{"id":204,"date":"2026-10-10T10:42:23","date_gmt":"2026-10-10T10:42:23","guid":{"rendered":"https:\/\/drpoletti.com\/blog\/?p=204"},"modified":"2026-10-11T13:47:31","modified_gmt":"2026-10-11T13:47:31","slug":"your-joints-dont-age-alone-testosterone-muscle-and-mens-health-after-50","status":"publish","type":"post","link":"https:\/\/drpoletti.com\/blog\/your-joints-dont-age-alone-testosterone-muscle-and-mens-health-after-50\/","title":{"rendered":"Your Joints Don\u2019t Age Alone: Testosterone, Muscle, and Men\u2019s Health After 50"},"content":{"rendered":"

Why I Look Beyond the Knee MRI: My Personal Approach to Orthopaedics, Metabolic Health and Hormonal Optimisation<\/strong><\/p>\n

Dr Fabi\u00e1n Poletti | Consultant Orthopaedic and Trauma Surgeon | Sports Medicine and Orthobiologics | Metabolic and Hormonal Optimisation<\/em><\/p>\n

\"\"<\/p>\n

When the problem is not just the knee<\/h2>\n

A 55-year-old man comes to see me because his knee hurts. His MRI shows some cartilage degeneration, a degenerative meniscal tear, or other changes commonly associated with ageing. So far, this is a fairly typical orthopaedic consultation. However, when we begin talking and explore his medical history in greater detail, a much more familiar picture starts to emerge.<\/p>\n

He tells me that over the past few years he has lost muscle mass, that he no longer recovers from exercise as he used to, and that he is accumulating abdominal fat despite having made relatively few changes to his lifestyle. His sleep has deteriorated, his energy levels have declined, and he feels that his physical capacity is deteriorating faster than he would expect. Sometimes he also acknowledges a reduction in his libido, although this is rarely the reason he originally sought an orthopaedic consultation. He is 55, but he feels that his body has changed dramatically in just five years.<\/p>\n

From a strictly orthopaedic perspective, I could concentrate on examining the knee, interpreting the imaging, and recommending a local treatment. The problem with this approach is that I might be overlooking an important part of what is happening to him. The question that interests me is not simply which structure within the joint is damaged, but what is happening within the body in which that joint has to function.<\/p>\n

Over the years, my personal interest in understanding the deeper mechanisms of health and ageing led me to pursue additional training in metabolic and hormonal optimisation, guided by my interest in integrative and functional medicine. This has shaped a clinical approach that combines my background in orthopaedic surgery, sports medicine and orthobiologics with a broader understanding of the metabolic, inflammatory and hormonal processes that influence musculoskeletal health.<\/p>\n

The more we understand about the physiology of ageing, the clearer it becomes that muscles, bones, tendons, and cartilage are not independent structures. They are tissues whose function is profoundly influenced by metabolism, inflammation, body composition, and the hormonal environment.<\/p>\n

And in middle-aged men, testosterone plays an important role in that relationship.<\/p>\n

Muscle is part of orthopaedic treatment<\/h2>\n

When we discuss knee osteoarthritis, attention usually turns immediately to cartilage. As an orthopaedic surgeon, however, I am just as interested in the articular surface as I am in the muscular system’s ability to control the forces acting upon it. The quadriceps, gluteal muscles, and other muscle groups of the lower limb are not merely supporting structures around the joint. They are essential for dynamic stability, load distribution, and efficient movement.<\/p>\n

A knee surrounded by strong, functional muscles is better equipped to cope with the mechanical demands of everyday life. Conversely, when a patient loses muscle mass and strength, relatively simple activities such as getting out of a chair, climbing stairs, or walking uphill can become considerably more demanding. This helps explain why two patients with similar radiological findings may experience very different levels of pain and functional limitation.<\/p>\n

As we age, progressive changes occur in muscle mass, strength, and particularly power, which is the ability to generate force quickly. Some of this deterioration is related to physical inactivity, inadequate nutrition, or metabolic disease, but hormonal mechanisms also contribute to the maintenance and renewal of muscle tissue.<\/p>\n

Muscle loss should therefore not be considered merely a cosmetic issue or an inevitable consequence of growing older. From an orthopaedic perspective, it represents a reduction in the body’s ability to protect joints, recover from injury, and maintain functional independence. Preserving muscle means preserving movement, stability, and physical capacity, which is why I believe it should be one of the central objectives of any men’s health strategy from the age of 40 or 50 onwards.<\/p>\n

Osteoarthritis is not simply wear and tear: it is also a metabolic and inflammatory disease<\/h2>\n

For decades, osteoarthritis has been explained primarily as the result of a mechanical process: a joint bears loads over many years, the cartilage progressively wears away, and eventually pain develops. This explanation remains deeply embedded in both public understanding and aspects of medical practice, but we now know that it captures only one dimension of a far more complex disease.<\/p>\n

Osteoarthritis affects the entire joint, not just the cartilage. The subchondral bone, synovial membrane, menisci, ligaments, joint capsule, and periarticular tissues are all involved in its development. Furthermore, research over recent decades has demonstrated that chronic low-grade inflammation contributes to the mechanisms underlying its onset and progression. We are not simply dealing with a structure that deteriorates through use, but with biologically active tissues that continuously respond to mechanical, metabolic, and inflammatory stimuli.<\/p>\n

This shift in perspective has significant implications, particularly when assessing patients with abdominal obesity, insulin resistance, or metabolic syndrome.<\/p>\n

Abdominal fat as a source of systemic inflammation<\/h3>\n

\"\"<\/p>\n

One of the most important concepts, in my view, is that body fat, particularly visceral fat accumulated around the abdomen, is not simply a passive store of energy. Adipose tissue is an active endocrine and metabolic organ, capable of producing numerous substances involved in the regulation of inflammation and metabolism.<\/p>\n

When this tissue expands and becomes dysfunctional, it can promote a state of chronic low-grade inflammation through the release of cytokines such as interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-\u03b1), as well as various adipokines, including leptin, resistin, and adiponectin. These mediators participate in complex cellular signalling pathways and can influence tissues far beyond the location where the inflammatory signals originate.<\/p>\n

Joints are no exception. Through several mechanisms, this metabolic environment can contribute to inflammatory processes within the synovium, disturbances in chondrocyte function, degradation of the cartilage extracellular matrix, and changes in subchondral bone remodelling.<\/p>\n

For this reason, reducing the relationship between obesity and osteoarthritis to a simple matter of additional kilograms acting on the knee is inadequate. Mechanical loading certainly matters, but in some patients the metabolic and inflammatory components may be equally important, or even dominant, contributors to the disease process.<\/p>\n

One particularly revealing observation is that people with obesity also have an increased risk of developing osteoarthritis in non-weight-bearing joints, such as those of the hands. This association is difficult to explain through mechanical overload alone and highlights the importance of systemic mechanisms.<\/p>\n

From this perspective, dysfunctional visceral adipose tissue behaves as a continuous source of inflammatory signals capable of influencing joint health far beyond its effects on body weight.<\/p>\n

Osteoarthritis as a manifestation of broader metabolic dysfunction<\/h3>\n

When we assess a patient with knee osteoarthritis, visceral obesity, and insulin resistance, we should consider the possibility that joint deterioration is part of a much broader metabolic problem. While inflammatory and degenerative changes are occurring within the joint, related processes may simultaneously be affecting the liver, cardiovascular system, skeletal muscle, and other organs.<\/p>\n

This does not mean that all osteoarthritis is necessarily metabolic in origin. Different phenotypes of the disease exist, with varying contributions from genetic, traumatic, biomechanical, and age-related factors. However, in a substantial number of patients, particularly those with abdominal obesity and metabolic abnormalities, adipose tissue dysfunction and low-grade inflammation form part of the underlying pathophysiology.<\/p>\n

This is what we refer to as metabolic osteoarthritis<\/em>, a concept that allows us to understand the joint as one of several possible organs affected by an unfavourable systemic metabolic environment.<\/p>\n

This interpretation also changes our therapeutic objectives. When I evaluate an arthritic knee in a patient with excess visceral fat, I am not interested solely in reducing the mechanical loads passing through that joint. I also want to understand what is happening to the patient’s metabolism, insulin sensitivity, body composition, and inflammatory state.<\/p>\n

The joint may be where the patient experiences the symptoms, but it is not necessarily the only tissue undergoing damage.<\/p>\n

Testosterone: much more than a sex hormone<\/h2>\n

\"\"<\/p>\n

For a long time, testosterone has been associated almost exclusively with libido, sexual function, and male secondary sexual characteristics. Its physiological influence, however, extends much further and becomes particularly relevant when we consider musculoskeletal ageing.<\/p>\n

Testosterone contributes to the maintenance of muscle mass, body composition, bone health, and several metabolic processes. Its effects occur through androgen receptors expressed in numerous tissues, where it participates in mechanisms involved in protein synthesis and the maintenance of muscle structure. In addition, some testosterone is converted into estradiol, a hormone that also plays a fundamental role in preserving bone mineral density in men.<\/p>\n

Clinical trials have consistently demonstrated that testosterone replacement therapy (TRT) can increase lean body mass and reduce fat mass in men with hypogonadism. Improvements in strength and physical performance are more variable, but the effects on body composition are well documented.<\/p>\n

From an orthopaedic perspective, this relationship is particularly relevant. A man who maintains good muscle mass, controls visceral adiposity, and preserves his ability to exercise is generally better positioned to manage the mechanical demands placed upon his joints and to undertake rehabilitation successfully.<\/p>\n

Testosterone is part of this balance, but its influence must be understood alongside other factors that continuously affect muscle health, including resistance training, nutrition, sleep, and metabolic function. This is precisely why integrating hormonal assessment into a broader clinical strategy makes considerably more sense than looking at hormones in isolation.<\/p>\n

The problem with calling everything within the reference range \u201cnormal\u201d<\/h2>\n

One aspect of medical practice that I believe deserves reconsideration is our tendency to interpret laboratory results primarily through reference intervals, without paying sufficient attention to the patient’s clinical trajectory.<\/p>\n

A man may have a testosterone concentration of 350 or 400 ng\/dL and receive a laboratory report describing the result as normal. Statistically, that classification may be correct, but the question that interests me is whether that number adequately reflects his physiological situation.<\/p>\n

Reference intervals are constructed using defined populations and analytical methods. They are useful clinical tools, but they do not necessarily represent the optimal functional state of every individual, nor do they tell us where that particular patient was during previous decades of his life.<\/p>\n

Consider a man who maintained substantially higher testosterone concentrations throughout much of his adult life and who has experienced a progressive decline over the years. If this change coincides with significant muscle loss, reduced libido, slower recovery, increased abdominal fat, and deteriorating general wellbeing, I believe the situation deserves further clinical investigation.<\/p>\n

Comparing his current levels with historical results does not, by itself, establish a diagnosis of hypogonadism, but it provides information about a trajectory that should not be ignored.<\/p>\n

In my clinical practice, I am interested in both the current laboratory value and the patient’s functional evolution. I want to understand what has changed, when those changes began, and which mechanisms may be contributing to them. This longitudinal perspective is one of the aspects I value most in functional medicine, because it encourages us to investigate relationships between physiological systems and potential causes of deterioration rather than simply classifying results as normal or abnormal.<\/p>\n

Total testosterone, free testosterone, and SHBG<\/h3>\n

Hormonal interpretation becomes even more interesting when we consider that total testosterone provides only part of the available information.<\/p>\n

Most circulating testosterone is bound to transport proteins, primarily sex hormone-binding globulin (SHBG) and albumin, while only a small proportion remains free. SHBG concentrations can vary according to age, body composition, insulin resistance, and several metabolic conditions, thereby altering the relationship between total and free testosterone.<\/p>\n

For this reason, assessing free testosterone alongside SHBG can be particularly valuable in selected patients. Depending on the clinical circumstances, it may also be appropriate to evaluate LH, FSH, and other parameters that help us understand how the hormonal axis is functioning and identify different causes of hormonal disturbance.<\/p>\n

When LH and FSH are measured, they can also help distinguish between primary and secondary hypogonadism. In primary hypogonadism, the problem originates in the testes, which fail to produce sufficient testosterone despite increased stimulation from the brain. As a result, LH and often FSH levels are elevated. In secondary hypogonadism, the problem lies in the hypothalamus or pituitary gland, which fail to provide adequate hormonal stimulation to the testes. In this case, LH and FSH levels are typically low or inappropriately normal despite reduced testosterone levels. This distinction is important because the underlying causes, clinical implications, and treatment approaches may be different.<\/p>\n

A well-structured hormonal assessment should aim to answer a specific clinical question and relate laboratory findings to symptoms, body composition, and functional changes. The purpose is to understand how the system is operating, rather than simply pursuing a particular number.<\/p>\n

Metabolism, visceral fat, and testosterone: a self-reinforcing cycle<\/h2>\n

The relationship between testosterone, visceral fat, and metabolism is one of the most interesting aspects of men’s health in middle age, precisely because none of these factors operates independently.<\/p>\n

Excess visceral adiposity is associated with insulin resistance, chronic low-grade metabolic inflammation, and hormonal disturbances. At the same time, low testosterone concentrations can contribute to unfavourable changes in body composition, including reduced lean mass and increased adiposity.<\/p>\n

These relationships can develop into a self-reinforcing cycle.<\/p>\n

A man begins to accumulate abdominal fat, gradually reduces his physical activity, and loses strength. His sleep deteriorates and his ability to recover declines. In this environment, metabolic and hormonal disturbances may develop, making it increasingly difficult to maintain a healthy body composition. If joint pain or a tendon injury then appears, the resulting reduction in physical activity may accelerate the process further.<\/p>\n

From an orthopaedic perspective, the consequences are particularly important because the joint is exposed to two problems simultaneously. On one hand, excess body weight alters mechanical demands; on the other, reduced muscle strength compromises the body’s ability to manage those loads. Added to this is the influence of a metabolic and inflammatory environment that can contribute directly to degenerative processes within the joint.<\/p>\n

What makes this especially significant is that the same environment may also be affecting other organs. A patient may develop osteoarthritis, insulin resistance, metabolic dysfunction-associated steatotic liver disease (MASLD), and vascular dysfunction within a shared pathophysiological context. These are not always completely independent conditions that happen to emerge at the same age; in many cases, they represent different manifestations of related metabolic mechanisms.<\/p>\n

This is why I consider body composition assessment far more informative than simply recording weight or body mass index. Two men may weigh exactly the same but have very different physiological profiles. One may preserve adequate muscle mass and carry relatively little visceral fat, while the other may have substantial abdominal adiposity, reduced muscle mass, and insulin resistance.<\/p>\n

Despite having identical body weights, their joints are not functioning within the same biological environment, nor are their cardiometabolic risk profiles necessarily comparable.<\/p>\n

For this reason, when the clinical history justifies it, my assessment does not end with the MRI scan. It also considers body composition, muscle strength, metabolic health, sleep quality, and hormonal status, with the aim of identifying modifiable factors that may improve both musculoskeletal function and long-term health.<\/p>\n

TRT: the evidence has changed, and our perspective should change with it<\/h2>\n

For many years, testosterone replacement therapy has been surrounded by considerable concern regarding its potential cardiovascular and prostate-related risks. Part of this perception was shaped by observational studies with significant methodological limitations, whose findings contributed to an excessively alarming view of the treatment.<\/p>\n

The publication of the TRAVERSE trial in 2023, in The New England Journal of Medicine<\/em>, represented an important turning point in this debate.<\/p>\n

TRAVERSE was a randomised clinical trial involving more than 5,200 men aged between 45 and 80 who had symptoms of hypogonadism, confirmed low testosterone, and either established cardiovascular disease or an elevated cardiovascular risk. Its primary objective was to evaluate the cardiovascular safety of testosterone therapy in a clinically relevant higher-risk population.<\/p>\n

The results showed that major adverse cardiovascular events occurred in 7.0% of men receiving testosterone, compared with 7.3% of those receiving placebo. The trial therefore demonstrated the non-inferiority of testosterone therapy compared with placebo for its primary cardiovascular safety outcome.<\/p>\n

These findings had important consequences and contributed to a change in the regulatory perspective on testosterone. In February 2025, the US Food and Drug Administration (FDA) announced class-wide labelling changes for testosterone products, including the removal of boxed-warning language concerning a possible increased risk of major adverse cardiovascular events, based on the evidence generated by TRAVERSE.<\/p>\n

The agency subsequently updated additional information concerning testosterone therapy and age-related hypogonadism.<\/p>\n

Taken together, these developments represent a significant change from the perception of risk that had dominated medical discussions for many years and allow TRT to be evaluated on a considerably stronger scientific foundation.<\/p>\n

What about prostate cancer?<\/h3>\n

Concern about prostate cancer has been another major historical barrier to prescribing testosterone.<\/p>\n

For decades, the idea that increasing testosterone levels might directly promote the development or progression of prostate cancer became widely accepted. However, clinical evidence accumulated over recent years has challenged this simplified interpretation.<\/p>\n

The prostate safety findings from the TRAVERSE programme, published in JAMA Network Open<\/em> in December 2023, were particularly relevant. In the population studied, there were no statistically significant differences between the testosterone and placebo groups in the incidence of prostate cancer, including high-grade disease.<\/p>\n

These findings are reassuring and challenge the assumption that administering testosterone to appropriately selected men necessarily increases their risk of developing prostate cancer.<\/p>\n

TRT should continue to involve individualised assessment and appropriate clinical monitoring, including haematocrit, blood pressure, and prostate health. We must also consider the adverse events reported more frequently in some TRAVERSE analyses, including atrial fibrillation and pulmonary embolism.<\/p>\n

Nevertheless, the broader conclusion is important: current evidence allows us to approach testosterone replacement therapy from a far more informed perspective, less constrained by the cardiovascular and prostate-related fears that dominated the debate for decades.<\/p>\n

More muscle does not mean indestructible tendons<\/h2>\n

One aspect of hormonal optimisation that particularly interests me, given my background in orthopaedic surgery and musculoskeletal medicine, is the relationship between improvements in muscle capacity and tendon adaptation.<\/p>\n

We know that muscles and tendons do not necessarily respond to training at the same rate. Muscle strength can improve relatively quickly, whereas the adaptation of tendinous structures to increasing mechanical demands requires a specific progression and, in some cases, considerably longer periods.<\/p>\n

This becomes especially relevant in a middle-aged man who begins appropriately indicated hormone therapy, improves his body composition, regains energy, and decides to return to intensive physical activity after years of inconsistent training.<\/p>\n

He may feel considerably stronger and capable of lifting weights that he has not attempted for a long time. However, this improvement does not necessarily mean that his tendons are ready to tolerate the same increase in mechanical demand.<\/p>\n

Over recent years, several observational studies have identified associations between testosterone treatment and certain tendon injuries, including Achilles tendon injuries. These findings do not establish that physiological TRT directly causes tendon rupture, but they raise interesting questions about the relationship between changes in strength, tissue adaptation, and exposure to higher loads.<\/p>\n

This is where orthopaedics and hormonal optimisation intersect in a particularly useful way. Improving muscle mass and physical capacity should be accompanied by appropriate exercise planning, progressive loading, and specific attention to tendon health.<\/p>\n

The objective should not simply be to make a patient feel stronger, but to develop a musculoskeletal system genuinely capable of using that strength safely and sustainably.<\/p>\n

My approach: from the joint to the whole person<\/h2>\n

Medicine is moving towards an increasingly integrated understanding of the processes associated with ageing, and this is the philosophy I have chosen to develop within my own practice.<\/p>\n

As an orthopaedic surgeon, I continue to regard clinical examination, accurate diagnosis, biomechanical assessment, imaging, and surgical treatment when indicated as fundamental parts of my work. However, my additional training and personal interest in integrative and functional medicine have led me to incorporate metabolic assessment, body composition, muscle strength, and hormonal health into my clinical approach. I recognise that all these factors contribute to the biological environment in which musculoskeletal problems develop and evolve.<\/p>\n

A patient with knee osteoarthritis is not simply a knee with osteoarthritis. He is an individual with a particular amount of muscle mass, a metabolic profile, a distribution of body fat, a hormonal environment, sleep habits, and a specific capacity for recovery. All these elements can influence both his clinical condition and his response to treatment.<\/p>\n

From a functional medicine perspective, I am interested in identifying the mechanisms contributing to deterioration and addressing those that can be modified. This may involve resistance training, nutritional optimisation, reduction of visceral fat, improved sleep, treatment of metabolic disturbances, and hormonal optimisation when appropriate.<\/p>\n

In osteoarthritis, it also means recognising that we may be dealing with a musculoskeletal manifestation of systemic metabolic dysfunction. Reducing visceral adiposity, improving insulin sensitivity, and restoring muscle mass are relevant interventions not only for general health but also for addressing some of the factors contributing to joint pain and functional deterioration.<\/p>\n

This approach does not replace traditional orthopaedic diagnosis. Rather, it places it within a broader physiological framework. My objective is not to pursue a specific testosterone concentration or an isolated laboratory value, but to improve the patient’s health, body composition, and physical capacity by integrating therapeutic strategies supported by scientific evidence.<\/p>\n

Conclusion: treating the man, not just his MRI<\/h2>\n

When a 55-year-old man comes to see me because his knee hurts, I will continue to assess that knee with all the precision that my speciality demands. However, if during the consultation I discover that he has also lost muscle mass, is accumulating abdominal fat, recovers poorly from exercise, sleeps badly, and has experienced significant changes in energy or sexual function, I do not believe that simply attributing everything to ageing is an adequate explanation.<\/p>\n

I want to understand what has changed within his body and which factors are contributing to that deterioration, because many of the changes we interpret as inevitable consequences of ageing are related to processes that can be influenced.<\/p>\n

We now understand that osteoarthritis is far more complex than simple cartilage wear and that metabolic inflammation, adipose tissue dysfunction, and insulin resistance can play important roles in certain patients. We also know that testosterone contributes to the maintenance of muscle, body composition, and bone health, and that the evidence surrounding the safety of therapeutic testosterone has evolved considerably in recent years.<\/p>\n

My own approach to men’s musculoskeletal health is grounded in integrating this knowledge into a clinical perspective that does not examine each joint as though it were an isolated mechanical structure.<\/p>\n

A knee ages within a body, and the metabolic, inflammatory, and hormonal processes affecting that body can have significant consequences for its function. Sometimes, what initially appears to be a local joint problem is also an opportunity to recognise a broader decline affecting the patient’s overall health.<\/p>\n

This is why I believe the real objective should not simply be to reach the age of 70 or 80, but to get there while preserving as much muscle, strength, mobility, energy, and independence as possible.<\/p>\n

Achieving that requires a broader clinical perspective, an understanding of the interactions between metabolism, hormones, and the musculoskeletal system, and a commitment to treating the patient as the integrated biological system that he truly is.<\/p>\n

\n
\n<\/div>\n

Dr Fabi\u00e1n Poletti<\/strong>
\nConsultant Orthopaedic and Trauma Surgeon<\/em>
\nSports Medicine and Orthobiologics<\/em>
\nMetabolic and Hormonal Optimisation<\/em><\/p>\n

Scientific references<\/h3>\n
    \n
  1. Lincoff AM, et al. Cardiovascular Safety of Testosterone-Replacement Therapy.<\/em> New England Journal of Medicine. 2023;389:107\u2013117. DOI: 10.1056\/NEJMoa2215025.<\/li>\n
  2. Bhasin S, et al. Prostate Safety Events During Testosterone Replacement Therapy in Men With Hypogonadism: A Randomized Clinical Trial.<\/em> JAMA Network Open. 2023;6(12).<\/li>\n
  3. FDA. FDA Issues Class-Wide Labeling Changes for Testosterone Products.<\/em> February 2025.<\/li>\n
  4. Albright JA, et al. Testosterone replacement therapy is associated with increased odds of Achilles tendon injury and subsequent surgery.<\/em> Journal of Foot and Ankle Research. 2023;16:76.<\/li>\n
  5. Peter Attia, MD, and Mohit Khera, MD. The Drive #260: Men’s Sexual Health.<\/em> 2023.<\/li>\n
  6. Peter Attia, MD, and Paul Turek, MD. The Drive #351: Male Fertility.<\/em> 2025.<\/li>\n
  7. Peter Attia, MD. AMA #28: All Things Testosterone.<\/em> 2021.<\/li>\n
  8. Binvignat M, et al. The role of obesity and adipose tissue dysfunction in osteoarthritis pain.<\/em> Nature Reviews Rheumatology. 2024;20:565\u2013584.<\/li>\n
  9. Hang W, Triantafilou K, Zhou Y. Adipose\u2013Joint Crosstalk in Obesity\u2013Induced Osteoarthritis: Mechanisms, Biomarkers, and Translational Therapeutic Opportunities.<\/em> Current Rheumatology Reports. 2026;28:22.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"

    Why I Look Beyond the Knee MRI: My Personal Approach to Orthopaedics, Metabolic Health and Hormonal Optimisation Dr Fabi\u00e1n Poletti | Consultant Orthopaedic and Trauma Surgeon | Sports Medicine and Orthobiologics | Metabolic and Hormonal Optimisation When the problem is not just the knee A 55-year-old man comes to see me because his knee hurts. 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