist, Saab Medical Library, American University of Beirut, for her assistance in designing comprehensive and complex searches of the various medical literature resources.

Conflicts of interest

René Rizzoli has received speaker or advisory board fees from Amgen, MSD, GSK, Servier, Danone and Takeda. Jean-Jacques Body has received speaker and consulting fees from Amgen and Novartis. Jorge B. Cannata-Andía has received research grants and speaker or advisory board fees from Amgen, Abbott, Servier and Shire. David Kendler has received honoraria for speaking, consulting and/or research grants from Amgen, Novartis, GSK, Eli Lily, Merck, Johnson&Johnson, Pfizer and Roche. Alexandra Papaioannou has been a consultant, or on a speaker’s bureau, or received unrestricted grants from Amgen, Eli Lilly, Merck Canada Inc., Novartis, Pfizer and Warner Chilcott. Tobias J de Villiers has received speaker or advisory board fees from Amgen, Merck, Adcock Ingram and Pfizer. Catherine Van Poznak has received research support from Amgen and Novartis. Ghada El-Hajj Fuleihan has received grants to support courses on osteoporosis from Novartis Pharmaceuticals and Les Laboratoires Servier. Abdellah El Maghraoui, Nicola Napoli, Dominique D Pierroz and Maria Rahme have no conflict of interest.

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Authors and Affiliations

  1. Division of Bone Diseases, Geneva University Hospitals and Faculty of Medicine, Geneva, Switzerland

    R. Rizzoli

  2. Department of Medicine, CHU Brugmann, Université Libre de Bruxelles, Brussels, Belgium

    J.-J. Body

  3. Department of Internal Medicine, University of Florence, Florence, Italy

    M.-L. Brandi

  4. Bone and Mineral Research Unit, Instituto Reina Sofía, REDinREN, ISCIII, Hospital Universario Central de Asturias, Universidad de Oviedo, Oviedo, Spain

    J. Cannata-Andia

  5. GEROM-Research Group on Bone Remodeling and bioMaterials, LUNAM University, Angers, France

    D. Chappard

  6. Rheumatology Department, Military Hospital Mohammed V, Rabat, Morocco

    A. El Maghraoui

  7. Sektion Biomedizinische Bildgebung, Klinik für Diagnostische Radiologie, Universitätsklinikum Schleswig-Holstein, Kiel, Germany

    C. C. Glüer

  8. Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada

    D. Kendler

  9. Division of Endocrinology, University Campus Bio-Medico, Rome, Italy

    N. Napoli

  10. Department of Medicine, McMaster University, Hamilton, Ontario, Canada

    A. Papaioannou

  11. International Osteoporosis Foundation (IOF), Nyon, Switzerland

    D. D. Pierroz

  12. Calcium Metabolism and Osteoporosis Program, WHO Collaborating Center for Osteoporosis and Metabolic Bone Disorders, American University of Beirut Medical Center, Beirut, Lebanon

    M. Rahme & G. El Hajj Fuleihan

  13. University of Michigan, Ann Arbor, MI, USA

    C. H. Van Poznak

  14. Panorama MediClinic and Department of Gynaecology, Faculty of Health Sciences, Stellenbosch University, Cape Town, South Africa

    T. J. de Villiers

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for the International Osteoporosis Foundation Committee of Scientific Advisors Working Group on Cancer-Induced Bone Disease

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Correspondence to R. Rizzoli.

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This position paper has been endorsed by the Committee of Scientific Advisors of IOF

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Rizzoli, R., Body, JJ., Brandi, ML. et al. Cancer-associated bone disease. Osteoporos Int 24, 2929–2953 (2013). https://doi.org/10.1007/s00198-013-2530-3

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