One of the hardest lessons of my career was learning that imaging does not reliably tell us what hurts, and structural change does not automatically mean tissue damage that requires surgery. Many of the so-called abnormalities we see on MRIs are age-appropriate findings, not a diagnosis of your future. I’ve seen far too many people with osteoarthritis elect to have surgery far too early. X-ray findings shouldn’t guide your decision-making. I run with people who have bone-on-bone knee X-rays. There’s far more to that decision-making. That’s why I wrote an entire book on knee osteoarthritis here on Substack.

I also believe we have framed far too much joint and tendon pain as a purely mechanical problem. Tendons do not usually fail because of one bad rep. Joints do not simply “wear out” because you stayed active.

• Biology matters.

• Tissue capacity matters.

• Load management matters.

• Metabolic health matters.

• Recovery matters.

In many cases, the answer is not rest, panic, or rushing toward a procedure. It is understanding the difference between a painful tissue and a dangerous problem, then building a plan around movement, progressive loading, time, and context.

My goal with this pillar is not to convince everyone to avoid surgery. It is to help people understand when surgery helps, when it does not, and why the right explanation is often as therapeutic as the treatment itself.

Top 6 posts to start with

1. Tendon Health Series
   This is one of the best entry points into how I think about tendon pain, rehab, loading, and the metabolic factors most people never hear about.

2. Why Your MRI Might Mislead You.. and Scare You
   If you only read one piece on imaging, make it this one. MRI findings can be useful, but they are often misunderstood and over-weighted.

3. Knee Osteoarthritis: An eye-opening book published here. How to manage osteoarthritic joints and when to consider surgery. Many have been able to delay surgery for years by following the principles discussed here.

4. Painful Tendons Want Load... Not Rest
   This is central to my tendon thesis: rest alone rarely solves tendinopathy, and rehab needs progressive loading.

5. Meniscus Tears: Podcast Episode 9
   A strong starting point for understanding what meniscus tears really mean, when they matter, and why most do not require surgery.

6. No, Exercise Doesn’t Cause or Worsen Osteoarthritis. Keep Moving.
   I wrote this to push back on one of the most damaging myths in orthopedics: that loading joints is what ruins them.

10 most common questions people ask on this subject

These reflect recurring search intent around MRI findings, meniscus tears, rotator cuff tears, tendon pain, arthritis, exercise, and surgery decisions, which show up consistently across major orthopedic and health information sources.

1. Does a meniscus tear always require surgery?
   Preview: No. Most degenerative meniscus tears in adults do not require surgery. I focus on symptoms, function, swelling, locking, and the full clinical picture—not just the MRI report.
   Read: Meniscus Tears: Podcast Episode 9

2. Can an MRI show the cause of my pain?
   Preview: Sometimes it helps, but it often misleads. Many people over 40 have “abnormal” findings that are completely age-appropriate and unrelated to symptoms.
   Read: Why Your MRI Might Mislead You.. and Scare You
   Also: When MRI Abnormalities Are Not Abnormal

3. Should I rest a painful tendon until it heals?
   Preview: Usually not. Tendons need the right amount of load to recover. Too little loading can make them weaker and prolong the problem.
   Read: Painful Tendons Want Load... Not Rest
   Also: Why We Should Not Immobilize Most Non-Surgical Tendon Injuries

4. What is tendinopathy, and how is it different from tendonitis?
   Preview: Most chronic tendon pain is not a short-lived inflammation problem. It is usually a tendon capacity and adaptation problem, which is why treatment has to go beyond rest and anti-inflammatories.
   Read: Tendon Health Series
   Also: Why Our Tendons Hurt: The Three Boneheads Podcast

5. Does exercise wear out my joints or make arthritis worse?
   Preview: No. That idea comes from an outdated mechanical model. Joints are living tissues that generally respond well to appropriate loading and movement.
   Read: No, Exercise Doesn’t Cause or Worsen Osteoarthritis. Keep Moving.

6. Do rotator cuff tears always need surgery?
   Preview: No. Many rotator cuff tears are age-related findings, and many people improve based on pain, strength, and function without surgery. The MRI should not make the decision on its own.
   Read: The Rotator Cuff: The Three Boneheads Podcast
   Also: The Real Reason Your Shoulder Hurts - And Why Rest Won’t Fix It

7. Why does the outside of my hip hurt? Is it bursitis?
   Preview: Often, it is not bursitis at all. Lateral hip pain is commonly a tendon problem, especially involving the gluteal tendons, and the treatment usually centers on load management and strength.
   Read: Why the Outside of Your Hip Hurts: Understanding Gluteal Tendinopathy

8. How do I know if arthritis is causing my pain?
   Preview: An X-ray can show arthritis, but it cannot tell you how much of your pain is coming from it. I look at the whole story: symptoms, irritability, function, movement, and what calms things down.
   Read: The (not so) Hidden Links Between Metabolic Health, Joints, Tendons and Longevity
   Also: Why Your MRI Might Mislead You.. and Scare You

9. Can metabolic health affect my joints and tendons?
   Preview: Absolutely. Blood sugar, insulin resistance, lipids, uric acid, and systemic inflammation all influence tissue quality, pain sensitivity, and healing capacity.
   Read: Tendon Health Part 2: When Tendons Meet Metabolism
   Also: The (not so) Hidden Links Between Metabolic Health, Joints, Tendons and Longevity

10. How do I decide whether I actually need orthopedic surgery?
    Preview: I do not start with the image. I start with function, weakness, instability, mechanical symptoms, failure of a well-run rehab plan, and what you need your body to do. Surgery can help — but only when it solves the right problem.
    Read: The Second Mountain of Medicine
    Also: The Power of Listening, Reassurance, and the Right Explanation

Next Steps

If you are trying to make sense of joint pain, tendon pain, arthritis, MRI findings, or a possible surgery recommendation, start here: Welcome to My Community. It is the best entry point into how I think about pain, imaging, movement, recovery, and staying active without being misled by fear.

Stay strong,
Howard Luks, MD

• Most tendon pain isn’t caused by an injury

• Tendons exist on a spectrum from reactive (reversible) to degenerative (manageable), and understanding where you are on that spectrum

• Metabolic health, hormones, medications, and aging all affect your tendons

• Loading, not resting, is how we restore tendon function, but the type, timing, and progression of that load matter

• MRI findings often look far worse than what you’re actually experiencing, and many people with “terrible” imaging have no pain at all.

I have written a lot about tendons over the past year. Probably more than most orthopedic surgeons write about tendons in a lifetime. Tendon problems are one of the most common complaints and misunderstood issues I see in the office. People come in thinking something tore. Whereas people with the most severe tendon pain often don’t have tears. Many come in thinking they need surgery. They come in convinced that a single event, like sleeping wrong, one bad swing, one heavy deadlift, or one morning of gardening, caused the issue. And almost always... that’s not what happened. Furthermore, many don’t understand why your elevated A1c, chronic inflammation levels, lipids, and uric acid affect your level of tendon pain and damage. This is a little complicated, but important to understand… Let’s get into this…

Despite all that I’ve written, I get a lot of questions from you about various tendon issues. So I felt it was time to revisit this broad topic. The problem is that I’ve written about this topic across many posts, each one approaching tendons from a slightly different angle. If you’re new here, or if you’ve been reading along but can’t remember which article covered what, it can be hard to find everything. So this article is going to organize it all.

Before we get into the specifics, we need to define tendinopathy. Tendinopathy is the term we use for the most common cause of tendon pain and dysfunction. It simply means “something is wrong with the tendon.” It’s not a tear, necessarily (some radiologists call it a partial tear on an MRI report). It’s not inflammation in the traditional sense. Instead… It’s a tendon that has undergone structural changes and is now signaling you through pain. The old term “tendinitis” implied that inflammation was the primary problem. We now know it’s rarely that simple.

Why Tendons Hurt

Most folks think their tendons hurt because of an injury. That can happen, although more tendons hurt because they’ve done too little. It’s intuitive to think of it like an injury. Then folks tend to rest whatever hurts, and this is often the exact opposite of what you should be doing.

Let’s assume you don’t train regularly, so your tendons see very little stress day to day. Then spring comes, and you need to clean out the garage or the garden. A few days later, your tendons hurt. You didn’t injure them or tear them… you just exposed them to more strain than they were adapted to.

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We call this initial phase a reactive tendinopathy because the tendon simply wasn’t prepared for what you asked it to do. The tendon responded by swelling, stiffening, and becoming painful. This is the earliest stage of the tendinopathy continuum, a model that describes tendon problems as existing on a spectrum.

On one end, you have this reactive stage, which is usually fully reversible with appropriate management. On the other end of the spectrum, you have severe degenerative tendinopathy, where the tendon has undergone enough structural changes that recovery is unlikely.

For this analogy, think of your tendon’s internal architecture as a tightly woven rope. That rope is made of collagen, the main structural protein in your body. In a healthy tendon, those collagen fibers are organized in neat, parallel bundles, all aligned in the direction of pull. They slide past one another smoothly, absorb force, and transmit it efficiently from muscle to bone.

In degenerative tendinopathy, that rope starts to fray. The normally parallel collagen fibers become disorganized. The tissue takes on water in some areas, loses its well-defined architecture, and the cells within the tendon change their behavior. New blood vessels grow into areas that are normally relatively avascular. These new blood vessels, a process called neovascularization, bring along small nerve endings. Those nerve endings may be one reason a degenerated tendon hurts.

Athletes can get into trouble with tendons despite their training… but it’s really the same issue. A runner whose achilles is used to 3 miles/ day and 20 miles/ week has a chance of developing achilles tendinopathy if the weather changes and they decide to run 5-6 miles/day.

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Sometimes, despite no obvious reason, our tendons start to hurt too. As we will discuss in a moment, our overall health and well-being, as well as some medications, have a role in te the etiology of tendinopathy. It’s not a 100% load mismatch problem.

Now…If the problem were simply tendon inflammation, then rest, ice, and anti-inflammatory medications would solve it. But tendinopathy isn’t primarily an inflammatory condition. It’s a failed response to the loading process. The tendon either received too much load too quickly, too little load for too long, or both. In either case, the solution is similar... You have to load the tendon… Carefully and progressively.

And I know that sounds counterintuitive. Your tendon hurts, and I’m telling you to use it more, not less. But this is what the research shows clearly, and it’s what I see works in the office every week. Rest might reduce pain temporarily, but it doesn’t rebuild the tendon’s capacity to handle the activities you want to do. Only progressive loading does that.

When we load a degenerated tendon through rehab, we are not necessarily restoring that frayed, disorganized tissue back to pristine condition. What the research suggests is that loading builds the capacity of the intact portion of the tendon, the healthy tissue that surrounds and coexists with the degenerative area. We are essentially working around the lesion, strengthening what’s still good, and building enough overall capacity that the tendon functions well despite the structural changes that may still show up on imaging. This is why someone can have a tendon that looks “terrible” on MRI but functions beautifully in real life. The imaging shows the degeneration. It doesn’t show you the functional capacity of the tendon as a whole.

Loading:

When we talk about loading, there are a few different approaches worth understanding.

• Isometric exercises are contractions in which the muscle generates force, but the joint doesn’t move. Think of holding a weight at a fixed angle and just maintaining that position. These are particularly useful early on because they can reduce tendon pain in the short term, giving you a window to begin more challenging work.

• Eccentric exercises involve lengthening the muscle under load, such as slowly lowering a weight after lifting it. Eccentric exercises have a role in the latter stages of the rehab process.

• Heavy slow resistance training involves both the lifting and lowering phases at slower speeds with heavier weights. More recent research suggests outcomes may be similar between eccentric-only and heavy slow resistance programs. But the key principle across all of them is the same... progressive, graduated loading that respects where your tendon is on that continuum and builds capacity over time.

Interpreting the Signals Your Tendon Is Sending:

There’s a difference between a tendon that’s stiff in the morning and loosens up as you move, versus a tendon that gets progressively worse the more you use it. Many people with achilles tendinopathy, for example, notice that the first few steps out of bed are uncomfortable, but within a few minutes of walking, the stiffness fades and the pain diminishes. That’s a tendon that’s responding to gentle loading. It’s a good sign, actually. Compare that to someone whose achilles feels fine at the start of a run but becomes increasingly painful mile after mile, or someone whose pain is markedly worse the day after activity. That pattern suggests you’re exceeding the tendon’s current capacity. Both signals are useful if you learn how to interpret them.

If you want the full exploration of why tendons prefer load over rest, including the research behind it and what this looks like in practice, start here.

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The Metabolic Connection

Tendons don’t exist in isolation. They’re part of a body that’s regulated by hormones, cytokines, blood sugar levels, medications, and subject to the cumulative effects of how you’ve lived for decades. Your metabolic health will affect your tendon health and how often tendinopathy occurs and how quickly it resolves.

Sustained high blood sugar (elevated Hemoglobin A1c) produces something called advanced glycation end products, or AGEs. Imagine sticky sugar molecules in your bloodstream gluing themselves to your collagen fibers. Over time, those sugar-glue bonds form permanent cross-links between the collagen strands in our tendons. Just like a rubber band left out in the sun for years. It loses its elasticity, becoming stiff and brittle. That’s essentially what AGEs do to tendon collagen. They make the tissue stiffer and less able to absorb and transmit force the way it should.

AGEs also impair the tendon cells’ ability to sense and respond to mechanical loading, a process called mechanotransduction. This is the very signaling pathway that your rehab program depends on. When you load a tendon during exercise, the cells inside are supposed to “feel” that mechanical stimulus and respond by producing new, healthy collagen. AGEs interfere with that process. So not only is the tissue stiffer and more vulnerable, but the biological machinery your tendon needs to adapt to loading, the whole reason rehab works, is compromised by chronically elevated blood sugar. This is one reason why tendinopathy can be very stubborn to treat in people with diabetes.

Hormones play a role as well. Women going through menopause experience a significant decline in estrogen, and estrogen is directly involved in collagen synthesis. Many women notice tendon pain showing up seemingly out of nowhere in their late 40s and 50s. Their tendons are losing one of the hormonal signals that helps maintain collagen quality. Testosterone decline in aging men also affects tendon collagen synthesis and repair capacity. The effect is generally more gradual than the relatively abrupt estrogen decline at menopause, but over time, lower testosterone levels contribute to reduced collagen production and slower tendon adaptation. This is part of why tendinopathy becomes more common as we age, regardless of sex.

Certain medications can also weaken tendons. Fluoroquinolone antibiotics, a class that includes ciprofloxacin and levofloxacin, are known to damage tendon tissue and have been associated with tendinopathy and even tendon rupture. Statins, while important for cardiovascular risk in many people, can also contribute to tendon complaints in some patients. These medication effects fit the broader theme here... your tendons are not isolated mechanical structures. They are living tissues embedded in your metabolic and hormonal environment, and anything that alters that environment can alter your tendons.

Lipid levels and uric acid need to be covered in this conversation, too. Multiple large studies have shown that elevated LDL roughly doubles the odds of rotator cuff disease and achilles tendon pathology. The mechanism is similar to what we see with blood sugar... lipids accumulate within the tendon matrix, stiffen the tissue, and activate inflammatory pathways that degrade collagen.

Uric acid may be even more relevant. Recent research shows that elevated uric acid, even without clinical gout, doubles to triple the odds of achilles tendon rupture. Urate crystals deposit silently in tendons, trigger inflammation, and weaken the collagen structure over time.

Cortisone injections should be mentioned in this context as well. For years, cortisone was a first-line treatment for tendon pain. We now know that cortisone injections are clearly harmful to tendon tissue. They may temporarily reduce pain, but they weaken the collagen structure and impair healing over time. A single, well-timed cortisone injection may occasionally be useful when pain is so severe that someone simply cannot begin a loading program at all. In that narrow circumstance, reducing pain enough to start rehab can be a reasonable choice. But it should be a considered decision, not a reflexive one, and it should not be repeated casually.

For a more in-depth discussion about how metabolic health connects to the health of our musculoskeletal system as a whole, including the research on AGEs, insulin resistance, and hormone effects, read this article. And for more information specific to the effects of our metabolic health on our tendons, this piece covers it in detail.

The Elbow

Lateral epicondylitis, or tennis elbow, is one of the most common tendon problems I see. And one of the most frustrating things for people is that it tends to stick around for a long time. Tennis elbow can interfere with gripping, lifting, and even holding a coffee cup.

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The tendons on the outside of your elbow, the common extensor origin, are the ones that let you extend your wrist and fingers and stabilize your grip. Every time you grip something, those tendons are working.

What I see in the office is people who’ve already tried bracing, ice, and rest, and they’re still not better. That’s because those approaches don’t rebuild capacity. The elbow tendons need progressive loading just like any other tendon. Wrist extensions with a light weight, eccentrics, slow heavy resistance, all following the same principles we discussed above.

I wrote a full article on elbow tendinopathy that covers the anatomy, the common mistakes, and what actually works. You can read it here.

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The Hip

Pain on the outside of the hip is incredibly common, especially in women over 40. People often think it’s bursitis. Sometimes that’s part of the picture, but more often the primary problem is gluteal tendinopathy, meaning the tendons of the muscles that stabilize your pelvis when you stand on one leg are upset.

The gluteal tendons have a unique challenge. Like all tendons, they need tensile loading, the pull of muscle contraction, to stay normal and healthy. But the gluteal tendons are also subject to compressive loading. That compression can be a provocative factor in gluteal tendinopathy. Think of a rope draped over the edge of a rock. That’s what happens to the gluteal tendon, where it wraps around the bony prominence on the outside of your hip, called the greater trochanter. Certain hip positions substantially increase this compression. Crossing the leg across the body, what we call adduction, presses the tendon harder against that bone. Standing with the hip dropped to one side does the same. Sleeping on the affected side can compress the tendon for hours.

This is why position modification is so important in the treatment of gluteal tendinopathy. It’s not just about progressively loading the tendon, though that remains essential. It’s also about reducing the compressive irritation that keeps aggravating it. Stretching our gluteal tendons has been proven to worsen our pain. Avoiding prolonged crossed-leg sitting, maintaining a mindful standing posture, and using a pillow between the knees at night can all help minimize compressive loading.

The loading program for gluteal tendinopathy focuses on hip abduction strengthening, the movement of taking your leg out to the side, and the muscles that control your pelvis in a single-leg stance. Standing, side-lying, and eventually single-leg exercises all have their place in the progression.

I wrote an entire post about gluteal tendinopathy. I included several exercises and shared videos showing how to perform them. My full article on lateral hip pain is here.

The Shoulder

The rotator cuff is a group of four tendons that stabilize the ball of the shoulder in its socket. As we age, these tendons undergo degenerative changes just like tendons everywhere else in the body, because they’re subject to the same metabolic, hormonal, and loading factors we discussed earlier.

For years, many surgeons blamed a bone spur for the symptoms of cuff tendinopathy. But current evidence suggests that intrinsic tendon degeneration explains most cases of rotator cuff tendinopathy, and rehab remains the first-line treatment regardless of imaging findings. Removing these bone spurs is no longer considered beneficial… even though the procedure is still commonly performed… go figure.

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Over 90% of people aged 40 or older have a rotator cuff abnormality on MRI. So do not expect your MRI result to say “normal”. Studies have also found full-thickness rotator cuff tears on imaging in roughly a quarter of people over 60 who have no shoulder pain at all. Many of the changes on our MRI’s are age-appropriate. And many rotator cuff tears do not require surgery.

So when you get an MRI, and it shows a rotator cuff tear, that finding alone doesn’t necessarily explain your pain. It might. But it also might be an incidental finding. Context matters. Your symptoms, your functional limitations, your response to loading, all of that matters far more than the image on the screen.

For most people with rotator cuff tendinopathy, a progressive loading program targeting the rotator cuff and scapular stabilizers is the most effective treatment. Surgery has its place for acute traumatic tears or for people who’ve truly failed an extended, well-designed rehab program. But the majority of people I see with shoulder pain related to the rotator cuff improve with loading.

My full article on shoulder tendinopathy and rotator cuff pain is here.

The Bigger Picture

If you’ve read this far, you’ve probably noticed a theme. It doesn’t matter whether we’re talking about the elbow, the hip, or the shoulder. The underlying story is remarkably consistent. Tendons that have lost capacity, either through underuse, overuse, metabolic compromise, hormonal change, medication effects, or simply the passage of time, eventually reach a point where normal activities exceed what they can handle.

Tendons don’t have the blood supply of muscle. They don’t adapt as quickly. A good tendon rehab program typically takes at least 12 weeks to see meaningful change, and for many people it’s much longer than that. This can be frustrating when you’re in pain and just want to feel better. I get that. But I’ve watched hundreds of patients go through this process, and the ones who commit to the loading program, who respect the timeline, who address their metabolic health simultaneously... they get better. Consistently.

We are all aging. We are all accumulating years of metabolic history. None of us can avoid the hormonal shifts that come with time. But we can load our tendons wisely, manage our blood sugar, address hormonal deficiencies when appropriate, and avoid the trap of thinking that rest is the answer to every ache. Your tendons are adaptable. They want to be loaded. They respond to progressive challenges at every age, as long as we give them the metabolic and hormonal support they need to do their job.

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The Full Reading List

If you want to go deeper on any of these topics, here are all the tendon posts I’ve published, in the order I’d recommend reading them:

1. Painful Tendons Want Load, Not Rest

2. Tendon Health Part 2: When Tendons Meet Metabolism

3. The Not-So-Hidden Links Between Metabolic Health and Tendon Pain

4. Why Does My Elbow Hurt So Much?

5. Why the Outside of Your Hip Hurts

6. Why Does the Outside of Your Shoulder Hurt?

I’ve talked a lot about the emergence of our current high-tech, low-touch healthcare environment. Visits are shorter. Fewer patients are being examined. These brief office conversations are also often built around the imaging report, perhaps with a sense of dread or urgency, and the assumption that surgery is the natural endpoint. That’s not how the conversation should go. Let’s get into this…

Rotator cuff issues are omnipresent with age. So this is one of the office conversations I have most often, and I thought it was worth writing about. As routine visits to orthopedic surgeons approach 8-10 minutes and often utilize a PA or NP, it is important that you know the pathology and options going into the conversation.

What Is The Rotator Cuff?

The rotator cuff is not a single muscle or tendon. It is a group of four small muscles that sit around the head of the humerus, the upper arm bone, and that work together to control how the arm moves at the shoulder. The four muscles are the supraspinatus on the top, the infraspinatus and teres minor on the back, and the subscapularis on the front. Each one originates on the scapula, the shoulder blade, and inserts into the head of the humerus through its own small tendon

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These muscles are small. The job of the rotator cuff is not, mostly, to move the arm. The power to move the arm is produced by the deltoid, lats, and pec muscles… the larger muscles that sit over the shoulder, chest, and back. The job of the rotator cuff is to keep the head of the humerus centered in the socket while the deltoid is doing the lifting, to fine-tune the position of the arm, and to provide the rotational control that lets you reach overhead, behind your back, and across your body. The cuff is the stabilizer. The other muscles are the engine.

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That distinction matters because it explains why almost all partial cuff tears or even most “full-thickness” defects are often compatible with full or nearly full arm shoulder function. The rotator cuff does not lift the arm. Well, it does a little, but it mostly controls the motion produced by other muscles. As long as the centering and rotational control are adequate, the arm can function well even when the cuff is not pristine or a tear is present. And since 90+% of people over 40 have rotator cuff abnormalities on MRI, that’s good. Read that again… 90+% of people have MRI abnormalities on their scan. So if you go see an Orthopedic Surgeon for shoulder pain, you should not assume that an abnormal MRI finding is…well, abnormal.

Continuity Is Not Required For Function

One of the most important and most underappreciated facts in shoulder medicine… A rotator cuff does not need to be in one continuous piece to do its job. The cuff is a load-bearing system, not a single rope (it doesn’t have a single point of failure), and it depends on an internal structure most patients (and many surgeons) have never heard of.

A little physics lesson… and it might save you from an unnecessary operation. In the early 1990s, the orthopedic surgeon Stephen Burkhart described what he called the rotator cable, a thick bundle of fibers that runs across the shoulder like the supporting cable of a suspension bridge. The rotator cable spans the insertions of the supraspinatus and most of the infraspinatus tendons and carries most of the load that the cuff transmits when the arm is used. Inside the cable, in the rotator crescent, the tissue is thinner and bears very little load. The cable is roughly 2.5 times as thick as the crescent it surrounds. The crescent is, in a real sense, stress-shielded by the cable. That means that there’s very little tension in the crescent… all the tension is borne by the cable.

The clinical implications of this on the integrity of the crescent area are huge. The supraspinatus tendon, the one most commonly described as ‘torn” on imaging reports, lies entirely in the rotator crescent. When the supraspinatus develops a defect, the load on the shoulder doesn’t change because the force in that region is distributed by the cable. The “tear” on the imaging report is often a region of the crescent that has gradually thinned due to stress shielding and developed a defect under the protection of the cable. The cable itself is intact, the load path through the shoulder is intact, and the arm continues to function normally.

This is the suspension bridge concept. The defect described by the MRI is often in a stress-shielded area, and its function depends on the cable system, which the MRI report does not even mention. If the rotator cuff doesn’t see stress or strain, it atrophies and disappears over time. That’s why most of these defects… not tears… occur. Tearing is not the right word. Tearing implies trauma… and very often there’s no trauma involved. Sure, you might have lifted something and felt a pop, but that was the straw that broke the camel’s back— it’s not a traumatic rotator cuff tear. Let’s dive deeper into this… It’s important.

Most Cuff Tears Are Not Tears In The Way You Think

The word tear implies an acute event. Something rips. Something breaks. The implication is that there was a before and an after, that something happened to produce the defect, and that the defect needs to be repaired.

That is not what most rotator cuff tears actually are.

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Pain on the outer side (lateral) of the shoulder is one of the most common reasons people come to see me. Lifters get it. Swimmers get it. Pickleball players get it. People who have never set foot in a gym get it. It can creep up gradually or appear after what seems like a minor change in activity.

Sleeping on that side becomes uncomfortable. Reaching into a cabinet feels different. Putting on a jacket demands more attention. Lifting a suitcase into the overhead bin produces a sharp reminder that something is wrong.

For decades, we called this bursitis. And everyone got injections for it. Lots of injections. But were we treating the right pathology? Often, no. And over time, repeated injections can weaken tendon tissue. So let’s walk through why lateral shoulder pain is so common and how to manage it properly.

The bursitis label stuck because it was simple. There is a bursa in the shoulder. If the area hurts, the bursa must be inflamed. And, to be fair, sometimes it does hurt. But most often the pain from the bursa is due to irritation from the actual primary pain generator.

Much like we once blamed bone spurs for shoulder pain (they’re not), we now understand that the rotator cuff tendons are far more often the primary issue. The bursa frequently reacts secondarily to an overloaded tendon.

What we have learned over the last twenty years is that lateral shoulder pain is most often due to rotator cuff disease- tendinopathy, partial or full thickness tear. Most often, not always. And no… impingement is a dead theory, too. Bone spurs very rarely are the cause shoulder pain.

Yes, there are other causes like calcium deposits, or a frozen shoulder… but they are far less common than rotator cuff related shoulder pain.

The supraspinatus is commonly involved, but the infraspinatus and other cuff tendons may contribute. Once you recognize this as a tendon capacity issue rather than an isolated inflammatory problem, the pattern becomes familiar. In fact, it behaves very much like gluteal tendinopathy at the hip.

As I discussed recently, nearly 100% of people over 40 have rotator cuff abnormalities on their MRI. While the abnormalities on MRI are common, pain from them is less common. Why do some hurt and others with the same abnormalities have no pain? Great question… modern medicine can’t answer that yet. Except that, your metabolic health- insulin resistance, type 2 diabetes, menopause can all affect how prone our tendons are to pain and inflammation.

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Like the gluteal tendons in the hip regions, the rotator cuff can be a troublemaker:

• Both can keep you up at night.

• Both can make everyday activity miserable.

• Both can hurt intensely without a significant tear.

• Both can show tears on imaging and not cause much pain.

• Both struggle when the load exceeds capacity.

• Both respond best to progressive strengthening.

• Both can be affected by your metabolic health.

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What these tendons actually do

The rotator cuff tendons attach around the humeral head. Their job is not simply to lift the arm. Their primary function is stabilization. They center the ball in the socket while larger muscles move the arm.

That means they are working constantly. Every time you reach forward, press overhead, push open a door, type with unsupported arms, or carry groceries, the cuff is firing to maintain joint control. And the rotator cuff muscles are far smaller than the large muscle groups that give us the power to move the shoulder. Over time, they can overpower the cuff and lead to an overuse tendinopathy that causes pain.

When the strength or resilience of the rotator cuff declines, but life continues to demand the same output, they protest. And sometimes that protest can be very loud. If you’re perimenopausal, diabetic or have thyroid disease, your shoulder is particularly prone to being cranky.

How lateral shoulder pain typically presents

The pattern is remarkably consistent. People report pain on the outside of the shoulder, often radiating toward the upper arm but rarely below the elbow. Sleeping on that side can be miserable. Reaching overhead or behind the back aggravates it. Lifting something away from the body becomes uncomfortable. Putting on a jacket or reaching into the back seat of the car becomes quite a challenge.

What often surprises patients is that there wasn’t a dramatic injury. No pop. No fall. No obvious moment of failure. Just a gradual increase in irritation until normal life activities began to feel very abnormal. That is how tendinopathies typically behave. Tendons tolerate what they are accustomed to. If that load changes or capacity declines, they become sensitive. Most of the adult joint pain that I see in the office was not accompanied by or initiated by an injury.

There are many reasons why that capacity might change. Activity may increase. Strength training may fade over time. Time sitting accumulates far too much. Our metabolic health shifts. Your metabolic health, the presence of metabolic disease, menopause and hormonal issues such as thyroid disease play a major role. Insulin resistance, elevated uric acid, and systemic inflammation influence tendon resilience in ways we are still learning to quantify.

None of this should be mysterious, yet it is. Like our cars and homes, our tissues require maintenance. When they are not asked to adapt and are exposed to an unfavorable metabolic environment, they lose the ability to tolerate normal load. Then comes the spring cleaning, or the need to shovel snow, or paint a room and a day or three later the shoulder begins to protest.

Why the bursitis story lasted so long

Because bursae exist, and they can become irritated. But when researchers began looking more carefully, isolated bursitis was relatively uncommon. Much more frequently, the tendon showed degenerative changes or signs of overload, with the bursa reacting secondarily.

In most cases, the bursa is not the primary problem. It is reacting to an unhappy neighbor- the rotator cuff.

A bone spur was blamed for lateral shoulder pain for decades. It still is. Despite little evidence. It’s strange to me that we still blame it. We get tendinopathy throughout our body and bone spurs are never mentioned. Yet, tendon pain in the shoulder was blamed on a bone spur?

What imaging shows—and why it scares people

MRI reports often sound alarming. Tendinosis. Partial tearing. Full-thickness tear. Degeneration. Fluid in the bursa. It can read like a structural disaster. But wait ;-).

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Imaging does not tell the whole story.

A recent population-based MRI study published in JAMA Internal Medicine examined adults between 41 and 76 years old and performed bilateral shoulder MRIs regardless of symptoms. Nearly every participant had a rotator cuff abnormality on imaging. These findings were present in the vast majority of people with pain and in nearly the same proportion of people without pain .

That is a critical point. Structural changes are extremely common after forty. Many so-called abnormalities represent normal aging rather than a clear pain generator. The presence of a tear on MRI does not automatically explain your symptoms.

Some people with dramatic imaging findings function well. Others with modest findings are very uncomfortable. The scan is information. Nothing more. It does not predict whether you will or will not have pain.

What the physical exam tells us…

A careful physical exam usually provides more practical guidance than the MRI. Pain with resisted abduction or external rotation, weakness in specific patterns, and altered scapular control often reveal the underlying issue. Cervical spine problems can also mimic lateral shoulder pain, so a neurological exam remains important.

In many cases, the exam clarifies what the scan cannot. Furthermore, a frozen shoulder may sound like a rotator cuff issue when we’re talking to you. And imaging may not see the classic changes associated with it… therefore, if you are not examined, a diagnosis of a frozen or stiff shoulder cannot be made.

Why rest rarely fixes it

It is natural to assume that if something hurts, it needs rest. A brief reduction in aggravating activities can be helpful early on. But prolonged rest almost always lowers tendon capacity further and exacerbates the issue at hand.

In the article I have linked to below I went into terrific detail about the changes that take place in the tendon to cause these issues and discomfort.

If rest becomes the primary strategy, the shoulder becomes less prepared for normal life demands. When lifting or overhead activity resumes, the same problem returns.

This is why so many people feel temporarily better, only to have symptoms recur.

For Members: What follows is a deep dive into the treatment protocols… including videos for the rehab portion, sleeping tips, and injection options.

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Sleeping on that side becomes uncomfortable. Long walks feel different. Stairs suddenly hurt a lot and demand much more attention. Getting in and out of the car produces that sharp reminder that something is wrong.

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For decades, we called this bursitis. And everyone got injections for it. Lots of injections. But were we treating the right pathology? No. And over time, injections can worsen the pathology. Let’s dive into why lateral hip pain is so common and how to manage it.

The bursitis label stuck. It was easy to say, easy to understand, and it made intuitive sense. There is a bursa on the outside of the hip, and if the area hurts, the bursa must be inflamed.

Except that usually isn’t what’s really going on. Much like shoulder pain used to be blamed on bursitis or a bone spur. We now know it’s usually the rotator cuff that started the process.

What we have learned over the last twenty years is that the problem is far more often the gluteal tendons—most commonly the gluteus medius and minimus. We have three gluteal muscles. The gluteus maximus is not usually involved in this. Once you understand that it’s primarily a tendon disorder, the condition begins to look very familiar. In fact, it behaves a lot like the rotator cuff in the shoulder.

• Both are troublemakers.

• Both can keep us up at night.

• Both can make everyday activity miserable.

• Both can hurt intensely without a tear.

• Both can show tears on imaging and not cause much pain.

• Both struggle when the load exceeds capacity.

• Both respond best to progressive strengthening. Not rest!!

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What these tendons actually do

The gluteal tendons attach to the outside of the femur at a bony prominence called the greater trochanter. Their job is simple but relentless: they stabilize your pelvis when you stand on one leg. They keep your pelvis level.

Which means they are working every time you walk. Every step.

If you walk a mile, that’s roughly two thousand repetitions of single-leg support. Add stairs, uneven ground, carrying groceries, chasing grandchildren, getting out of a chair, and you start to appreciate how busy these tendons are.

When their strength or resilience declines, but life continues to demand the same output, they protest.

How lateral hip pain typically presents

The pattern is remarkably consistent. People report pain on the outside of the hip. It’s tender to touch. Lying on that side can be miserable. Longer walks or hills tend to aggravate it. Sometimes the discomfort radiates down the outside of the thigh, but rarely below the knee.

What often surprises patients is that there wasn’t a dramatic injury. No pop. No fall. Just a gradual increase in irritation until normal life activities began to feel abnormal. This is a very common presentation for tendinopathies. No, you didn’t sleep the wrong way on them one day. Our tendons get used to doing what they do day in and day out. That’s the amount of load they can handle. If that load starts to change, they will begin to protest- sometimes loudly.

There are many other reasons why our tendons might start to bother us. Menopause, poor metabolic health, elevated uric acid are relatively common causes. I discussed how our metabolism influences our tendon health in the following article.

Why the bursitis story lasted so long

Because bursae exist, and they can become irritated. But when researchers and surgeons began looking more closely, they found that isolated bursitis was relatively uncommon. Much more frequently, the tendon showed “degenerative” changes or signs of overload, with the bursa reacting secondarily.

In many cases, the bursa is not the primary problem. It’s reacting to unhappy neighbors.

What’s actually happening inside the tendon

Most of the time, this is not a raging inflammatory process. It is a capacity mismatch.

The tendon is being asked to tolerate more than it is currently prepared for.

That mismatch can develop for many reasons. Activity may have increased. Body weight may have changed. Strength training may have faded away over the years. Gait can shift. Time sitting accumulates. Previous injuries alter mechanics.

Sometimes, the only real change is that we stopped preparing the tissue for what daily life requires. Reason 1245 to be in a gym.

Who gets lateral hip pain?

I see it most in midlife and beyond, and more often in women. Deconditioning plays a role. Rapid changes in walking or running volume play a role. Years of avoiding strength work play a role. Menopause, type 2 diabetes, fatty liver, elevated uric acid, and many other confounding issues almost certainly play a role too.

None of this should be mysterious. Our tissues require maintenance. When tissues are not asked to adapt and are exposed to inflammatory mediators or lack the hormones that protect them, they lose the ability to adapt.

What imaging shows—and why it scares people

MRIs frequently look dramatic. Words like tendinosis, partial tearing, degeneration, and fluid in the bursa. It can read like a disaster report.

But we’ve learned the same lesson here as with the rotator cuff: imaging findings and pain intensity often do not correlate well. Some people with ugly scans function quite well. Others with modest findings are very uncomfortable.

The scan is information. Nothing more. It doens’t predict whether you will or won’t have pain.

What the exam tells us

A careful physical exam usually gives the diagnosis away. Standing on one leg often reproduces pain. Resisting abduction hurts. Pressing over the tendon is tender.

In many cases, the exam provides more practical guidance than the MRI. Lateral hip pain can also be caused by lumbar spine issues. So a careful exam will include a neurological exam as well.

Why rest rarely fixes it

People naturally assume that if something hurts, it needs rest. A brief reduction of irritating activity can be helpful early on. But absolute rest is virtually never needed. I go into far more detail in this highly relevant post on tendon pain.

If rest becomes the primary strategy, the tendon’s capacity continues to fall. Then, when you resume walking or climbing stairs, the same problem recurs.

This is why so many people feel better temporarily, only to have the pain return.

What about stretching?

This surprises people. When something hurts, our reflex is often to stretch it. We assume the muscle is tight and needs to be lengthened. With gluteal tendinopathy, that approach frequently backfires. This has been studied a lot. Gluteal tendinopathy symptoms often worsen when these tendons are stretched.

Deep hip stretches—especially crossing the leg, pulling the knee toward the opposite shoulder, or dropping the hip into adduction—increase compression of the tendon against the bone. Remember, compression is one of the main things that irritates this tissue in the first place.

So instead of calming it down, aggressive stretching can keep the tendon sensitive.

This doesn’t mean flexibility is bad or that the hip should never move through these positions again. It means that in the irritated phase, repeatedly compressing the tendon is usually not helpful.

Early on, strength and controlled loading tend to outperform stretching.

As tolerance improves and the tendon becomes more resilient, those movements can gradually return.

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What actually helps

Eventually, treatment almost always comes back to load. And we usually need far more load than you think. Tendons are strong. They require a lot of load to convince the tendon tissue to reorganize and heal. And this is also a very long process. It can take 3-8 months, or longer, for progressive loading to resolve severe cases of gluteal tendinopathy.

Appropriate, progressive loading.

Tendons remodel in response to demand. They get stronger when asked, gradually, to do more.

This is where physical therapy shines, especially when the program is thoughtful and progresses over time rather than stopping at the first sign of improvement. And clamshells with a band will never be enough. Not even close. You might start there… but you should progress beyond them rapidly.

Early exercises might be simple. Side-lying raises. Clamshells. Supported movements. As tolerance improves, we work toward more functional challenges, such as step-downs, carries, and single-leg deadlifts.

The treatment of gluteal tendinopathy will require load. Different types of loads and exercises. The following sections will dive deep into how we approach loading this area appropriately. Including work you should do to avoid lateral hip pain in the future.

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Summary:

• Frozen shoulder isn’t mechanical. It’s metabolic dysfunction showing up in your shoulder capsule.

• Perimenopausal women have 99% higher odds of developing it—estrogen loss removes the brake on inflammatory scarring pathways.

• Diabetics get it 5x more often, and their frozen shoulder often doesn’t fully resolve. AGEs (advanced glycation end products) permanently stiffen collagen.

• The diagnostic trap: MRI shows a “cuff tear,” you get surgery, then your shoulder gets worse. The tear was incidental—the real problem was inflammatory, not structural. Many people have surgery for an MRI finding, when the problem was a frozen shoulder.

• Early intervention (first 1-2 months) can prevent months or years of disability. Most people wait too long. We get into this… super important.

• Your musculoskeletal system is an end-organ of metabolic disease, not just infrastructure that wears out with age. We dive deep into the science of why this happens.

• I conclude with the tips and guidance on what I would do if I had a frozen shoulder.

ICYMI:

Heart rate training isn’t about going as hard as possible—or staying easy forever. Most people train at the wrong intensity because they don’t understand what’s actually happening inside their cells at different heart-rate zones. This post breaks down why low-HR work builds the base that protects your joints, metabolism, and recovery—and why small, intentional doses of intensity matter more as we age. If Zone 2, fat burning, and “train harder” advice have left you confused, this is a good place to start.

HRV has gone mainstream—but most people either overreact to it or ignore what it’s actually telling them. This post explains what heart rate variability really measures, when it’s useful, when it’s just noise, and how to interpret trends without obsessing over daily numbers. If your watch, ring, or app is leaving you confused about recovery, stress, or readiness to train, this is a good place to reset your thinking.

A frozen shoulder—adhesive capsulitis, is one of those conditions that sounds benign until you’ve experienced it. They can be miserable. The medical term doesn’t capture the reality: a very painful shoulder that progressively loses motion until sleeping, reaching into the back seat of your car, or fastening a bra becomes excruciating, if not impossible. This is a far more complex issue than even most Orthopedic Surgeons know. Let’s get into it…

It affects at least 2-5% of the general population, but jumps to 10-36% in people with diabetes, and is significantly more prevalent in perimenopausal women… so common in some Asian countries it’s simply called “fifty-year shoulder.” The pattern is consistent: ages 40-65, women more than men, strong associations with metabolic and hormonal conditions.

For decades, we treated this as a mechanical problem. Inflammation, fibrosis (scarring), stiffness, and eventual resolution. But that framework never explained why certain people develop it, and others don’t. Why does a minor shoulder tweak in one person resolve in days, while in another it triggers months or years of disability?

Let’s Meet Sarah…

Sarah is 52, a runner and avid gardener. She’s navigating perimenopause—irregular periods, some sleep disruption, nothing she can’t manage. Three months ago, she tweaked her shoulder lifting a suitcase into an overhead bin. It hurt, but not dramatically. She iced it, took some ibuprofen, and moved on with her life.

Two months later, she couldn’t lift her arm high enough to blow-dry her hair. Reaching behind her back was impossible. The pain at night was severe enough to wake her. Simple movements like grabbing something off a high shelf or pulling on a jacket became agonizing.

Her primary care doctor ordered an MRI. It showed a small partial-thickness rotator cuff tear. Nothing terrible, but there it was. The orthopedic surgeon she was referred to recommended arthroscopic repair. “We’ll clean that up, get you back to normal,” he told her.

Three months post-surgery, Sarah’s shoulder is worse than before the operation. Much worse. She can barely move it.

What actually happened? Sarah had a frozen shoulder brewing before she ever had surgery. The MRI finding was a red herring—an incidental “tear” that wasn’t causing her problems. The surgery, with its necessary post-operative immobilization and inflammatory response, poured gasoline on a fire that was already burning.

What Actually Triggers Frozen Shoulder?

The latest research points to alarmins—molecules such as HMGB1 (high-mobility group box 1) and other damage-associated molecular patterns as the initial triggers. These are danger signals your body releases when tissue gets injured, even from minor trauma.

In a metabolically healthy person, that minor shoulder tweak heals normally. The alarmins trigger controlled inflammation and tissue repair, and everything resolves. But in someone who’s metabolically primed—diabetes, perimenopausal estrogen depletion, thyroid dysfunction—something different can happen.

These alarmins bind to RAGE—the receptor for advanced glycation end products. RAGE is upregulated in states of chronic low-grade inflammation. When activated, it triggers the NF-κB pathway, unleashing an inflammatory cytokine cascade: interleukin-1, interleukin-6, tumor necrosis factor-alpha, and critically, transforming growth factor-beta (TGF-β).

TGF-β drives fibroblast proliferation and differentiation into myofibroblasts (that produce scar tissue). These contractile cells produce excessive collagen (particularly type III) and are mechanosensitive… meaning that mechanical stress activates MAP kinases through β1-integrin receptors, which further amplifies cytokine (inflammation) production. The process becomes self-perpetuating. Move your shoulder, and you stimulate more inflammation. The more fibroblasts differentiate, the more the capsule contracts and thickens.

This explains the characteristic progression: initial injury, a lag period of a month or two as the inflammatory cascade ramps up, then progressive “freezing” as the capsule becomes increasingly fibrotic (scarred) and contracted.

Why Perimenopause?

The connection between frozen shoulder and perimenopause is mechanistic. Recent research has identified the specific pathway.

Estrogen receptors are present throughout the shoulder’s connective (collagen-containing) tissues—capsule, ligaments, and surrounding structures. Research published in 2025 showed that estrogen acts through GPER (G protein-coupled estrogen receptor) to suppress the PI3K/AKT signaling pathway. This suppression prevents fibroblast activation and blocks progression to fibrosis.

During perimenopause, estrogen doesn’t just decline; it can fluctuate wildly and ultimately crash. When estrogen drops, you lose GPER activation. Without GPER suppressing PI3K/AKT, fibroblasts proliferate freely and differentiate into myofibroblasts. You also lose estrogen’s anti-inflammatory effects and its protective influence on collagen metabolism.

The Duke Health study found that postmenopausal women not receiving hormone replacement therapy had 99% greater odds of developing a frozen shoulder compared to those on HRT.

Estrogen also influences muscle tone and coordination around the shoulder joint. Declining levels can cause subtle changes in muscle function and joint mechanics that may contribute to that initial “innocuous” injury.

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• Tendinopathy is the leading cause of tendon pain, a broad term encompassing failed adaptation, structural changes, and associated pain.

• Causes include abrupt load increase, repetitive cycles, compression + tension, intrinsic tissue limitations, and failed repair responses.

• Rest alone is never sufficient. Tendons need load to remodel and regain capacity.

• A smart rehab progression moves from isometrics to strength loading. Tendons eventually require heavy loads to heal.

• Prevention is as important as treatment.

Tendon-related pain is exceptionally common. I see more people in the office for tendon pain than for any other issue. Most of these “injuries” are self-inflicted, either from doing too little or too much.

And although I’m biased… this is a very good, in-depth overview of why our tendons hurt and how to treat them. I can guarantee you that most (including doctors) do not understand these principles.

Tendons adapt to load. They require a load to be healthy. But how that load is applied matters.

When someone says, “My tendon hurts,” it helps to pause and think: why?

Many people reflexively say “inflammation” and “tendinitis,” but tendinitis is actually rare in adults.

Tendinopathy is a far more common cause.

Let me explain.

Why Tendons Hurt — Tendinitis vs. Tendinopathy

“Tendinitis” suggests inflammation: swelling, redness, infiltration by immune cells… a classic “itis.” That model works in cases of acute overload or acute tears. However, chronic tendon pain rarely exhibits a strong inflammatory cell presence under the microscope.

Instead, it tends to show disorganized collagen near its attachment to bone, microruptures, increased ground substance (which I’ll explain), excessive vascular and neural (including pain) ingrowth, and “degenerative” changes. I hate using the term degeneration… but it’s relevant.

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Now… many of you have probably had MRIs that have shown evidence of tendinopathy. Most people with tendinopathy have no pain. But some people with tendinopathy have terrible pain.

We’re not always sure why that happens. However, towards the end of this article, I delve into the common training errors. (or lack of training) that can lead to painful tendons.

When we biopsy or examine tendons in chronic painful states, traditional inflammatory markers (neutrophils, massive inflammatory cell infiltrates) are often absent or minimal.

That doesn’t mean that inflammatory mediators (cytokines, signaling molecules) aren’t involved, but the concept of a purely “inflamed tendon” fails to capture what’s going on.

Thus, the preferred term is tendinopathy. This captures the broader idea: pain, dysfunction, structural changes, failed adaptation, partial degeneration.

It does not assume that inflammation is the sole culprit, but rather allows for variable contributions from multiple processes.

Tendinopathy means the tendon is not adapting well to load. Alternatively, it may be failing due to the absence of a load. In tendinopathy, the tendon is struggling. It may have microdamage, disordered collagen, and zones that are less capable of repair.

Pain and structure don’t always align: sometimes a tendon “looks bad” but causes no symptoms, while sometimes pain is present despite mild changes. So we must treat the person, not just the MRI or ultrasound images.

For Members, I dive into the details of why common tendinopathies, such as tennis elbow, achilles tendinopathy, patella tendinopathy, and rotator cuff tendinopathy, occur, and how to manage them.

And, no, the treatment is not simply rest. It’s never rest. Furthermore, since prevention is the most effective strategy, the final section provides robust guidelines to follow to minimize the risk of tendon issues.

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