Everything you were told to stretch is what is compressing it.

PRP FOR GLUTEAL TENDINOPATHY

Pain on the outside of the hip that makes lying on that side impossible is almost never the hip joint. It is the gluteal tendons, and it is one of the most frequently misdiagnosed problems in musculoskeletal medicine.

It was called bursitis for decades and mostly was not

“Trochanteric bursitis” was the standard label, and the standard treatment was a steroid injection into the bursa. Imaging and surgical series then showed that the dominant pathology is tendinopathy of the gluteus medius and minimus at their insertion on the greater trochanter, with bursal inflammation secondary or absent.

The name matters because it drove treatment. Injecting steroid into a bursa to treat a degenerate tendon relieves symptoms for a couple of months and weakens the tendon — and in this location, where the tendons are already failing, that is a poor exchange. The current term is greater trochanteric pain syndrome, and the underlying problem is a tendon.

Why compression is the key idea

Gluteal tendons fail under compression more than under tension. The iliotibial band runs directly over them, and anything that adducts the hip — bringing the knee toward the midline — presses the band into the tendon and its insertion.

That single mechanism explains the entire symptom pattern, and it explains what to stop doing:

• Lying on the affected side compresses it directly, which is why night pain dominates.
• Lying on the good side lets the painful leg drop across the midline, which compresses it too — a pillow between the knees fixes this.
• Standing hanging on one hip, the classic waiting posture, adducts and compresses.
• Crossing the legs, deep stretching of the ITB, and downhill walking all do the same.
• Stretching the outside of the hip — the instinctive response — makes it worse, reliably, and is the most common self-inflicted error.

Who gets it, and the hormonal reason it is mostly women

This is overwhelmingly a condition of women around and after menopause, and that pattern is a clue rather than a coincidence. Estrogen influences tendon collagen synthesis and tendon stiffness, and the gluteal tendons sit at a site where declining estrogen and increasing compression arrive at roughly the same stage of life.

That hypothesis has actually been tested. A 2 × 2 factorial randomized trial enrolled 132 postmenopausal women with greater trochanteric pain syndrome, randomizing them to menopausal hormone therapy or placebo cream, and to tendon-specific or sham exercise. Every group also received education about avoiding gluteal tendon compression and managing load. Three findings, all useful:

• Everybody improved — at 12 weeks and still at 52 weeks, in every arm.
• Targeted exercise did not beat sham exercise on any outcome. What all four groups had in common was the education about compression and load, which is the strongest available argument that the compression message on this page is the active ingredient rather than the particular exercises.
• Hormone therapy did beat placebo — but only in the women with a BMI under 25, where the difference on the gluteal tendinopathy score reached 20.7 points at 12 weeks (95% CI 10.2 to 31.2) and still measured 16.7 points at 52. There was a significant interaction between the cream and BMI.

That last result is the reason this page exists in the form it does. One terrain variable's effect was gated by another terrain variable. Hormonal status mattered, and it mattered only where the metabolic picture allowed it to. It is the clearest demonstration on this site that these factors are not a checklist to be ticked off individually — they interact, and the interaction is where the result lives. What we measure is on the metabolic health page.

Two boundaries on that. Hormone therapy is a decision for you and the physician who manages it, made on the whole picture rather than on a tendon, and nothing here is a recommendation to start it. And this was one trial in postmenopausal women; it does not describe men or younger women with the same diagnosis.

What PRP contributes

A reasonable indication, and one where the comparison against corticosteroid has been studied directly. A randomized trial of gluteal tendinopathy found PRP superior to corticosteroid at twelve weeks with the advantage maintained at two years — one of the cleaner results in the regenerative literature.

That fits the biology: a degenerate tendon does not need suppression, and steroid injected around already-compromised gluteal tendons has been associated with progression to tearing.

What else it might be

• Hip osteoarthritis — groin pain and lost internal rotation, not lateral tenderness
• Lumbar referral — L4–L5 pathology referring laterally, with a normal local examination
• Gluteal tendon tear — marked weakness and a positive Trendelenburg sign, which changes management
• Sacroiliac pain — posterior rather than lateral

The loading program

Load management first, then strengthening. Removing compression is what stops the tendon getting worse; abductor strength is what stops it recurring.

• Weeks 0–2 Compression removed — pillow between the knees, no crossed legs, no ITB stretching, no hanging on one hip. Isometric abduction holds.
• Weeks 2–8 Progressive abduction strengthening in neutral, avoiding positions that adduct the hip. Side-lying work is introduced carefully because the position itself compresses.
• Weeks 8–16 Loaded single-leg work, step-ups, and gait retraining to stop the pelvis dropping.
• Ongoing Abductor strength maintained indefinitely. This tendon recurs in people who stop.

What has to be true for this to hold

The compression idea above is not background — it decides who this works for. A tendon that is being compressed for eight hours a day will keep failing whatever is injected into it, so the honest entry requirement here is behavioral as much as anatomical.

The person this suits has had lateral hip pain for more than three months, is tender over the greater trochanter, cannot lie on that side at night, and has no findings that point into the joint itself. A steroid injection that helped for a few weeks and then wore off fits the picture rather than arguing against it. And — this is the part that decides it — they are willing to change how they sit, stand and sleep, because the crossed legs, the hip-dropped standing posture and the side-lying without a pillow between the knees are what keep loading the tendon against the bone.

It does not suit a full-thickness gluteal tendon tear with real weakness, which is a structural problem. It does not suit hip arthritis presenting as groin pain, which is treated as hip osteoarthritis. It does not suit referred pain from an untreated lumbar spine, which is why telling the hip from the back comes first. And it does not suit anyone unwilling to address the compression, because the tendon does not care what was injected if the load never changes.

Why it is so often missed

Three things send this diagnosis wrong, and between them they account for years of unnecessary treatment in a lot of people.

The scan finds something else. A hip X-ray in a fifty-five-year-old often shows some degenerative change, and once a report mentions arthritis the lateral pain gets attributed to it. The two coexist frequently and the tendon is usually what hurts.

The word bursitis persists. It is still in wide use, it still prompts bursal steroid injection, and it still frames the problem as inflammation to be suppressed rather than a tendon to be rebuilt.

The advice is backward. Patients are commonly told to stretch the iliotibial band and to foam-roll the outside of the hip. Both compress the tendons against the trochanter, which is precisely the mechanism causing the problem. People who follow that advice diligently get worse and conclude they are doing it wrong.

What tends to work, in order

• Remove compression. Free, immediate, and the single highest-yield step. Sleeping position, standing habits, leg crossing, and stopping the stretching.
• Load the abductors. Isometrics first for pain relief, then progressive strengthening. This is the treatment that changes the trajectory.
• Address the drivers above it. Gait, pelvic control, and the deconditioning that started the loop.
• Then consider injection, where three months of the above has not been enough — and PRP rather than corticosteroid, for the reasons above.
• Shockwave therapy as a further option with its own evidence base.
• Surgical repair reserved for genuine full-thickness tears with weakness.

An injection offered before the first three have been tried is an injection offered too early, and it will be undone by the compression that nobody removed.

What people ask when they cannot lie on that side

Is this bursitis?

Usually not — it is tendinopathy, and the distinction changes the treatment. What we treat.

Why does stretching make it worse?

Stretching the ITB compresses the tendons underneath it. It is the most common self-inflicted mistake. What to expect.

Should I have a cortisone injection?

PRP outperformed corticosteroid at two years in a randomized comparison here. The comparison.

Is my hip joint the problem?

If the pain is in your groin and rotation is limited, possibly. Lateral pain is usually tendon. PRP for hip osteoarthritis.

Related reading

• Hip, SI joint or lumbar spine?
• PRP for hip osteoarthritis
• PRP compared with cortisone
• Recovery timeline
• Am I a candidate?