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Review
. 2025 Mar 27;116(1):54.
doi: 10.1007/s00223-025-01362-0.

Bone Effects of Anti-Cancer Treatments in 2024

Marie Teissonnière  1 , Mathieu Point  2 , Emmanuel Biver  3 , Peyman Hadji  4 , Edith Bonnelye  5 , Peter R Ebeling  6 , David Kendler  7 , Tobias de Villiers  8 , Gerold Holzer  9 , Jean-Jacques Body  10 , Ghada El Hajj Fuleihan  11 , Maria Luisa Brandi  12 , René Rizzoli  13 , Cyrille B Confavreux  14   15   16
Affiliations
Review

Bone Effects of Anti-Cancer Treatments in 2024

Marie Teissonnière et al. Calcif Tissue Int. .

Abstract

Considerable progress has been made in the management of cancer patients in the last decade with the arrival of anti-cancer immunotherapies (immune checkpoint inhibitors) and targeted therapies. As a result, a broad spectrum of cancers, not just hormone-sensitive ones, have seen several patients achieve profound and prolonged remissions, or even cures. The management of medium- and long-term side-effects of treatment and quality of life of patients are essential considerations. This is especially true for bone, as bone fragility can lead to increased fractures and loss of autonomy, ultimately reducing the possibility of resuming physical activity. Physical activity is essential for lasting oncological remission and prevention of fatigue. While the issue of hormone therapies and their association with breast cancer has been recognized for some time, the situation is relatively new with regards to targeted therapies and immunotherapies. This is particularly challenging given the wide range of available targeted therapies and their application to numerous cancer types. This article provides a comprehensive review of the bone effects of the main anti-cancer therapies currently in use. The review goes beyond glucocorticoids and hormone therapies and discusses for each drug category what is known regarding cellular effects, BMD effects, and fracture incidence.

Keywords: Bone mineral densitometry; Cancer treatment induced bone loss (CTIBL); Fracture risk; Osteoblast; Osteoclast; Side effects.

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Conflict of interest statement

Declarations. Conflict of interest: The following authors MT, MP, EB, EB, TV, GH, GEHF, MLB and RR declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. The authors declare the following conflicts of interests: Research grants: PH (Stada), PE (Amgen, Alexion, Sanofi) and CC (Amgen, MSD avenir). Conferences: PH (UCB), PE (Amgen, Kyowa-Kirin, Alexion), DK (Amgen, Radius Pharma), JJB (Amgen), CC (Amgen, BMS, Lilly, MSD, Theramex).

Figures

Fig. 1
Fig. 1
PRISMA flow diagram for identification, screening/eligibility, and inclusion of the studies
Fig. 2
Fig. 2
Schematic representation of bone effects of anti-cancer drugs according to three levels of evidence: osteoblast and osteoclast, bone mineral density and fracture. BMD: Bone Mineral Density, SERM: Selective Estrogen Receptor Modulator, TKI:Tyrosine Kinase Inhibitor 5-FU: 5-fluorouracil and AI: aromatase inhibitor. In red: increase, in green: decrease and in blue: neutral
Fig. 3
Fig. 3
Integration of tyrosine kinase inhibitor (TKI) pathways in osteoblast signaling. Each membrane receptor may act on one or several intracellular pathway(s) resulting on biological effect(s) on osteoblast (OB) precursor proliferation, early and/or late OB differentiation. Intracellularly, TKI act mainly on PI3K/AKT/mTOR and MEK/ERK pathways
Fig. 4
Fig. 4
Integration of tyrosine kinase inhibitor (TKI) pathways in osteoclast signaling. Each membrane receptor may act on one or several intracellular pathway(s) resulting on biological effect(s) on osteoclast (OC) progenitor proliferation, OC progenitor differentiation and/or OC resorption activity
See this image and copyright information in PMC

References

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