Men treated for prostate cancer may be winning the fight against their tumor only to face a quieter, slower-moving threat: crumbling bones. A sweeping new systematic review and meta-analysis, published in Supportive Care in Cancer, has pooled data from 52 studies covering 91,913 men with prostate cancer and concluded that roughly one in five of them has osteoporosis, while more than four in ten carry a diagnosis of low bone mass, or osteopenia. The findings, drawn from research published between January 1994 and October 2025, represent the most comprehensive attempt yet to quantify the skeletal toll of the disease and, crucially, of the hormone-suppressing therapies that form the backbone of prostate cancer treatment worldwide.
The numbers are stark. Across all included studies, 7,042 cases of osteoporosis were reported, yielding a pooled prevalence of 22.0 percent, with a 95 percent confidence interval of 19.9 to 24.1 percent. For low bone mass, defined by bone mineral density T-scores between greater than −2.5 and less than −1.0, the pooled prevalence across 42 studies was 41.7 percent, with a confidence interval of 36.6 to 46.9 percent. Taken together, the analysis suggests that in a typical clinic population of men with prostate cancer, more than six in ten may have bone density below the normal range, a burden that vastly exceeds what would be expected in age-matched men without the disease or its treatments.
The biological explanation lies in the central role of testosterone in maintaining the male skeleton. Androgen-deprivation therapy, or ADT, the standard treatment for advanced, high-risk, and recurrent prostate cancer, deliberately suppresses testicular androgen production to starve hormone-sensitive tumors. But the same sex steroids that fuel prostate cancer cell growth also restrain the bone-resorbing cells known as osteoclasts. When androgens are stripped away, bone remodeling tips toward resorption, bone mineral density declines at an accelerated rate, and fracture risk climbs. Earlier cohort studies, including a landmark analysis of Medicare beneficiaries published in the New England Journal of Medicine in 2005, documented increased fracture rates among men receiving ADT, and subsequent population-based studies in Korea, Taiwan, and elsewhere have reinforced the association. Vertebral fractures, in particular, have been found at strikingly high rates even at the initiation of therapy, before measurable density loss accumulates.
To assemble the new estimates, the research team, led by investigators at Tehran University of Medical Sciences with collaborators in Brazil, searched six major databases: PubMed, Scopus, Web of Science, Embase, CINAHL, and ProQuest. They included population- and institution-based cross-sectional and cohort studies reporting the prevalence of osteoporosis or low bone mass among adult men with prostate cancer at any disease stage. Osteoporosis was classified primarily by the conventional dual-energy X-ray absorptiometry, or DXA, threshold of a T-score at or below −2.5, while low bone mass covered the intermediate band above that cutoff. Risk of bias was assessed independently using the Joanna Briggs Institute checklist, and pooled estimates were calculated with random-effects meta-analysis, the appropriate model when underlying true prevalences are expected to differ across populations.
That expectation was borne out dramatically. Heterogeneity, measured by the I-squared statistic, reached 99.49 percent for osteoporosis and 95.85 percent for low bone mass, meaning that almost all of the observed variation among studies reflects real differences rather than statistical noise. Subgroup analyses showed that pooled estimates shifted depending on how bone mineral density was measured, how the outcomes were defined, which category of ADT patients had received, which geographic region the study came from, and whether the design was cross-sectional or longitudinal. Notably, the authors report that the largest differences were methodological rather than clinical, and that many subgroups contained only one or two studies, so all such comparisons should be read as exploratory rather than definitive.
The methodological point deserves emphasis, because it cuts to the heart of how bone disease is detected in men. Central DXA scanners measure the spine and hip, the gold-standard sites, whereas peripheral devices assess the forearm, heel, or finger and can yield systematically different classifications. Quantitative ultrasound of the calcaneus, used in some screening studies, is cheaper and portable but less precise. Studies that relied on study-specific definitions or on diagnostic codes rather than densitometry contributed additional noise. The result is a literature in which the same underlying patient population could plausibly generate prevalence estimates differing by tens of percentage points depending on the instrument and cutoff employed, a problem the authors argue can only be resolved through standardized assessment protocols.
Meta-regression, a technique that tests whether study-level characteristics predict the size of the pooled effect, found no statistically significant association between publication year or ADT duration and overall prevalence. But the authors are careful about what this null result means. Duration data were available for only 24 of the studies contributing to the osteoporosis analysis and 20 of those contributing to the low bone mass analysis, and even after accounting for these variables, residual heterogeneity remained above 92 percent. In other words, the analysis lacked the power and the homogeneity needed to detect a true dose-response relationship if one exists, and the absence of a detected link should not be mistaken for evidence that longer hormone therapy is harmless to bone. Sensitivity analyses, meanwhile, produced results consistent with the main findings, offering some reassurance that no single outlier study was driving the pooled estimates.
The clinical implications are considerable. Prostate cancer is the second most common cancer in men globally, and ADT is prescribed to a large fraction of patients, often for years. If roughly a fifth of these men have frank osteoporosis and another two-fifths have low bone mass, then bone health belongs in every prostate cancer management pathway, not only in oncology clinics but in primary care and survivorship programs. Yet prior studies cited in the review suggest that screening rates remain low, that physicians frequently fail to order bone density testing or prescribe antiresorptive agents during ADT, and that patients themselves often lack knowledge about osteoporosis risk. Automated outpatient systems that flag men starting ADT for DXA screening have been shown to improve screening rates, pointing to practical, low-cost interventions.
At the same time, the authors draw a firm boundary around what their review can and cannot claim. It assessed prevalence only. It did not evaluate fracture incidence, the effectiveness of screening programs, or the efficacy of any preventive or therapeutic intervention, and it therefore cannot confirm that any particular strategy, from calcium and vitamin D supplementation to bisphosphonates and denosumab, actually reduces fractures in this population. That question requires randomized trials and longitudinal cohorts with harmonized bone mineral density assessment, which the authors identify as the field’s most urgent unmet need. Until such studies arrive, the review’s central message stands on its own: the skeleton is a silent casualty of prostate cancer care, and the first step toward protecting it is simply counting the damage, which this analysis has now done at unprecedented scale.
Subject of Research: Prevalence of osteoporosis and low bone mass in men with prostate cancer
Article Title: Prevalence of osteoporosis and low bone mass in men with prostate cancer: a systematic review and meta-analysis
Article References: Ebrahimi, M., Mohammadi, A., Sarmadi, S., Rahimnia, R., Zare-Kaseb, A., Reis, L. O., Shabestari, A. N., Sanaie, N., Keshtkar, A., & Aghamir, S. M. K. (2026). Prevalence of osteoporosis and low bone mass in men with prostate cancer: a systematic review and meta-analysis. Supportive Care in Cancer, 34(10), Article 1053. https://doi.org/10.1007/s00520-026-11289-3
Image Credits: AI Generated
DOI: 10.1007/s00520-026-11289-3
Keywords: prostate cancer, osteoporosis, low bone mass, osteopenia, androgen-deprivation therapy, bone mineral density, meta-analysis, systematic review, fracture risk, DXA, supportive care, men’s health
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Nathaniel Bowman. (October 3, 2026). One in Five Men With Prostate Cancer Has Osteoporosis, Global Analysis Finds. Scienmag. https://scienmag.com/one-in-five-men-with-prostate-cancer-has-osteoporosis-global-analysis-finds/
Nathaniel Bowman. “One in Five Men With Prostate Cancer Has Osteoporosis, Global Analysis Finds.” Scienmag, 3 October 2026, https://scienmag.com/one-in-five-men-with-prostate-cancer-has-osteoporosis-global-analysis-finds/. Accessed 3 October 2026.
Nathaniel Bowman. “One in Five Men With Prostate Cancer Has Osteoporosis, Global Analysis Finds.” Scienmag. October 3, 2026. https://scienmag.com/one-in-five-men-with-prostate-cancer-has-osteoporosis-global-analysis-finds/
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