HRT and Bone Health: Osteoporosis Prevention with Estrogen and Testosterone

Bones are not static scaffolding. They are living tissue under constant renovation, with specialized cells removing old mineral and laying down new matrix. That balance holds steady for decades, then, after midlife hormonal shifts, the scale tips. The result can be an accelerated drop in bone density and a jump in fracture risk that disrupts independence and quality of life. Hormone therapy, when chosen and monitored well, can be one of the most effective tools to steady that balance.

I have sat with patients in their fifties, sixties, and seventies whose first sign of osteoporosis was a wrist fracture after a minor fall or a vertebral compression that stole two inches from their height and left a persistent ache. Many had given their bones little thought until then. The science and my experience both support a simple message: hormone levels matter to skeletal health, and smart hormone treatment can prevent a lot of trouble.

What hormones do inside bone

Estrogen and testosterone act directly on bone cells and indirectly on the systems that feed bone. Estrogen reduces the activity of osteoclasts, the cells that resorb bone. When estrogen drops, osteoclasts become more active, bone turnover speeds up, and net loss begins. Estrogen also improves calcium absorption in the gut and curbs calcium loss in urine, preserving mineral supply for remodeling.

Testosterone affects bone partly through aromatization to estradiol, which then acts like estrogen in bone. It also stimulates osteoblasts, the cells that build bone, and supports muscle mass and strength, which translates to better balance and fewer falls. Progesterone likely has a smaller role, but some data suggest it can support osteoblast function when cyclically present.

In both sexes, peak bone mass is set by genetics, nutrition, activity, and hormonal environment before age 30. After that, bone remodeling maintains density until hormones shift. Estrogen deficiency in women and clinically low testosterone in men accelerate loss. That is why hormone balancing and hormone optimization are part of a legitimate osteoporosis prevention strategy, alongside calcium, vitamin D, resistance training, and fall prevention.

The cliff after menopause

The steepest decline in bone density for women arrives in the first 3 to 5 years after the final menstrual period. Estradiol levels fall by over 90 percent from late reproductive years to postmenopause. Many women lose 2 to 3 percent of bone density per year in that early window, then about 1 percent annually afterward. The risk becomes visible in population data: hip and vertebral fractures jump in the seventh decade.

Here is the crux: estrogen therapy reliably lowers this risk when started around the time of menopause in appropriate candidates. Clinical trials and observational follow up have shown significant improvements in bone mineral density at the spine and hip, often in the range of 3 to 5 percent gain over two to three years, and a reduction in vertebral and nonvertebral fractures. Estrogen replacement therapy is not just about hot flashes or mood swings. It is a powerful bone medication when used correctly.

I remember a 52 year old physician who came in with drenching night sweats, brain fog, and a DEXA showing osteopenia at the spine. She had no thrombotic risk factors, healthy blood pressure, and wanted nonpharmacologic options only. We discussed a plan heavy on strength training and protein, with vitamin D repletion. After 9 months she felt stronger, but her repeat scan was unchanged. We started transdermal estradiol with micronized progesterone. Two years later, night sweats were gone, and her spine density rose by 4 percent. The numbers fit what we expect.

Timing and route matter

Not all hormone replacement therapy looks the same, and details affect both benefit and risk.

Transdermal estradiol in patch, gel, or spray form absorbs through the skin into the bloodstream without first-pass liver metabolism. That route appears to have a lower risk of venous thromboembolism compared with oral estrogen, particularly in women over 60 or those with higher BMI. For bone, both routes raise estradiol into a protective range, so I tend to favor transdermal delivery for most patients who need long-term HRT for bone and menopausal symptoms.

Doses vary with symptom control and Extra resources baseline labs, but common transdermal estradiol patch strengths are 0.025 to 0.1 mg per day, applied once or twice weekly. For women with a uterus, add a progestogen to protect the endometrium. Micronized progesterone 100 mg nightly or 200 mg cyclically is well tolerated for many. If hot flashes are the primary issue and bone health is a secondary aim, the lower estradiol range often suffices. If a DEXA shows low bone density or rapid decline, titrating to a mid physiologic estradiol level, confirmed by serum testing, is reasonable.

The window of opportunity concept applies here. Starting estrogen therapy within 10 years of menopause, or before age 60, yields the best balance of benefits and risks across systems, bones included. Initiating therapy later can still help bone, but cardiovascular and thrombotic risks shift, so the conversation becomes more nuanced. There are safe paths in later years, often with lower transdermal doses and careful screening.

What about bioidentical hormone therapy, compounded bioidentical hormones, and synthetic hormone therapy? The term bioidentical refers to hormones with the same molecular structure as endogenous hormones, like 17 beta estradiol and micronized progesterone. Many FDA approved products fall into this category. Compounded hormone therapy can be useful for unusual dosing or allergies, but it lacks the manufacturing consistency and safety data of approved formulations. For most, I recommend FDA approved estradiol and progesterone first, then consider compounded bioidentical hormones if a specific need arises. Natural hormone therapy is a popular phrase, but the biology cares about molecular structure and dose, not the marketing language.

Testosterone, men, and the skeleton

Men typically lose bone more slowly than women until late life, largely because they avoid the menopause cliff. When men do develop osteoporosis, up to 20 percent carry a history of hypogonadism. In these cases, testosterone replacement therapy can improve bone mineral density and reduce vertebral fracture risk over time. The gains do not happen overnight. Expect to see lumbar spine BMD increase by 5 to 10 percent after two to three years of TRT in men with low T at baseline. Hip density changes are smaller but directionally positive.

I think of a 63 year old man with fatigue, low libido, and a total testosterone repeatedly under 220 ng/dL, along with osteopenia at the femoral neck. After a shared decision making process, he chose testosterone injections every 1 to 2 weeks. We aimed for a mid normal trough level, not peaks that pushed erythrocytosis or irritability. Twelve months later, his lean mass rose by about 3 kg, hematocrit nudged up but stayed under 52 percent with dose adjustment, and his hip T score stabilized rather than slipping further. Over three years, his spine density improved and he had no fractures. The muscle gained likely mattered as much as the bone density gain.

TRT is not a cure all. If a man has normal hormone levels, using testosterone for bone alone does not make sense and carries risk. If prostate cancer is active or high risk, if untreated severe sleep apnea is present, or if there is significant polycythemia, TRT may be unsafe. Work with a hormone doctor who understands indications, contraindications, and monitoring. Endocrine therapy is powerful when guided carefully.

Testosterone in women

Low dose testosterone therapy for women draws interest for libido, energy, and sometimes for muscle and bone support. The evidence for fracture prevention is limited, though some studies show improvements in lean mass and modest gains in BMD when physiologic female testosterone levels are restored. I do not consider testosterone a first line osteoporosis treatment in women. If low desire is a major concern and estrogen and progesterone therapy are already optimized, a carefully dosed transdermal testosterone under close lab guidance can be reasonable. The target is a total testosterone level in the upper physiologic female range, not male ranges. Watch for acne, hair growth, or voice changes, and stop if these occur.

Pellet hormone therapy is fashionable, including pellet hormone implants that deliver estradiol or testosterone for months. Pellets can create high early levels and unpredictable tails, which complicates dose titration and side effect management. I have had to treat women with months of androgenic side effects after a single pellet. This is why I favor patches, gels, sprays, or injections where we can adjust dose every few weeks. Hormone injections work well for testosterone in men, and sometimes in masculinizing care, but for estrogen replacement therapy, transdermal forms usually offer steadier levels with fewer risks.

Gender affirming hormone therapy and bone

Transgender and gender diverse patients bring specific bone health questions. Estrogen treatment in transfeminine individuals, often combined with an antiandrogen, generally preserves or improves bone density when estradiol levels are maintained in the physiologic female range. The risk arises when therapy is interrupted or underdosed. I have seen gaps around surgery or gaps due to access issues cause a measurable dip in spine density within a year.

For transmasculine individuals, testosterone therapy supports bone and muscle when maintained in a male physiologic range. If ovaries are removed and testosterone doses are inconsistent, bone health can suffer. Whether MTF hormone therapy or FTM hormone therapy, long term hormone balance therapy should include DEXA at baseline and periodic reassessment, with attention to vitamin D status and strength training. This is classic hormone health treatment, tailored to individual goals.

Weighing risks and trade offs

Every hormone treatment has benefits and risks, and the calculus changes with age and medical history. For estrogen and progesterone therapy, the main serious risks are venous thromboembolism, stroke, and, depending on the progestogen, a small change in breast cancer risk with long duration use. Transdermal estradiol plus micronized progesterone appears to have a more favorable profile than oral estrogen with certain synthetic progestins. A family history of breast cancer is not an automatic stop sign, but it does shape the discussion and follow up strategy.

For testosterone therapy in men, risks include increased hematocrit with potential for hyperviscosity, acne or oily skin, male pattern hair loss, potential worsening of sleep apnea, and fertility suppression. The relationship with cardiovascular events is complex and depends on comorbidities and dosing. For both sexes, poorly monitored or supraphysiologic dosing is what creates most of the problems I see referred to our hormone clinic.

I do not recommend growth hormone therapy, HGH therapy, or IGF 1 therapy to treat osteoporosis outside of specific deficiency syndromes under endocrine specialist care. DHEA therapy can have small effects on androgens and estrogens, but for bone it is not a primary tool. Thyroid hormone replacement is essential for hypothyroidism, but overtreatment raises fracture risk, so aim for a TSH in target range. Cortisol treatment for adrenal insufficiency must be carefully dosed, since excess glucocorticoid accelerates bone loss.

Practical prescribing patterns that work

For postmenopausal women at high fracture risk who will accept HRT, I often start with transdermal estradiol at 0.0375 to 0.05 mg per day, plus oral micronized progesterone 100 mg at bedtime if they have a uterus. If vasomotor symptoms are severe, 0.075 mg per day may be needed short term. I recheck estradiol levels after 8 to 12 weeks, aiming for a mid physiologic postmenopausal replacement range that relieves symptoms and supports bone. Calcium intake should total roughly 1,200 mg daily from food and supplements combined, and vitamin D should keep serum 25 hydroxyvitamin D around 30 to 50 ng/mL.

In hypogonadal men with osteoporosis or high fracture risk, testosterone replacement therapy can be a foundational piece, paired with a bone specific agent if needed. Typical starting options are testosterone cypionate 60 to 80 mg weekly, or 120 to 160 mg every two weeks, adjusted to keep trough total testosterone around 400 to 700 ng/dL and free testosterone in range. Alternatives include transdermal gels delivering 50 to 75 mg daily. I recheck labs at 6 to 8 weeks, then every 3 to 6 months, including hematocrit, PSA for appropriate ages, lipids, and liver enzymes.

When HRT is not an option due to risk or preference, we use nonhormonal osteoporosis medications, often for a finite period, then reconsider HRT for symptoms if needed. There is no virtue in rigid ideology around hormone balance therapy. Use the right tool for the job, at the right time.

Monitoring that actually changes outcomes

Bone mineral density measured by DEXA is the anchor test. I order a baseline scan when symptoms and history suggest risk, then repeat every 1 to 2 years until the trend is clear. In early menopause on HRT, a two year interval is often enough. If someone is on aromatase inhibitors for breast cancer or on long term steroids, annual scans are justified. I watch the lumbar spine and total hip closely, since they behave differently over time.

Serum labs guide hormone levels treatment. For estrogen therapy, estradiol levels help with dose titration, though clinical response is king. For testosterone therapy, total and free testosterone, sex hormone binding globulin, hematocrit, and in men over 40 to 50, PSA, are standard. Thyroid function deserves periodic review since both hyper and hypothyroidism affect bone. Celiac screening or secondary workup comes into play with unexplained accelerated loss.

Here is a concise follow up blueprint I share with patients on HRT for bone:

DEXA baseline, then every 1 to 2 years until stable, then every 2 to 3 years Labs at 8 to 12 weeks after dose changes, then every 6 to 12 months: estradiol or testosterone, SHBG, CBC, CMP, lipid panel, 25 hydroxy vitamin D, PSA for men as indicated Blood pressure, weight, waist circumference, and symptom review at each visit Review of supplements and medications that affect bone, including PPIs, SSRIs, steroids, and aromatase inhibitors Fall risk screen yearly, with referrals for balance and strength training as needed

Routes and formulations, distilled

Patients often ask what form of hormone replacement will be easiest to live with and safest over the long haul. Here is a quick comparison to help frame that discussion:

Transdermal estradiol patch, gel, spray: steady levels, lower clot risk than oral, easy to adjust. Skin irritation is the main nuisance. Oral estradiol: effective for bone and symptoms, higher impact on liver proteins and clotting. Consider in younger healthy women without risk factors. Micronized progesterone: endometrial protection, often improves sleep. Can cause grogginess, so taking at night helps. Testosterone injections: predictable, low cost, peaks and troughs manageable with weekly dosing. Watch hematocrit. Testosterone gel: smooth levels, skin contact precautions required, adherence is key.

Two notes from the trenches. First, pellets can produce very high early levels that make side effects hard to reel in. Second, compounded creams can work, but quality varies across pharmacies. If compounded bioidentical hormones are used, pick a pharmacy with strong quality controls and be consistent in brand.

When to add a bone specific drug

Hormone therapy is not a stand alone solution for every patient. If someone already has a hip or vertebral fracture, or a DEXA T score under about minus 2.5 with additional risk factors, I will often add a bone specific medication either up front or after a limited trial of HRT and lifestyle. Bisphosphonates like alendronate and zoledronic acid are the workhorses. Denosumab is potent but requires a plan for transition when stopping. Anabolic agents like teriparatide or abaloparatide can rebuild trabecular bone rapidly in very high risk patients, then we maintain the gain with an antiresorptive.

With HRT layered underneath, bone turnover quiets further and the skeleton is less likely to slide backward when these medications are paused. Stopping denosumab without a follow on plan is a classic pitfall that leads to rebound bone loss. I flag calendars for this.

Edge cases that deserve attention

Secondary osteoporosis is common and underappreciated. I see bone loss in men on androgen deprivation therapy for prostate cancer, in women on aromatase inhibitors for breast cancer, and in both sexes on chronic prednisone. In these settings, estrogen or testosterone replacement are not appropriate, but aggressive bone protection is. Start antiresorptives early, maintain vitamin D sufficiency, and push resistance training.

Bariatric surgery patients and those with chronic malabsorption need higher vigilance. Celiac disease, inflammatory bowel disease, and long term PPI use can all chip away at bone density through reduced calcium absorption. Thyroid hormone dose creep over years can do the same. These are the moments when a broad hormone panel treatment mindset helps, because you find and fix the upstream issue rather than just chasing T scores.

Lifestyle, the multiplier

No hormone plan rescues bone without load bearing movement and protein. Twice weekly resistance training, ideally progressing to three sessions, transforms the musculoskeletal system. I ask patients to aim for 1.0 to 1.2 grams of protein per kilogram of body weight daily, spread across meals, and to pay attention to calcium in food first, supplements second. Walking is excellent for the heart, but your spine wants deadlifts, rows, and carries with perfect form. Even simple sit to stands and heel raises, done daily with progressive challenge, add up.

Sleep and alcohol intake matter. Poor sleep disrupts hormones and bone remodeling. Heavy alcohol weakens bone and destroys balance. Sunlight and vitamin D are simple, but powerful. Fall proofing the home is boring until you hear what a hip fracture costs in independence. I have patients photograph their throw rugs and cords so we can make a plan.

Bringing it together

Hormone therapy, used thoughtfully, is one of the most potent osteoporosis prevention tools we have. Estrogen and progesterone therapy around menopause protects spine and hip, relieves vasomotor symptoms, and, for many, improves sleep and mood. Testosterone replacement therapy in men with confirmed low T preserves bone and adds muscle, which reduces falls. In gender affirming care, consistent hormone levels are essential to preserve bone during and after transition.

This is hormone rebalancing, not one size fits all. Start with a clear indication, choose a route that fits the risk profile, set realistic targets, and monitor. Combine HRT with resistance training, adequate calcium and vitamin D, and judicious use of bone specific drugs when fracture risk is high. Be wary of pellet hormone implants that outpace control, and prefer FDA approved bioidentical hormones over unregulated compounded mixtures unless a specific need drives the choice.

I have seen women reclaim dense, resilient spines and men abandon the slow slump toward fragility when the plan is cohesive. The measures are straightforward, but the judgment comes from listening to history, balancing trade offs, and adjusting course early. If you are unsure where to start, partner with a hormone specialist or an endocrinologist who is comfortable with both menopause treatment and male hormone therapy. The work you do together today pays dividends every time you slip on the stairs and catch yourself with strong legs and a solid hip.

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Pub: 28 Feb 2026 15:13 UTC

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