Testosterone replacement therapy (TRT) increases measured bone density in older men with low testosterone.

The Verdict

At Longevity Benchmark, we review clinical trials to evaluate what hormone therapies deliver in practice. The bone density findings look clear on paper. However, density alone does not guarantee fewer broken bones. The largest clinical trial to date evaluated both markers and found that fractures did not decline.

Volumetric Density Changes in the 2017 Trial

A 12-month clinical trial showed substantial increases in volumetric bone mineral density from testosterone gel. The Bone Trial of the Testosterone Trials enrolled 211 men aged 65 or older. Every participant had two morning testosterone blood tests averaging below 275 ng/dL. The average participant age was 72.3 years. Participants applied either daily testosterone gel or a placebo gel. Researchers analysed scans from 189 men who completed the evaluation period. The team published their findings in JAMA Internal Medicine.

Investigators measured volumetric bone mineral density, known as vBMD, using quantitative computed tomography (QCT). In the spine, trabecular vBMD increased 7.5% in the testosterone group. The 95% confidence interval (CI) for that gain ranged from 4.8% to 10.3%. Men receiving placebo saw a 0.8% rise, with a confidence interval between -1.9% and 3.4%. The net treatment effect in spine trabecular bone was 6.8%. Its confidence interval spanned 4.8% to 8.7%. The trial also estimated spine trabecular bone strength. Estimated strength rose 10.8% with testosterone against 2.4% with placebo. This produced an 8.5% net treatment effect, with a confidence interval of 6.0% to 10.9%.

Gains varied across different parts of the skeleton. Spine peripheral vBMD showed a treatment effect of 2.9%. Hip trabecular vBMD gained 1.5%, while hip peripheral vBMD gained 1.0%. Every density gain achieved statistical significance at P<.001.

Skeletal Site and MeasurementTreatment Effect95% Confidence IntervalP Value
Spine trabecular vBMD 6.8% 4.8% to 8.7% <.001
Spine peripheral vBMD 2.9% 2.1% to 3.7% <.001
Hip trabecular vBMD 1.5% 0.9% to 2.0% <.001
Hip peripheral vBMD 1.0% 0.5% to 1.5% <.001
Estimated spine trabecular strength 8.5% 6.0% to 10.9% <.001

Limitations of Density as a Stand-In for Fracture Risk

A measurable rise in bone mineral density does not confirm that fractures will decrease. The investigators in the 2017 study stated this limitation directly. Over 12 months, only 12 men experienced a broken bone. Six fractures occurred in the testosterone arm. Six fractures occurred in the placebo arm. A total of 12 events across 211 men cannot show whether a treatment prevents skeletal injury.

The study authors noted that clinical relevance depends entirely on whether testosterone reduces fracture risk in larger trials. Surrogate markers show biological movement. They do not guarantee fewer hospital visits or intact bones. Men evaluate signs of low testosterone across multiple body systems, but skeletal protection requires fracture data.

Clinical Fracture Findings in the TRAVERSE Study

The TRAVERSE fracture subtrial found that testosterone therapy did not reduce clinical fractures in older men. Researchers published the subtrial results in The New England Journal of Medicine in 2024. The trial enrolled 5,204 men between the ages of 45 and 80. All participants had diagnosed hypogonadism alongside established cardiovascular disease or multiple cardiovascular risk factors. Investigators randomly assigned participants to daily testosterone gel or an identical placebo gel. Median follow-up lasted 3.19 years.

During the study, 91 men on testosterone experienced a clinical fracture. That represented 3.50% of the testosterone cohort. In the placebo group, 64 men suffered a fracture, representing 2.46% of participants. The hazard ratio reached 1.43, with a 95% confidence interval of 1.04 to 1.97. By year 3, the cumulative fracture incidence stood at 3.8% for testosterone against 2.8% for placebo.

The trial concluded that testosterone treatment did not lower fracture incidence. Instead, fracture rates were numerically higher in the testosterone group. The most common fracture sites were the ribs, wrist, and ankle. More than 80% followed trauma. Most were falls. The overall injury pattern closely resembled typical osteoporotic fractures in older men.

Skeletal Compartments and Potential Biological Mechanisms

Testosterone reaches trabecular bone and cortical bone by separate structural routes, and the trial results differ accordingly. The 2017 density trial revealed a clear anatomical split. Net gains reached 6.8% in spine trabecular bone. In contrast, net gains were only 1.0% in peripheral hip bone. Peripheral skeletal sites contain a high proportion of dense cortical bone. The TRAVERSE authors suggested that testosterone might exert neutral or detrimental effects on cortical bone. However, they cautioned that the exact biological mechanisms remain unproven.

Steven Nissen addressed the idea that men on testosterone moved more and so fell more. Cardiologist Steven Nissen rejected that behavioral explanation. He pointed out that the trial recorded an excess of non-impact fractures. That non-impact excess roughly matched the increase observed across all clinical fractures.

Hormone metabolism adds further complexity. In 2013, researchers published a 2013 gonadal-steroid study in The New England Journal of Medicine. That trial showed that estrogen deficiency primarily accounted for increases in body fat among men. Androgen deficiency accounted for the loss of lean mass, muscle size, and strength. Testosterone aromatizes into estradiol in male tissue. Testosterone's skeletal effects in men run partly through estradiol, so estradiol is part of this picture rather than an afterthought.

Differences Between Quantitative CT and DXA Scans

Volumetric bone mineral density from a quantitative CT scan does not convert directly to a DXA T-score. Patients frequently confuse these two imaging technologies. The 2017 trial relied on quantitative computed tomography, often abbreviated as QCT. QCT measures volumetric bone density in three dimensions. It isolates internal trabecular bone from external cortical bone.

In contrast, most clinical practices use dual-energy x-ray absorptiometry, or a DXA scan. DXA produces a two-dimensional areal measurement expressed in grams per square centimeter. That reading generates a comparative T-score. Our guide to DXA scan T-scores explains how clinicians interpret these readings. A percentage increase in volumetric density does not equal a T-score increase. Reviewing when to get a DXA scan helps determine appropriate timing for clinical testing.

Study Population Limits and Patient Selection

Clinical trials on testosterone and bone describe narrow patient groups. The 2017 study enrolled men aged 65 and older with verified low hormone levels. Morning testosterone had to average under 275 ng/dL. In contrast, TRAVERSE enrolled men aged 45 to 80 with preexisting cardiovascular disease or multiple cardiovascular risk factors.

These trials do not describe every patient. A 38-year-old man with a pituitary disorder does not match either study population. Younger men without heart risks cannot assume these fracture numbers apply to them.

Evaluating free vs total testosterone clarifies hormone status, while a comprehensive men's hormone panel checks baseline safety.

Male Osteoporosis Diagnosis Rates and Scope of Therapy

Major clinical trials measured treatment responses rather than the prevalence of undiagnosed male osteoporosis. Neither the 2017 trial nor TRAVERSE evaluated how frequently bone loss goes undetected in men. The studies enrolled men based on low testosterone and specific medical criteria. They did not assess community diagnosis patterns.

Furthermore, neither trial evaluated testosterone as a targeted medical treatment for diagnosed osteoporosis. Investigators did not compare testosterone against established, bone-specific medications. Because of this design, the trials cannot show whether testosterone should treat established bone disease.

Patients on therapy also monitor blood thickness. Our analysis of high hematocrit on TRT outlines how clinicians manage elevated red blood cell counts. Reviewing TRT side effects and risks ensures a complete view of potential treatment outcomes.

Evidence Thresholds and Clinician Discussion Topics

Our assessment of testosterone and bone outcomes would change with fresh trial data. New trials could challenge the findings. A second large study evaluating fractures could clarify the risk. Subgroup analyses might also explain why fractures rose. Until then, men should not assume that higher density prevents broken bones. Review your skeletal health with your physician. Bring these questions to your next appointment before changing any aspect of your care.

  • Fracture history review. Discuss prior low-trauma fractures or broken bones with your prescribing doctor.
  • Scan technology evaluation. Ask your clinician which imaging method they recommend and how they interpret your baseline score.
  • Estradiol monitoring. Verify whether your routine blood panels measure circulating estradiol alongside testosterone levels.
  • Cardiovascular risk context. Check whether your personal health history mirrors the high-risk population studied in the TRAVERSE trial.

Frequently Asked Questions

Does TRT increase bone density?

Testosterone replacement therapy reliably raises measured bone mineral density in older men with low testosterone. In the 2017 Bone Trial of the Testosterone Trials, 12 months of daily testosterone gel produced a 6.8% net treatment effect in spine trabecular volumetric bone mineral density compared to placebo. It also produced an 8.5% net gain in estimated spine trabecular bone strength. Smaller gains occurred in peripheral bone and in the hip. However, these volumetric improvements were measured with quantitative computed tomography and do not convert directly to standard DXA T-scores.

Does testosterone therapy prevent fractures?

Testosterone therapy has not been shown to prevent clinical fractures in clinical trials. The 2024 TRAVERSE fracture subtrial evaluated 5,204 men aged 45 to 80 over a median of 3.19 years. In that study, 91 men on testosterone (3.50%) experienced a clinical fracture compared to 64 men on placebo (2.46%). The hazard ratio was 1.43, with a 95% confidence interval of 1.04 to 1.97. By year 3, cumulative fracture incidence reached 3.8% in the testosterone group versus 2.8% in the placebo group. The trial concluded that testosterone treatment did not reduce fractures.

Why did the testosterone group have more fractures?

The exact biological reason why the testosterone group experienced more fractures in the TRAVERSE trial remains unproven. The study authors noted that testosterone might have detrimental or neutral effects on cortical bone, which forms the dense outer shell of the skeleton. In the 2017 trial, density gains were smallest in cortical-rich peripheral bone. Some hypothesized that men on testosterone were more physically active and fell more often. However, researchers noted that an excess of non-impact fractures occurred in the testosterone group roughly equal to the increase in all clinical fractures, suggesting increased falls alone cannot explain the difference.

Is TRT a treatment for osteoporosis in men?

Testosterone therapy is not an established standalone treatment for male osteoporosis in clinical practice. Neither the 2017 Bone Trial nor the 2024 TRAVERSE trial compared testosterone against bone-specific osteoporosis medications. The trials evaluated men with low testosterone rather than men selected specifically for severe osteoporosis. Because TRAVERSE found no reduction in clinical fractures and a numerically higher fracture rate in the testosterone group, testosterone cannot be assumed to protect against osteoporotic fractures. Men with diagnosed bone loss must consult their physician to evaluate therapies specifically tested for fracture reduction.

How long does it take for testosterone to affect bone density?

Clinical trials demonstrate measurable increases in volumetric bone mineral density after 12 months of daily testosterone gel application. In the 2017 Testosterone Trials, researchers observed statistically significant increases in spine and hip volumetric density at the one-year mark. The trial did not report interim scan intervals between baseline and 12 months, so earlier shifts remain unverified in that dataset. In TRAVERSE, the fracture figures at year 3 were 3.8% on testosterone and 2.8% on placebo. Men tracking skeletal changes typically follow testing intervals established by their personal clinician.

Should I get a DEXA scan before starting TRT?

The clinical trials evaluating testosterone and bone density did not establish whether every man should receive a DXA scan before starting therapy. In the 2017 trial, researchers used quantitative computed tomography rather than standard dual-energy x-ray absorptiometry to assess volumetric bone density. Deciding whether to obtain a baseline DXA scan depends on your personal clinical history, age, and existing risk factors. If you have experienced prior broken bones or have clinical concerns regarding bone thinning, ask your doctor whether baseline skeletal imaging is appropriate for your care.

Does low testosterone cause osteoporosis?

Androgen deficiency contributes to changes in male body composition, but the clinical trials evaluated here focused on treatment effects rather than the primary causes of bone loss. A 2013 study published in The New England Journal of Medicine demonstrated that androgen deficiency in men led to decreases in lean mass, muscle size, and strength, while estrogen deficiency accounted for increases in body fat. Because testosterone aromatizes into estradiol, both hormones influence male skeletal health. However, neither the 2017 trial nor TRAVERSE tracked community prevalence or proved that low testosterone alone causes osteoporosis.

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