AndroGel Bone Health and Density Impact

Does testosterone gel actually raise bone density?

The strongest controlled evidence comes from the bone study inside the Testosterone Trials. It enrolled 211 men aged 65 or older with low testosterone on two measurements (mean age 72.3) at nine US academic medical centers between December 2011 and June 2014 [1]. Men received testosterone gel, with the dose adjusted to keep serum testosterone inside the normal range for young men, or placebo gel, for 12 months [1].

Measured by quantitative computed tomography (QCT), spine trabecular volumetric bone mineral density rose 7.5% (95% CI 4.8 to 10.3) on testosterone and 0.8% (95% CI -1.9 to 3.4) on placebo, a treatment effect of 6.8% (P<.001) [1]. Estimated strength of spine trabecular bone, calculated from the same scans, rose 10.8% (95% CI 7.4 to 14.3) against 2.4% (95% CI -1.0 to 5.7), a treatment effect of 8.5% (P<.001) [1].

Testosterone also raised spine peripheral vBMD and hip trabecular and peripheral vBMD, and it raised spine areal bone density by DXA, though the areal measure rose less than the volumetric one [1]. The estimated strength gains were larger in trabecular than peripheral bone and larger in the spine than the hip [1].

What those numbers do and do not mean

QCT reports density per volume of bone and separates trabecular from cortical bone. DXA, the scan most clinics use, reports areal density, and in this trial it moved less than the QCT measure [1]. The result is a 12-month density change in 211 men, not a count of broken bones [1].

Does testosterone gel prevent fractures?

The 12-month bone trial measured density and estimated strength, not fractures, so it did not show whether the density gain translates into fewer fractures [1].

TRAVERSE enrolled 5,246 men aged 45 to 80 with hypogonadism and existing or high cardiovascular risk, who took daily 1.62% testosterone gel or placebo gel for a mean of 21.7 months, with 33 months of mean follow-up [2]. Its primary endpoint was the first occurrence of cardiovascular death, nonfatal myocardial infarction or nonfatal stroke, which occurred in 7.0% of men on testosterone and 7.3% on placebo, meeting noninferiority [2]. Bone fracture was among the events more frequent with testosterone gel than placebo, at 3.5% versus 2.5% [2].

Regulatory status matters here. FDA's February 2025 class-wide labeling action kept the limitation-of-use language stating that safety and efficacy in age-related hypogonadism have not been established [6], and in June 2026 FDA requested removal of that limitation and revision of prostate safety information [4]. FDA says approved testosterone products are for men whose low testosterone comes with a medical condition, such as testicular failure or a pituitary or hypothalamic disorder [4]. Treating osteoporosis is not among the labeled uses of testosterone gel.

The Endocrine Society's 2012 guideline on osteoporosis in men recommends drug treatment for men 50 or older who have had a spine or hip fracture, who have a T-score of -2.5 or below, or who are at high fracture risk, with monitoring by serial DXA [7]. The testosterone bone trial did not compare testosterone with any osteoporosis drug, so it cannot show whether testosterone alone is enough for a man who meets those thresholds [1].

How fast does density change, and does it hold?

The longer-term studies below used injections and scrotal patches rather than gel [3][8][9].

In a long-term cohort, 72 hypogonadal men received testosterone substitution for up to 16 years, 32 of them followed from before treatment: trabecular spine density by QCT rose from 95.2 to 120.0 mg/cm3 in the first year, and continued treatment kept density within the age-related reference range. Transdermal testosterone patches applied to the scrotum normalized density as effectively as intramuscular enanthate [3].

In a 36-month randomized trial of 70 men aged 65 and older, testosterone enanthate 200 mg intramuscularly every 2 weeks raised lumbar spine density by 10.2% versus 1.3% with placebo, and hip density by 2.7% versus a fall of 0.2% [9]. Fifty of the 70 men completed the 36 months, and low bone density was not required to enter [9].

In a study of 36 men with acquired hypogonadism, 29 received testosterone enanthate 100 mg weekly; after 18 months, spinal density rose 5% and trabecular density rose 14% in the treated men, radial density did not change, and markers of bone formation and resorption both fell [8].

Estradiol and bone

Testosterone is converted to estradiol by the enzyme aromatase, and loss of the estrogen receptor ESR1 or of aromatase affects bone and other nonreproductive tissues in males [10]. A one-year randomized trial of 69 men aged 60 and older with low or borderline testosterone tested what happens when that conversion is blocked: anastrozole 1 mg daily raised testosterone from 319 to 524 ng/dL at three months while estradiol fell from 15 to 12 pg/mL, and spine areal density fell from 1.121 to 1.102 g/cm2 while placebo rose from 1.180 to 1.189 g/cm2 (P=0.0014) [11]. Bone turnover markers were unchanged [11]. In that trial, raising testosterone while blocking its conversion to estradiol did not protect the spine [11].

Dose and serum levels

In the bone trial, the gel dose was adjusted to keep testosterone within the normal range for young men [1]. In TRAVERSE, the gel dose was adjusted to keep testosterone between 350 and 750 ng/dL [2].

Monitoring

The Endocrine Society's 2012 guideline recommends central DXA testing for men aged 70 and older, and for men aged 50 to 69 who have risk factors, with serial DXA used to monitor treatment [7]. Its 2018 testosterone guideline recommends monitoring symptoms, serum testosterone, hematocrit and prostate cancer risk during the first year of therapy [12].

Hematocrit is also tracked during testosterone therapy. A network meta-analysis of 29 placebo-controlled trials in 3,393 men found every formulation raised mean hematocrit versus placebo: gel by 3.0% (95% CI 1.8 to 4.3) and intramuscular enanthate or cypionate by 4.0% (95% CI 2.9 to 5.1) [5].