Does Testosterone Replacement Therapy Affect Orthopedic Surgery Outcomes?

Curated by Nelson Vergel | B.S. Chemical Engineering, MBA | Founder, ExcelMale.com | 34+ years on TRT | NIH and FDA advisory panel service | Author: Testosterone: A Man's Guide, Beyond Testosterone, The Peptide Consensus
| ExcelMale.com | Updated July 2026

ExcelMale Consensus
Testosterone replacement therapy is linked to higher rates of two orthopedic problems: failed spinal fusion and Achilles tendon injury. In a propensity-matched analysis of lumbar fusion patients, TRT users had a roughly 1.5-fold higher rate of pseudarthrosis (bone that never fully fuses) at one year. This holds even though TRT raises bone mineral density on a scan. The practical takeaway: TRT is not a reason to cancel surgery, but your surgeon should know you are on it and plan for it.

Key Takeaways

• TRT users had a 49.5% higher relative risk of failed lumbar fusion at one year (14.9% vs 10.0%) and 40.7% higher at two years.
• Denser bone on a DXA scan does not mean better fusion biology. Many TRT patients stay in the osteopenic range even after density gains.
• Consistent TRT use (3+ months) was linked to 24% higher odds of Achilles tendon injury and 54% higher odds of needing surgery after that injury.
• In lumbar fusion patients, TRT did not raise 90-day blood clot, sepsis, or pneumonia risk, unlike some joint replacement data.
• These are retrospective database studies. They show association, not proof of cause. Do not stop TRT on your own before surgery. Talk to your surgeon.

Testosterone builds bone. Older men on TRT gain roughly 7 to 7.5% in lumbar spine bone density in a single year, so you would expect a spine on TRT to fuse better after surgery. The data points the other way. A propensity-matched study of lumbar fusion patients found that men on testosterone replacement therapy had a higher rate of pseudarthrosis, the term for a fusion that fails to knit into solid bone. That gap between what the scan shows and what the bone actually does is the whole story of TRT and orthopedic surgery outcomes, and it changes how you should prepare for any elective bone or tendon procedure.

Does TRT Increase the Risk of Failed Spinal Fusion?​

Yes, based on the best data we have. Researchers used a large insurance database to match men on TRT against nearly identical men who were not, then tracked what happened after single-level lumbar fusion. They matched for the things that usually wreck a fusion, including smoking, diabetes, age, and BMI, so the comparison was as fair as claims data allows.

The pseudarthrosis numbers were consistent at both time points.

Interval	TRT users	Non-users	Relative risk
Pseudarthrosis at 1 year	14.9%	10.0%	1.50
Pseudarthrosis at 2 years	16.7%	11.9%	1.41

Put plainly, TRT users failed to fuse about half again as often at one year. That effect size is larger than what you see from smoking or advanced age, which is saying something, because both are well-known enemies of a good fusion.

Reoperation rates told a softer story. They ran higher in the TRT group but did not reach statistical significance. There are two likely reasons. A nonunion that does not hurt often gets watched rather than cut on again. And some TRT patients carry enough underlying frailty that surgeons hesitate to put them through a revision. So the true burden of failed fusion may be undercounted by looking at reoperations alone.

One reassuring finding: in these spine patients, TRT was not tied to more 90-day blood clots, pulmonary embolism, sepsis, or pneumonia. That runs against some total joint replacement data, where TRT has been flagged for higher clot and revision risk. The likely explanation is baseline risk. Spine surgery carries a lower baseline clot rate than joint replacement, often under 1% versus about 2%, so the blood-thickening effect of testosterone has less room to show up. The TRAVERSE trial did report a 1.8-fold higher pulmonary embolism risk in testosterone users overall, so this is context-dependent, not a green light to ignore clotting.

Why Would TRT Raise Nonunion and Fracture Risk If It Builds Bone?​

This is the core paradox, and it comes down to a simple distinction. Bone mineral density measures how much mineral is packed into the bone. Fusion biology measures whether living bone can remodel and bridge a gap. Those are not the same thing, and TRT seems to help the first while leaving the second short.

Two explanations fit the data. The first is confounding by indication. Men who get prescribed TRT often started from a worse place: longer duration of low testosterone, poorer baseline bone quality, more frailty. A 7% density bump sounds good, but if you begin deep in the osteopenic range, that gain may not carry you to a bone that fuses well. The therapy improves the number without normalizing the underlying biology.

The second is the vigor effect. TRT gives men more energy and drive. Some return to heavy activity sooner than a healing fusion can tolerate, which loads the surgical site before it is ready. More movement also means more chances to fall. This may help explain a separate and striking finding: despite denser bone, TRT users in some analyses show markedly higher vertebral fracture rates. Denser bone that gets loaded harder and falls more often can still break.

The honest answer is that we cannot yet separate these fully. Both probably contribute. What matters for you is the conclusion they share: a good DXA score is not proof that your spine is ready to fuse.

Does TRT Increase Achilles and Other Tendon Injury Risk?​

The tendon data is larger and cleaner than the spine data. Albright and colleagues matched hundreds of thousands of TRT users against controls and followed Achilles tendon health for two years. Men and women on TRT for at least three consecutive months were injured more often, and when they were injured, the damage was worse.

The injury rate ran 377.8 per 100,000 person-years in TRT users versus 245.8 in controls. The adjusted odds of an Achilles injury rose 24%. More telling, once injured, TRT users were 54% more likely to need surgery rather than heal in a boot, which suggests these were more complete, more severe ruptures.

The mechanism is a mismatch between muscle and cable. Testosterone grows muscle fast. Tendon adapts slowly. When a stronger muscle pulls on a tendon that has not caught up, the tendon is the weak link. On top of that, androgens appear to stiffen tendon tissue, blunt the relaxin response that keeps tissue pliable, and inhibit matrix metalloproteinases, the enzymes that let a tendon remodel and repair micro-damage. A stiffer tendon that cannot remodel well, pulled by a muscle that got strong quickly, is a setup for rupture.

Which Age Groups Are Most at Risk?​

Not the young lifters you might expect. The highest odds landed in the 66 to 75 age group, with an adjusted odds ratio of 1.66 for men and 1.82 for women. Aging tendons already have fewer cells and more disorganized collagen. Add the energy and strength surge of TRT and you get older people pushing stiffer, more brittle tendons harder than those tendons can handle. The risk increase was nearly equal between sexes, which tells you this is a tendon biology issue, not a male-specific one.

Should You Stop TRT Before Orthopedic Surgery?​

Not on your own, and probably not at all in most cases. Current guidance does not require stopping non-estrogen hormone therapy before surgery. Stopping TRT abruptly has its own downsides, including a crash in energy and mood during an already stressful recovery. This is a decision to make with your surgeon and prescriber together, weighing the specific procedure.

What the data supports is planning, not panic. If you are heading into a spinal fusion, your surgeon may lower the threshold for osteoinductive materials such as BMP-2 or bone graft adjuncts to overcome weaker fusion biology. If you are having a tendon repair or any procedure where you will be tempted to load early, the plan should include a more conservative return-to-activity schedule. The point is to match the surgical strategy to the real risk, not to yank a hormone you may need.

What Should You Tell Your Surgeon If You're on TRT?​

Tell them you are on it, how long you have been on it, and your dose and delivery method. That belongs in your history next to smoking and diabetes, because it carries similar weight for fusion outcomes. Ask directly whether your procedure warrants extra fusion support or a slower loading protocol.

Bring your recent labs and bone density if you have them, but say out loud that you understand a good density score does not guarantee good fusion. That single sentence tells a surgeon you get the paradox and moves the conversation toward biology instead of just the scan. Nail down the modifiable risks you can still control before the date: keep nicotine at zero, get your HbA1c in range, and sort out nutrition. Those levers matter more in a TRT patient, because they stack on top of an already higher baseline risk.

Frequently Asked Questions​

Does TRT make bones stronger or weaker?​

Both, in different senses. TRT reliably increases bone mineral density, so bones look denser on a DXA scan. But denser bone is not the same as bone that heals and fuses well, and TRT users show higher rates of nonunion and, in some data, vertebral fracture. Density up, healing biology not necessarily up.

Can I still have spinal fusion surgery if I'm on testosterone?​

Yes. TRT is not a reason to deny surgery. It is a reason for your surgeon to plan for a higher chance of nonunion, which may mean using extra fusion-promoting materials and watching your recovery more closely.

How long should I wait to return to lifting after a tendon injury on TRT?​

Longer than you feel you need to. The whole risk pattern in TRT users comes from strong muscle pulling on a tendon that has not caught up. Follow your surgeon's or physical therapist's loading schedule even when your energy says you are ready sooner.

Do these risks mean I should quit TRT?​

No, and do not stop on your own. These are association studies, not proof that TRT causes these problems, and TRT treats real symptoms of low testosterone. The right move is to tell your surgical team you are on it and let them adjust the plan.

Related ExcelMale Forum Discussions​

Patients taking hormones seem to be at a higher risk of tendon injury breaks down the orthopedic review on TRT and tendon rupture, with members debating whether harder training, not the hormone, drives the signal.

Does testosterone decrease collagen? digs into how androgens affect collagen synthesis and tendon structure, which is the mechanism behind the injury data.

My experience repairing my torn biceps tendon is a firsthand recovery account from a member on TRT, useful if you are facing a tendon repair yourself.

Key References​

Miller M, Delgadillo B, Meade M, et al. Testosterone Replacement Therapy in Posterior Lumbar Fusion Patients: A Propensity Score-Matched Analysis of Long-Term Outcomes. Global Spine Journal. 2026. https://doi.org/10.1177/21925682261467396

Albright JA, et al. Testosterone replacement therapy is associated with increased odds of Achilles tendon injury and subsequent surgery: a matched retrospective analysis. Journal of Foot and Ankle Research. 2023;16:76. https://doi.org/10.1186/s13047-023-00678-0

Lincoff AM, Bhasin S, Flevaris P, et al. Cardiovascular Safety of Testosterone-Replacement Therapy (TRAVERSE). New England Journal of Medicine. 2023;389:107-117. https://doi.org/10.1056/NEJMoa2215025

Snyder PJ, Kopperdahl DL, Stephens-Shields AJ, et al. Effect of Testosterone Treatment on Volumetric Bone Density and Strength in Older Men With Low Testosterone. JAMA Internal Medicine. 2017;177(4):471-479. https://doi.org/10.1001/jamainternmed.2016.9539

Cancienne JM, Brockmeier SF, Rodeo SA, Werner BC. The Effect of Sex Hormone Deficiency on the Incidence of Rotator Cuff Repair: Analysis of a Large Insurance Database. Journal of Bone and Joint Surgery. 2022. The Effect of Sex Hormone Deficiency on the Incidence of Rotator Cuff Repair: Analysis of a Large Insurance Database - PubMed

Bhasin S, Brito JP, Cunningham GR, et al. Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline. Journal of Clinical Endocrinology and Metabolism. 2018;103(5):1715-1744. https://doi.org/10.1210/jc.2018-00229

Vigen R, O'Donnell CI, Baron AE, et al. Association of testosterone therapy with mortality, myocardial infarction, and stroke in men with low testosterone levels. JAMA. 2013;310(17):1829-1836. https://doi.org/10.1001/jama.2013.280386

Corona G, Rastrelli G, Di Pasquale G, et al. Testosterone and Cardiovascular Risk: Meta-Analysis of Interventional Studies. Journal of Sexual Medicine. 2018;15(6):820-838. https://doi.org/10.1016/j.jsxm.2018.04.641

Conclusion​

One thing the studies hint at but never say outright: the men most likely to fail a fusion on TRT may be the ones who feel the best on it. Renewed energy sends you back to heavy activity, and stronger muscle loads bone and tendon that are still catching up. The dangerous window opens once testosterone has done its job and you feel capable again, while the surgical site is still weeks from ready. If you are heading into a bone or tendon procedure, respect the recovery timeline even when you feel ready to skip it. For more on how testosterone actually behaves in the body, see our SHBG guide and our exercise on TRT guide.

Medical Disclaimer
This article is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before starting or modifying any hormone therapy or medical treatment.

About ExcelMale​

ExcelMale.com is a men's health community with more than 24,000 members and over 20 years of archives, founded by Nelson Vergel. Nelson is a chemical engineer with 34+ years on TRT and has served on NIH and FDA advisory panels. He is the author of Testosterone: A Man's Guide and Beyond Testosterone.

 

Thread 'Testosterone Therapy and Skeletal Health: What Older Men on TRT Need to Know About Fractures and Tendon Risk'

Apr 15, 2026

Curated By Nelson Vergel | ExcelMale.com | Updated April 2026

Summary: TRT improves bone density on imaging scans, but landmark clinical data from the TRAVERSE trial reveal a paradox: men on testosterone experienced significantly more clinical fractures than men on placebo. Add emerging evidence linking TRT to Achilles, rotator cuff, and quadriceps tendon injuries, and the picture becomes clear - TRT is a powerful treatment for hypogonadism symptoms, but it is not an anti-fracture or anti-injury therapy. This article explains why, what you can do about it, and how to...

• Nelson Vergel
• bone fractures trt fractures trt tendons
• Replies: 2
• Forum: Testosterone Side Effect Management

• 

 

The Androgen Paradox: Reconciling Bone Mineralization with Connective Tissue Fragility and Surgical Nonunion​

1. Introduction: The Clinical Landscape of Testosterone Replacement Therapy (TRT)​

The strategic landscape of endocrine and orthopedic medicine has shifted significantly over the last two decades. Between 2001 and 2011, prescriptions for testosterone replacement therapy (TRT) in the United States increased more than threefold. This trend coincides with a rising volume of elective lumbar fusion procedures, driven largely by an aging global population seeking relief from spinal stenosis and degenerative conditions. For the clinical researcher, the intersection of these two trends is critical; as TRT becomes a common component of the preoperative medical profile, understanding its impact on surgical outcomes is a mandatory requirement for risk stratification and successful postoperative management.
The central challenge in managing the TRT patient is the "Androgen Paradox." Androgens are traditionally recognized for their anabolic properties, specifically their ability to increase bone mineral density (BMD) and muscle mass. However, emerging clinical data suggests a troubling disconnect: while TRT successfully improves static markers of bone health, it appears to correlate with higher rates of structural integration failure and connective tissue injury. In short, the therapy that makes the bone appear "stronger" on a scan may simultaneously undermine the biological environment necessary for those bones to fuse or for tendons to remain resilient under strain. This synthesis explores this paradox, moving from the specific data regarding lumbar spinal fusion and the incidence of pseudarthrosis to systemic musculoskeletal failures.

2. The Bone Density Dilemma: BMD Gains vs. Pseudarthrosis Risk​

In orthopedic surgery, a critical distinction must be made between static bone mineral density and functional bone healing, or fusion biology. While TRT is known to increase volumetric BMD in the lumbar spine by approximately 7% to 7.5% after one year of treatment, these gains do not necessarily translate into successful osseointegration following surgery. The successful union of a spinal fusion requires a complex, dynamic remodeling process that may be compromised by the presence of exogenous androgens.
Recent findings from Stump et al. (2026) highlight this disparity. Despite the documented androgen-driven increase in bone density, patients on TRT exhibited significantly higher rates of pseudarthrosis compared to matched controls.
Bone Mineral Density vs. Clinical Outcomes in TRT Patients

Metric	TRT Patient Group Findings
Documented BMD Increase	~7.0–7.5% in the lumbar spine after 1 year
Incidence of Pseudarthrosis at 1 Year	14.9% (vs. 10.0% in Controls)
Incidence of Pseudarthrosis at 2 Years	16.7% (vs. 11.9% in Controls)
Relative Risk (RR) and Confidence Intervals	1-Year: 1.495 (1.165–1.917); 2-Year: 1.407 (1.119–1.769)

One prevailing theory to explain this outcome is "Confounding by Indication." This hypothesis suggests that patients prescribed TRT may represent a "severe phenotype" of hypogonadism or frailty. In these cases, the baseline bone quality and regenerative capacity are so profoundly impaired that even the density gains afforded by androgen supplementation cannot normalize the biology of a spinal fusion. This suggests that the observed association between TRT and pseudarthrosis might stem from an underlying deficiency that TRT fails to rectify, rather than a direct negative effect of the hormone itself. Regardless of the cause, the failure of bone to successfully integrate mirrors a parallel vulnerability observed in the body's connective tissues; the "Androgen Paradox" is ultimately a systemic failure of the "chassis" to support a chemically supercharged "engine."

3. Connective Tissue Vulnerability: Tendinopathy and Rupture​

Beyond the skeleton, the androgen paradox manifests in the "Muscle-Tendon Gap." This phenomenon occurs when TRT-induced rapid muscle hypertrophy outpaces the slower, more methodical adaptive capacity of the surrounding connective tissues. The result is a musculoskeletal system where the engine (the muscle) has become too powerful for the chassis (the tendon), leading to failure at the interface.
Data from Albright et al. (2023) regarding Achilles tendon health provides a stark illustration of this vulnerability. Their research into over 400,000 patients identifies several key markers of risk:

• Incidence Rates: TRT patients showed an incidence of 377.8 Achilles tendon injuries per 100,000 person-years, contrasted with 245.8 in matched controls.
• Surgical Odds: Following an initial injury, TRT users demonstrated an adjusted odds ratio (aOR 1.54) for progressing to surgery, indicating a higher severity of tissue failure.
• Demographic Vulnerability: The risk is most pronounced in the 66–75 age cohort for both males (aOR 1.66) and females (aOR 1.82). This specific vulnerability is driven by the interplay between aging tenocyte activity—characterized by reduced proliferation and collagen organization—and the TRT-induced increase in physical vigor and mechanical loading.

These findings must be reconciled with documented risks in other regions, specifically the baseline risks of hormone deficiency. While testosterone-deficient males show an 89% increase in rotator cuff repairs and estrogen-deficient females show a 48% increase, the addition of TRT does not appear to normalize this risk, but rather introduces a new profile of mechanical vulnerability. This suggests a systemic failure of the tissue to adapt to new mechanical loads, driven by underlying biochemical disruptions.

4. Biochemical Hypotheses: MMP Inhibition and Collagen Dysplasia​

Understanding molecular-level remodeling is critical for predicting long-term orthopedic success in patients on exogenous androgens. Successful orthopedic healing requires a precise homeostatic balance between the degradation of old tissue and the synthesis of new, organized collagen.
The primary drivers of this balance are Matrix Metalloproteinases (MMPs) and Tissue Inhibitors of Matrix Metalloproteinases (TIMPs). Exogenous androgens disrupt this equilibrium, specifically through the inhibition of MMP-1, MMP-2, and MMP-3 activity. This disruption leads to the following structural consequences:

1. Collagen Dysplasia: Androgen use is directly linked to damaged tendon structures in experimental models. Fibers are improperly organized, leading to inherent structural weakness despite increased muscle mass.
2. Increased Stiffness: Androgens are associated with increased tendon stiffness and a significant reduction in the relaxin response. This makes the tissue less compliant and more susceptible to failure under repeated strain.
3. Remodeling Failure: By altering the MMP/TIMP ratio, TRT leads to "dysfunctional adaptation." The tissue cannot effectively repair the micro-damage caused by increased physical activity, eventually leading to macro-failure such as rupture or impaired osseointegration at a surgical site.

5. Clinical Synthesis and Risk Mitigation Strategies​

Clinical vigilance and aggressive patient optimization are of strategic importance before elective orthopedic procedures. While TRT patients may not show elevated rates of acute 90-day medical complications in spinal fusion contexts, their long-term structural risk profile is distinct and requires targeted intervention.
TRT-Associated Complications: Documented vs. Refuted

Documented Risks (General/Other Trials)	Refuted Findings (Stump et al. Lumbar Study)
Pseudarthrosis: 1.4-fold increased risk	Pneumonia & Sepsis: No significant difference
Tendon Rupture: aOR 1.54 for surgery (Albright)	Acute Renal Failure (AKI): No difference in lumbar study
VTE/PE: 1.8-fold PE risk in TRAVERSE trial	VTE/PE: No significant difference in lumbar study
Revision Surgery: Increased risk in TJA cohorts	ED Utilization & Readmission: No difference

The "So What?" Layer for Surgeons The data necessitates a high level of clinical assertiveness. Based on the 1.4-fold increased risk of pseudarthrosis, it is mandatory for clinicians to perform comprehensive preoperative screenings for bone quality in TRT patients. Surgeons should adopt a lower threshold for—and potentially prioritize—the aggressive utilization of osteoinductive adjuncts, such as bone morphogenetic protein-2 (BMP-2), to overcome impaired fusion biology. Furthermore, because these patients often possess increased physical vigor, postoperative protocols must be more demanding regarding the optimization of modifiable risk factors and more conservative regarding weight-bearing schedules to prevent "engine-over-chassis" failures.
Ultimately, the increased risk of fracture and nonunion is a non-negotiable factor in surgical planning. Prospective research is essential to establish clear causality and to determine if specific dosing can mitigate these structural risks.

6. Final Summary of Findings​

The overarching paradox of androgen therapy is clinically significant: while TRT effectively restores physiological levels and improves bone mineral density, it simultaneously introduces structural vulnerabilities that compromise surgical outcomes and tendon integrity. The "stronger" bone observed on radiographic imaging often masks a weakened biological infrastructure and impaired remodeling capacity. Clinicians must recognize that TRT successfuly increases the "static" strength of the musculoskeletal system while potentially undermining its "dynamic" healing potential, necessitating heightened vigilance and robust surgical augmentation.