Osteoporosis in men is significantly under-recognised and under-treated compared to the same condition in women. Approximately one in four men over the age of 50 will sustain a fragility fracture in their remaining lifetime, yet men are far less likely than women to receive a DEXA bone density scan, be assessed with the FRAX tool, or be started on pharmacological bone protection after a fracture. Part of the reason is historical — early research focused on postmenopausal women, and the clinical narrative of osteoporosis as a “women’s disease” persisted long after the epidemiological evidence showed otherwise. Men who sustain hip fractures have a significantly higher 12-month mortality than women with the same fracture — approximately 37% versus 20% — partly because of later diagnosis, older age at fracture, and higher burden of comorbidities.
Understanding the specific biology of male bone loss, the secondary causes that are more common in men, and the treatment approaches available is important for men, their families, and the clinicians managing their health in middle age and beyond.
The under-recognition of osteoporosis in men operates at multiple levels. Many men are unaware that osteoporosis is a risk for their sex. Many GPs do not routinely discuss bone health with male patients at the kind of midlife health reviews that routinely address it in women. And when men do sustain a fragility fracture, they are less likely than women to receive a DEXA scan, a FRAX risk assessment, or a prescription for bone protection — a gap in care that the fracture liaison service (FLS) model has been specifically designed to address, with measurable success where FLS access is equitable. Addressing this gap requires both patient awareness and clinical practice change, starting with recognition that osteoporosis in men is common, consequential, and treatable.
How Bone Loss Develops in Men
Men do not experience the equivalent of the female menopause — there is no abrupt, age-defined withdrawal of sex hormones. Instead, testosterone levels in men decline gradually from approximately the age of 30 onwards, at a rate of roughly 1–2% per year. This gradual decline means that male bone loss is less dramatic than the acute postmenopausal trajectory in women, but it is cumulative and accelerates in the 70s when testosterone falls more steeply.
Testosterone supports bone health through two mechanisms: direct androgen receptor activity in osteoblasts and osteoclasts, and conversion (aromatisation) to oestradiol — which, counterintuitively, is the primary mediator of bone turnover in men as well as women. Low oestradiol (below approximately 40 pmol/L) in men is associated with more rapid bone loss and higher fracture risk than low testosterone alone. This means that conditions causing low oestradiol in men — not just conditions causing low testosterone — are relevant to fracture risk.
Peak bone mass in men is approximately 20–25% higher than in women, largely because testosterone-driven periosteal expansion during puberty results in wider, thicker bones. This higher structural reserve means that men generally need more bone loss to reach the osteoporosis diagnostic threshold, and fractures typically occur approximately ten years later in men than in women for an equivalent skeletal condition. Hip fractures in women peak in frequency in the late 70s; in men, the equivalent peak is in the mid-80s.
Secondary Causes: More Common in Men
Secondary causes of osteoporosis — medical conditions and medications that independently reduce bone density — are identifiable in up to 60% of men who present with osteoporosis or a fragility fracture. This is a substantially higher proportion than in postmenopausal women, where the dominant cause is usually oestrogen deficiency with secondary causes present in approximately 30%. The implication is that when a man presents with osteoporosis or an unexpectedly low T-score, a thorough investigation for secondary causes is always warranted.
The most clinically important secondary causes in men are:
- Hypogonadism — low testosterone (and consequent low oestradiol) from any cause: Klinefelter syndrome, pituitary disease, chronic opioid use, haemochromatosis, or age-related decline below the reference range. Testosterone replacement can stabilise bone density in men with confirmed hypogonadism and osteoporosis.
- Androgen deprivation therapy (ADT) — used in the treatment of hormone-receptor-positive prostate cancer; suppresses testosterone to castrate levels, resulting in bone loss of 2–5% per year at the spine; fracture risk is markedly increased with prolonged ADT. Bone protection (bisphosphonate or denosumab) should be co-prescribed from the start of ADT for men with existing osteoporosis or significant fracture risk.
- Glucocorticoids — long-term prednisolone use for inflammatory conditions (COPD, inflammatory bowel disease, polymyalgia rheumatica) directly suppresses osteoblast function and increases osteoclast activity; the bone-loss effect is dose-dependent and begins within the first months of treatment
- Alcohol excess — chronic heavy alcohol use is independently associated with low bone density and increased fracture risk through direct toxic effects on osteoblasts, nutritional deficiency (calcium, vitamin D, protein), and increased falls risk
- Coeliac disease — malabsorption of calcium and vitamin D; often under-diagnosed in men; serological screening (anti-tissue transglutaminase IgA) is appropriate in men with unexplained low bone density
- Chronic kidney disease (CKD) — impairs conversion of vitamin D to its active form (calcitriol), disrupts calcium-phosphate-PTH balance, and causes renal osteodystrophy in advanced stages
Diagnosis and the FRAX Tool
The diagnostic threshold for osteoporosis in men — a DEXA T-score at the hip or spine of −2.5 or below — is the same as for women. T-scores for men are calculated against a male reference population, meaning a T-score of −2.5 in a man represents the same degree of deviation from the male peak bone mass standard deviation as it does from the female standard in women.
The FRAX tool has a specific calculation for men that accounts for the higher peak bone mass, later fracture age, and different risk factor weighting in men compared with women. FRAX inputs for men include age, body weight and height, prior fragility fracture, parental hip fracture, current smoking, alcohol use above 3 units per day, glucocorticoid use, rheumatoid arthritis, and secondary osteoporosis — with optional BMD input if a DEXA has been performed. The FRAX output gives a 10-year major fracture probability and a 10-year hip fracture probability, from which treatment decisions are made. More detail on FRAX and DEXA is in our guides to osteoporosis risk factors and bone density test: a simple guide.
Z-scores (age-matched comparisons) are particularly relevant in men under 50, where a Z-score below −2.0 indicates bone density significantly lower than expected for age and sex and should prompt thorough investigation for secondary causes.
Androgen Deprivation Therapy and Bone
ADT for prostate cancer deserves specific attention because it represents the single most common cause of severe, rapidly progressive osteoporosis in men. ADT suppresses testosterone to near-zero by either surgical castration (orchidectomy) or chemical castration (LHRH agonists such as leuprorelin or LHRH antagonists such as degarelix). The consequence is the equivalent of a sudden male menopause — oestradiol levels (which depend on peripheral aromatisation of testosterone) fall alongside testosterone, and osteoclast activity increases rapidly.
Men on ADT for two or more years who do not receive bone protection lose approximately 5–8% of spinal BMD and experience a 30–40% increase in fracture risk relative to similarly aged men not on ADT. Both zoledronate (annual intravenous infusion) and denosumab (six-monthly subcutaneous injection) have established evidence for preventing bone loss in ADT-treated men and are recommended by NICE for men with existing osteoporosis or high fracture risk on ADT. For men with a normal DEXA T-score starting ADT, baseline DEXA and monitoring are appropriate; pharmacological bone protection is initiated when the T-score falls into the osteoporosis range or fracture risk becomes sufficiently elevated on FRAX assessment.
Falls Risk and Fracture Prevention in Older Men
Falls are the proximate cause of the majority of fragility fractures in both men and women, and falls risk in older men carries its own specific profile. Men aged 75 and over who fall are more likely to sustain a hip fracture per fall than younger men, and the consequences — higher mortality, longer hospital stay, greater loss of independent living — make falls prevention as important as bone density management in this age group.
Risk factors for falls that are particularly relevant in older men include:
- Sarcopenia — age-related muscle mass loss and reduced grip strength; more prevalent and more rapidly progressive in men with hypogonadism; contributes to reduced postural stability and slower corrective responses to balance perturbation
- Orthostatic hypotension — a postural blood pressure drop of ≥20 mmHg systolic; commonly caused by antihypertensive medications, alpha-blockers used for prostate symptoms (tamsulosin, doxazosin), and dehydration; responsible for a significant proportion of falls in men with prostate-related comorbidities
- Visual impairment — uncorrected refractive error, cataracts, and glaucoma are modifiable contributions to falls risk; cataract removal has been shown to reduce hip fracture rates in older adults
- Polypharmacy — men over 75 on five or more medications have substantially higher falls risk; sedatives, antidepressants, antipsychotics, and diuretics are particularly associated with balance impairment and falls
- Balance and gait impairment — Parkinson’s disease, peripheral neuropathy (including diabetic neuropathy), and prior stroke are more prevalent in older men and significantly increase falls risk
The interaction between falls risk and bone fragility is multiplicative — a man with a T-score of −2.5 who falls twice per year has a much higher absolute fracture risk than the same T-score in a man who falls rarely. The FRAX tool accounts for falls as a secondary osteoporosis indicator via the “previous fragility fracture” variable, but does not directly incorporate falls frequency as an input — meaning clinical assessment of falls risk is an essential complement to FRAX and DEXA in older men.
Post-fracture care for men is an area of systematic underprovision. Men who sustain a hip, vertebral, or wrist fragility fracture are less likely to be referred to a fracture liaison service (FLS), less likely to receive a DEXA scan, and less likely to be started on pharmacological bone protection after the fracture than women with the same injury. Studies of FLS programmes show that proactive identification and treatment of men after fracture reduces re-fracture rates by 20–30%, equivalent to the benefit seen in women — making equitable access to post-fracture bone health services a clinical priority. Men who sustain a fragility fracture and are not automatically referred to an FLS or bone health service should ask their GP or hospital team about this specifically.
Treatment
Treatment for osteoporosis in men follows the same general principles as in women, with bisphosphonates (alendronate 70 mg weekly or risedronate 35 mg weekly) as the first-line pharmacological intervention. Alendronate has marketing authorisation for male osteoporosis in the UK and is NICE-recommended. The evidence for fracture reduction in men is less extensive than in women, but bisphosphonate-treated men with osteoporosis show comparable improvements in BMD to women, and the mechanism of action — osteoclast inhibition — is the same in both sexes.
Denosumab (60 mg subcutaneous injection every six months) is licensed for male osteoporosis and is an effective alternative for men who cannot tolerate oral bisphosphonates or have renal impairment that precludes bisphosphonate use. Teriparatide (recombinant PTH, used for two years in severe osteoporosis with multiple vertebral fractures) is also licensed for use in men. Full detail on pharmacological treatments is in our guide to osteoporosis: symptoms, causes, and prevention.
Calcium (700–1,200 mg/day) and vitamin D (400–800 IU/day supplementation) are co-prescribed with all pharmacological treatments. Weight-bearing and resistance exercise maintains bone density and reduces falls risk in men as well as women. Smoking cessation and reduction of alcohol to within recommended limits are important modifiable interventions for men with bone health concerns. Our guides on calcium and bone health and vitamin D and bone health cover the nutritional aspects in detail.
Frequently Asked Questions
Can men get osteoporosis?
Yes. Osteoporosis affects approximately 1.2 million men in the UK. One in four men over 50 will sustain a fragility fracture in their lifetime. Men develop osteoporosis on average about ten years later than women, because higher peak bone mass and a more gradual sex hormone decline provide a longer protective window. However, when men do sustain a hip fracture, their outcomes are worse than women’s — 12-month mortality is approximately 37% in men versus 20% in women, partly because of later recognition, older age at fracture, and higher comorbidity burden. The belief that osteoporosis is a women’s condition contributes to delayed diagnosis and undertreatment in men.
What causes osteoporosis in men specifically?
Unlike women, where oestrogen deficiency at menopause is the dominant driver in the majority, up to 60% of men with osteoporosis have an identifiable secondary cause. The most common are hypogonadism (low testosterone and consequently low oestradiol), androgen deprivation therapy for prostate cancer, long-term glucocorticoid use, alcohol excess, coeliac disease, and chronic kidney disease. This means that a man presenting with osteoporosis or a fragility fracture should have a thorough blood investigation including testosterone, LH, FSH, oestradiol, calcium, vitamin D, PTH, thyroid function, coeliac screen, renal function, and liver function — at minimum — to identify or exclude secondary causes that may be treatable in their own right.
Does testosterone replacement help with bone density in men?
Testosterone replacement therapy (TRT) can stabilise bone density in men with confirmed hypogonadism — serum testosterone consistently below the reference range with associated symptoms. Studies show that TRT in hypogonadal men increases BMD at the lumbar spine by 5–8% over two years, an effect comparable to bisphosphonate treatment in some populations. However, the evidence for fracture reduction with TRT specifically is less robust than for bisphosphonates, and in men with confirmed hypogonadism and osteoporosis, co-prescribing a bisphosphonate alongside TRT is often appropriate. TRT in men with normal testosterone levels does not provide additional bone benefit and is not indicated for bone protection in eugonadal men.
How does ADT for prostate cancer affect bone?
Androgen deprivation therapy (ADT) suppresses testosterone — and consequently oestradiol — to near-zero, triggering the male equivalent of a sudden menopause. Bone mineral density loss of 2–5% per year at the lumbar spine occurs in untreated men on ADT, with fracture risk increasing by 30–40% over two years of treatment. Bone loss is most rapid in the first year of ADT and then continues at a lower rate. All men starting long-term ADT should have a baseline DEXA scan, and those with existing osteoporosis or high FRAX scores should receive pharmacological bone protection — typically denosumab or zoledronate — from the start of treatment. Annual DEXA monitoring is appropriate during long-term ADT.
Are the same medications used for osteoporosis in men and women?
Yes, mostly. Alendronate 70 mg weekly is NICE-recommended for male osteoporosis and is the standard first-line agent. Risedronate and zoledronate are alternatives. Denosumab is licensed for male osteoporosis (and for bone protection during ADT). Teriparatide (recombinant PTH) is licensed for severe male osteoporosis with multiple vertebral fractures, as it is for women. The dosages are the same as in women — unlike some medications where sex-based dosing differences exist. The main difference is that HRT (oestrogen), which is an important bone-protective option in postmenopausal women, is not used in men; testosterone replacement therapy is the male equivalent for men with confirmed hypogonadism.
What should men do to protect their bone health?
The foundations of bone health for men are the same as for women: weight-bearing and resistance exercise throughout life, adequate calcium and vitamin D, smoking cessation, and limiting alcohol to within recommended limits. For men aged 50 and over with one or more risk factors — prior fragility fracture, long-term steroid use, alcohol excess, known hypogonadism, prostate cancer on ADT, low body weight — discussing fracture risk assessment with a GP and requesting FRAX calculation (and DEXA if the score is above the assessment threshold) is appropriate and worthwhile. Men with a prior fragility fracture who have not been referred to a fracture liaison service or started on bone protection should ask about this specifically; post-fracture bone health management is an area where men are systematically less well served than women.
Are FRAX scores interpreted the same way for men and women?
The FRAX tool has sex-specific calculations that account for differences in peak bone mass, fracture age distribution, and absolute fracture risk between men and women. A FRAX major fracture probability of 20% in a 65-year-old man represents a different population-level risk profile than the same probability in a 65-year-old woman. The intervention thresholds recommended by NICE are also age-specific and have been separately calibrated for men and women using UK fracture incidence data. This means that treatment decisions based on FRAX are appropriately sex-specific, even though the tool uses the same input variables for both sexes. Clinicians using FRAX for men should ensure the sex field is set correctly, as using the female calculation would overestimate fracture probability for a given BMD in most age groups.
Summary
Osteoporosis in men is common, under-recognised, and associated with worse outcomes after hip fracture than in women. Unlike postmenopausal osteoporosis in women, which is primarily oestrogen-driven, male osteoporosis has an identifiable secondary cause in up to 60% of cases — making thorough investigation essential when it presents. Androgen deprivation therapy for prostate cancer is the single most common cause of rapidly progressive osteoporosis in men and requires proactive bone protection from treatment initiation. Bisphosphonates, denosumab, and teriparatide are effective treatments for male osteoporosis. Falls risk management is as important as pharmacological treatment in older men, and post-fracture care through fracture liaison services should be equally accessible to men and women. The same foundations of bone health apply to men as women: weight-bearing exercise, calcium and vitamin D adequacy, and avoiding smoking and excess alcohol. Any man aged 50 or over with one or more risk factors should ask their GP about fracture risk assessment. Our full series of bone health guides covers osteoporosis: symptoms, causes, and prevention, osteoporosis in women after menopause, and DEXA scan: what adults should know.
Medical disclaimer: This article is for general educational purposes and does not constitute medical advice. Consult a qualified healthcare professional for personalised bone health assessment and management.
References:
NHS. Osteoporosis. nhs.uk. 2023.
NICE CG146. Osteoporosis: assessing the risk of fragility fracture. NICE. 2023.
Royal Osteoporosis Society. Clinical guidance for the prevention and treatment of osteoporosis. theros.org.uk. 2023.
Watts NB, et al. Osteoporosis in men: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2012;97(6):1802–1822.
Golds G, Houdek D, Arnason T. Male hypogonadism and osteoporosis: the effects, clinical consequences, and treatment of testosterone deficiency in bone health. Int J Endocrinol. 2017:4602129.


I’ve been on LHRH agonist ADT for prostate cancer for three years and my oncologist did mention at the start that bone density would be affected, but I wasn’t given a baseline DEXA or any bone protection at that point. At my two-year oncology review I raised it myself — I’d read about ADT and bone loss — and was finally referred for a DEXA. My T-scores were −2.4 at the spine and −1.9 at the hip — just crossing the osteoporosis threshold at the spine. I was started on six-monthly denosumab injections and calcium and vitamin D. My oncologist said the guidelines do recommend a baseline DEXA and bone protection discussion at ADT initiation, but it had been missed in my initial planning. I’ve since had a 12-month DEXA and my spine T-score has improved to −2.1 on denosumab. This article’s point that all men starting long-term ADT should have a baseline DEXA and bone protection consideration from initiation reflects what should have happened for me from the beginning.
Malcolm, your case is a clear example of the ADT bone protection gap that persists in clinical practice despite established guidelines. A baseline DEXA and formal bone risk discussion at ADT initiation is recommended by both the Royal Osteoporosis Society and NICE guidance for prostate cancer, but implementation remains inconsistent. Your DEXA at two years showing a spine T-score of −2.4 — just crossing the osteoporosis threshold — is a better outcome than many men experience; some patients are not assessed until after a fracture occurs three to five years into ADT. The response to denosumab (T-score improving from −2.4 to −2.1 at 12 months) is consistent with the expected bone density gain from denosumab in ADT-treated men, which typically runs at 4–7% at the spine over 12 months in the trials. Continuing annual DEXA during long-term ADT is appropriate monitoring. George, your coeliac-related osteoporosis trajectory is clinically characteristic: long-standing untreated coeliac disease causes calcium malabsorption for years before diagnosis, resulting in BMD loss that accumulates silently. The response to combined gluten-free diet (which restores intestinal calcium absorption) plus alendronate over 18 months — improving from −2.1 to −1.8 at the spine — is a meaningful gain and reflects the additive effect of eliminating the secondary cause alongside the bisphosphonate. Continued DEXA monitoring at two to three year intervals is appropriate to track whether the improvement is sustained and whether the spine T-score can be maintained out of the osteoporosis range long-term.
I was diagnosed with coeliac disease at 58 after years of vague GI symptoms and fatigue. Within six months of the coeliac diagnosis my GP organised a DEXA scan, because coeliac can cause significant calcium malabsorption. My T-scores were −2.1 at the spine and −1.6 at the hip — osteopenia at the hip, just into osteoporosis at the spine. My GP said the bone density loss had likely been accumulating silently for years while the coeliac was undiagnosed and untreated. I was started on a strict gluten-free diet, calcium and vitamin D supplementation, and alendronate after my FRAX score was calculated. After 18 months on a gluten-free diet and alendronate, repeat DEXA showed improvement to −1.8 at the spine. The article’s mention of coeliac disease as an under-diagnosed secondary cause of osteoporosis in men particularly resonates — I had no idea until this was found that my gut condition had been silently affecting my bones for what turned out to be over a decade.