Anıl Köktürk1, Erdem Aras Sezgin2, O. Şahap Atik3

1Department of Orthopedics and Traumatology, Zonguldak Devrek State Hospital, Zonguldak, Türkiye
2Department of Orthopedics and Traumatology, Gazi University Faculty of Medicine, Ankara, Türkiye
3President, Turkish Joint Diseases Foundation, Ankara, Türkiye

Prostate and breast cancers are classified as hormone-sensitive malignancies, as the survival and proliferation of their tumor cells are closely dependent on the binding of steroid hormones to their respective receptors, notably the androgen receptor.[1] Hormonal ablation therapies used in patients with hormone-sensitive cancers, accelerate bone loss via estrogen and androgen suppression, thereby leading to secondary osteoporosis and an increased risk of fractures.[2-6] According to the International Osteoporosis Foundation (IOF) review, women with non-metastatic breast cancer exhibit an approximately five-fold increased risk of vertebral fracture compared to the general population.[3] The American Society of Clinical Oncology (ASCO) guidelines also state that men with prostate cancer undergoing androgen deprivation therapy experience an approximately nine-fold greater loss in bone mineral density during the first year compared to normal aging.[4]

A key diagnostic challenge in these patients lies in the radiographic indistinguishability between vertebral fractures caused by metastatic involvement and those resulting from therapy-induced bone fragility.[7-10] The most confusing aspect of this overlap is the presence of bone marrow edema on magnetic resonance imaging (MRI) images in both acute osteoporotic fractures and early metastatic infiltration.[9] To overcome this issue, diffusionweighted imaging (DWI) using low b-values (<500 s/mm2) has been shown to effectively distinguish benign from malignant lesions.[9] However, current literature reports an unexpected malignancy rate of up to 6 to 7% in routine transpedicular biopsies, even when preoperative MRI shows no evidence of metastasis.[8,10] Considering these findings, vertebral biopsy should be primarily considered in patients with a history of cancer and in those exhibiting imaging features suspicious for malignancy on MRI, such as convexity of the posterior vertebral border, epidural or paravertebral soft-tissue masses, and involvement of the posterior vertebral elements.[10]

It is of utmost importance to assess the risk of fracture before treatment in patients planning to receive aromatase inhibitors, gonadotropin-releasing hormone (GnRH) analogs, or androgen deprivation therapy, and to initiate preventive measures in at-risk individuals.[2-6] Cancer treatment–induced bone loss differs from postmenopausal or age-related osteoporosis, progressing approximately seven times more rapidly and representing a significant cause of secondary osteoporosis.[4] Consequently, preventing vertebral fractures through prophylactic treatments such as bisphosphonates and denosumab can be considered in patients with hormonesensitive cancers.[2-6] A multi-center randomizedcontrolled trial involving patients with painful vertebral compression fractures demonstrated that minimally invasive interventions such as balloon kyphoplasty provide rapid and sustained analgesic relief.[11] Furthermore, compared to non-surgical management, these procedures significantly improve back-specific functional status and overall quality of life.[11]

In conclusion, osteoporosis associated with hormone ablation therapy progresses rapidly; therefore, ensuring high patient compliance and implementing appropriate preventive measures to manage the risk is essential. Although MRI demonstrates high accuracy in differentiating osteoporotic fractures from metastatic involvement, a targeted biopsy should be considered in patients with a history of cancer.

Citation: Köktürk A, Sezgin EA, Atik OŞ. Vertebral fragility fractures mimicking metastases in patients with hormone-sensitive cancers: A clinical highlight. Jt Dis Relat Surg 2026;37(2):563-564. doi: 10.52312/jdrs.2026.57933.

Author Contributions

All authors contributed equally to this article.

Conflict of Interest

The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Financial Disclosure

The authors received no financial support for the research and/or authorship of this article.

Data Sharing Statement

The data that support the findings of this study are available from the corresponding author upon reasonable request.

AI Disclosure:
The authors declare that artificial intelligence (AI) tools were not used, or were used solely for language editing, and had no role in data analysis, interpretation, or the formulation of conclusions. All scientific content, data interpretation, and conclusions are the sole responsibility of the authors. The authors further confirm that AI tools were not used to generate, fabricate, or ‘hallucinate’ references, and that all references have been carefully verified for accuracy.

References

  1. Proverbs-Singh T, Feldman JL, Morris MJ, Autio KA, Traina TA. Targeting the androgen receptor in prostate and breast cancer: Several new agents in development. Endocr Relat Cancer 2015;22:R87-106. doi: 10.1530/ERC-14-0543.
  2. Nicolopoulos K, Moshi MR, Stringer D, Ma N, Jenal M, Vreugdenburg T. The clinical effectiveness of denosumab (Prolia®) in patients with hormone-sensitive cancer receiving endocrine therapy, compared to bisphosphonates, Selective Estrogen Receptor Modulators (SERM), and placebo: A systematic review and network meta-analysis. Arch Osteoporos 2023;18:18. doi: 10.1007/s11657-023-01211-3.
  3. Rizzoli R, Body JJ, Brandi ML, Cannata-Andia J, Chappard D, El Maghraoui A, et al. Cancer-associated bone disease. Osteoporos Int 2013;24:2929-53. doi: 10.1007/s00198-013- 2530-3.
  4. Shapiro CL, Van Poznak C, Lacchetti C, Kirshner J, Eastell R, Gagel R, et al. Management of osteoporosis in survivors of adult cancers with nonmetastatic disease: ASCO clinical practice guideline. J Clin Oncol 2019;37:2916-46. doi: 10.1200/ JCO.19.01696.
  5. Coleman R, Hadji P, Body JJ, Santini D, Chow E, Terpos E, et al. Electronic address: clinicalguidelines@esmo.org. Bone health in cancer: ESMO clinical practice guidelines. Ann Oncol 2020;31:1650-63. doi: 10.1016/j.annonc.2020.07.019.
  6. Ottanelli S. Prevention and treatment of bone fragility in cancer patient. Clin Cases Miner Bone Metab 2015;12:116-29. doi: 10.11138/ccmbm/2015.12.2.116.
  7. Kourtis E, Zygogiannis K, Fanourgiakis I, Koulalis D, Stathopoulos KD. Understanding and managing fracture risk in patients with cancer: A literature review. Cureus 2025;17:e83082. doi: 10.7759/cureus.83082.
  8. Osterhoff G, Scheyerer MJ, Spiegl UJA, Schnake KJ. The role of routine transpedicular biopsies during kyphoplasty or vertebroplasty for vertebral compression fractures in the detection of malignant diseases: A systematic review. Arch Orthop Trauma Surg 2023;143:1887-93. doi: 10.1007/s00402- 022-04392-7.
  9. Luo Z, Litao L, Gu S, Luo X, Li D, Yu L, et al. Standard-b- value vs low-b-value DWI for differentiation of benign and malignant vertebral fractures: A meta-analysis. Br J Radiol 2016;89:20150384. doi: 10.1259/bjr.20150384.
  10. Chou KN, Lin BJ, Chien LY, Tsai WC, Ma HI, Hueng DY. Simple transpedicular vertebral biopsy for diagnosis of malignancy in vertebral compression fracture. Neurol India 2013;61:587-92. doi: 10.4103/0028-3886.125249.
  11. Berenson J, Pflugmacher R, Jarzem P, Zonder J, Schechtman K, Tillman JB, et al. Balloon kyphoplasty versus non-surgical fracture management for treatment of painful vertebral body compression fractures in patients with cancer: A multicentre, randomised controlled trial. Lancet Oncol 2011;12:225-35. doi: 10.1016/S1470-2045(11)70008-0.