Greater trochanteric pain syndrome (GTPS) Updated 2026

Clinical synthesis based on LEAP 2018, recent meta-analyses (Bremer 2025, Harding 2024) and landmark reviews (Grimaldi & Fearon 2015, Speers 2017): gluteus medius and gluteus minimus tendinopathy.

1.1. How is this condition defined, who is affected and what are the risk factors?

• Lifetime prevalence : 10 to 25% of the general population experience at least one episode (reviews based on the Segal 2007 and Lievense 2005 cohorts).⁴⁻⁵
• Incidence in primary care : 1.8 patients per 1,000 per year (retrospective Lievense 2005 cohort, n = 164, mean age 55 years, 80% women).⁵
• Female-to-male ratio ≈ 4:1 (Fearon 2013, Speers 2017, Grimaldi 2015) with a peak of incidence between 40 and 60 years, particularly marked after the menopause.¹⁻³

• High BMI : one of the most powerful factors; a markedly increased risk in overweight and obese people (Segal 2007).⁴
• Female sex and age between 40 and 60 years, with a post-menopausal exacerbation (Fearon 2013, Speers 2017).¹⁻³
• Concomitant low back pain : an association documented by several cohorts; GTPS prevalence reaches 20 to 35% in patients referred for lumbar spine surgery (Tortolani 2002).⁶
• Ipsilateral osteoarthritis (hip or knee) (Segal 2007).⁴
• Hip abductor weakness : Allison 2016 (MSSE) shows, in comparison with asymptomatic controls, a significant reduction in isometric abductor strength on the symptomatic side AND on the contralateral side.⁷
• Increased pelvic width and the female Q angle (biomechanics): both promote relative adduction and tendon compression.²

1.2. What happens inside the body, and how does GTPS evolve naturally?

1. Tendinopathy reactive (acute response to overload, non-inflammatory, reversible thickening);
2. Tendon « in disrepair » (dysrepair): a disorganised attempt at healing;
3. Tendinopathy degenerative : advanced structural changes with loss of collagen fibre organisation, neovascularisation and sensory hyperinnervation contributing to pain.

2.1. Which questions should you ask to understand the patient and their history? 🧐

• “Does your pain wake you at night, especially when you sleep on the painful side?” This is answered yes by the majority of patients with GTPS.¹
• “Which activities bring on or aggravate the pain?” Typically: prolonged walking, going up and down stairs, single-leg stance (putting on trousers), sitting with the legs crossed or on a low seat.³
• “Have you changed your activity habits recently?” A rapid increase in walking volume, recent weight gain or a return to sport are typical contexts.¹
• “Where exactly do you feel the pain?” Typically over the greater trochanter, sometimes radiating along the lateral aspect of the thigh without clearly descending below the knee (a discriminating sign versus L5 radiculopathy).⁴
• “Do you have associated low back pain?” A frequent comorbidity, but an essential one to distinguish (see the differential below).

2.2. Which clinical tests should you perform, and which other conditions must you rule out? 🤸

• L4-L5 radiculopathy : pain along the lateral aspect of the thigh that may travel down to the foot, radicular motor deficit, dermatomal dysaesthesia, positive neurodynamic signs (Slump, SLR). Several cases have been reported of a false radiculopathy that was in fact GTPS, and the reverse.⁴
• Hip osteoarthritis : pain rather in the groin, morning stiffness, restricted range (especially internal rotation), positive FADIR test.⁶
• Femoroacetabular impingement (FAI) : a young, athletic patient, predominantly anterior pain, positive FADIR.
• Meralgia paraesthetica : neurological symptoms of burning or paraesthesia in the territory of the lateral femoral cutaneous nerve (anterolateral thigh); Tinel's test over the anterior superior iliac spine is sometimes positive.⁷
• Piriformis syndrome or sacroiliac pathology: posterior buttock pain rather than lateral pain.
• Proximal hamstring tendinopathy : low buttock pain, brought on by prolonged sitting.
• Stress fracture of the femoral neck or of the trochanter (endurance athlete, woman with RED-S, elderly osteoporotic patient): progressive pain of increasing intensity, sometimes with a sudden loss of function.

2.3. Should patients with GTPS be classified, and what is gained from it? 🎯

1. Reactive tendinopathy (often a young adult, recent onset < 6 weeks): pain of rapid onset after overload. Management favours a temporary reduction in load and pain-free isometric exercise. Early heavy strengthening is thought to be harmful.
2. Tendon in disrepair (3-6 months): the intermediate phase; progressive introduction of isotonic exercise without high compressive loads.
3. Degenerative tendinopathy (often > 6 months, in an older patient): an approach based on progressive heavy strengthening (HSR: heavy slow resistance) to improve functional capacity, even if the tendon structure is not restored.

3.1. Where do you start? What is the recommended hierarchy of interventions?

1. First line (always): education + graded exercise. High level of evidence.
2. Second line for cases that resist at 8-12 weeks : extracorporeal shockwave therapy (ESWT, Harding 2024).⁵
3. Third line : corticosteroid injection, only for short-term relief (≤ 6 weeks) while waiting for exercise to take over. Harmful effect on tendon integrity when repeated (Coombes 2010, Lancet).⁶
4. Alternative to corticosteroids : PRP (platelet-rich plasma). Fitzpatrick 2019 (AJSM, RCT n=80) shows an improvement maintained at 2 years, unlike corticosteroids, whose benefit is lost by 6 weeks.⁷
5. Last line : surgery (endoscopic repair of the gluteal tendons, Walker-Santiago 2020) where at least 6 months of conservative management has failed, or where a complete tendon tear is documented.⁸

3.2. What is the place of exercise, and is there a superior approach?

1. Phase 1: pain modulation and decompression (weeks 1-2) :
   • Education on managing compressive positions (see the self-management section) the absolute priority.
   • Abduction isometrics in supine (without compressive load): 30-45 s holds × 4-5 repetitions, 1-2 times a day.
   • Avoidance of positions of prolonged adduction.
2. Phase 2: targeted isotonic strengthening (weeks 3-6) :
   • Single-leg glute bridge (progressing towards 20-30 quality repetitions);
   • Side-lying abduction without letting the thigh drop into adduction, with a resistance band or a light weight;
   • modified “clam shell” without lateral compression;
   • Hip hike (raising one half of the pelvis) in controlled single-leg stance.
3. Phase 3: functional strengthening (weeks 6-12) :
   • Partial single-leg squat with control of pelvis-knee alignment;
   • Controlled step-ups and step-downs;
   • Progressive uphill walking;
   • Heavy slow resistance (HSR) with increasing load for degenerative patients.
4. Phase 4: return to specific activities (beyond 12 weeks) : running, sport, hiking; see chapter 4.

3.3. Manual therapy, shockwave therapy, injections: how effective are they really?

3.4. Beyond the physical: how do you educate the patient and address psychological factors?

• An impairment of conditioned pain modulation (CPM) , a marker of central sensitisation.
• An impairment of psychological health (anxiety, depression, quality of life).
• Raised catastrophising and kinesiophobia scores.

4.1. How do you make the patient an active participant in their own recovery through self-management?

1. Day-to-day management of compressive loads 🧑‍🏫 :
   • Do not cross the legs when sitting;
   • Avoid low seats (knees higher than hips);
   • Standing: spread the weight over both legs, avoid prolonged “hip-hitched” standing;
   • Sleep: prefer the side that is not painful, with a pillow between the knees ; avoid side-lying on the affected side.³
2. Pain monitoring ⚖️ : a simple rule the patient can apply alone: pain during an activity may reach 4-5/10 provided it does not worsen over the following 24 h (adapted Silbernagel model).⁴
3. Adherence to the home programme 💪 : consistency > intensity. A short daily session beats a long weekly session that gets missed.
4. Identifying psychosocial factors 🧠 : recognising one's own catastrophising thoughts or avoidance behaviours; open dialogue with the clinician about movement-related fears.

4.2. When and how do you plan a safe return to sport and to activity? 🏃

1. Restoration of pain-free everyday function : 30 min of walking, pain-free stair climbing, prolonged standing tolerated.
2. Strength and motor control criteria :
   • 20-30 repetitions of the single-leg glute bridge without compensation;
   • 30 s Trendelenburg test with no drop of ≥ 2 cm;
   • Isometric abductor strength symmetry ≥ 90% (dynamometer measurement).
3. Progressive reintroduction of specific loads (a runner, for example):
   • Weeks 1-2: alternating walk/run programme (1 min running + 4 min walking × 5);
   • Weeks 3-6: increase the volume by ≤ 10% per week ⚠️ (the Gabbett 2016 rule: beyond that, injury risk rises);⁶
   • Weeks 6+: introduce only one new variable at a time (hills, speed, surface).
4. Long-term maintenance : 1-2 gluteal strengthening sessions a week for life in at-risk patients (post-menopausal women, recreational runners).

5.1. Pelvic anatomy and biomechanics: why are women more exposed?

• A wider pelvis : the bi-trochanteric distance is on average 5 to 10% greater in women, which increases the lever arm in relative adduction and the tension in the iliotibial band that overlies the gluteal tendons.²
• An increased Q angle (quadriceps angle) : more pronounced dynamic knee valgus during walking, squatting and running, contributing to a hip adduction and internal rotation that compresses the lateral gluteal tendons.
• Femoral neck geometry : mean femoral anteversion 4 to 6 ° greater, which alters the path of the fascia lata over the greater trochanter.
• Relative abductor weakness : the Allison 2016 cohort (MSSE) showed significantly lower isometric abductor strength in women with GTPS than in asymptomatic controls, even on the pain-free side , which suggests a baseline vulnerability before the condition is ever triggered.⁴

5.2. Menopause, oestrogens and tendon health: an unfavourable combination?

• Reduced type I collagen synthesis and increasingly impaired cross-link maturation → a tendon less resilient to compressive loads.
• Altered fibre architecture : disturbed tenocyte turnover.
• Low-grade systemic inflammation (oestrogen deprivation): heightened sensitivity to repeated micro-trauma.
• Changes in body composition : increased abdominopelvic fat mass, frequent weight gain, global muscular deconditioning.

5.3. How do you stratify risk and adapt management?

• 📋 Systematically screen for other tendinopathies : lateral epicondylitis, rotator cuff tendinopathy, plantar fasciitis, all more frequent after the menopause.
• 🦴 Assess bone status (DXA where indicated): in a post-menopausal woman with progressive trochanteric pain, a stress fracture or an underlying bone fragility must be ruled out.
• 💊 Discuss whether to seek a gynaecological opinion for women with menopausal symptoms (HRT, raloxifene, and so on): a shared decision outside the physiotherapy remit.
• 🥗 A metabolic approach : suitable nutrition, sufficient protein, vitamin D, regular physical activity. BMI is one of the two major modifiable risk factors.

6.1. Analysis of a “classic” case: from assessment to resolution

• A woman aged 50 to 65, BMI often > 27, lateral hip pain of insidious onset over several months.
• Night pain when lying on the affected side, pain on climbing stairs, pain on prolonged walking.
• Failure of an initial treatment (NSAIDs, relative rest, sometimes an earlier injection that worked only briefly).
• Physical examination: trochanteric palpation reproduces the pain, positive 30 s single-leg stance, positive FADER.

1. Initial assessment (1 session): history, clinical examination with the test cluster, identification of modifiable risk factors, screening for red and yellow flags.
2. Patient education (built into every session): dismantling the “bursitis” myth, the principles of decompression, position management.
3. Supervised exercise programme over 8 weeks (14 sessions in LEAP): isometric phase → isotonic → functional.
4. Daily home programme alongside it: 10-15 min a day.
5. Reassessment at 6 and 12 weeks : load adjusted to the response, introduction of the return to activity.

6.2. The diagnostic challenge: when GTPS mimics another condition

6.3. A complex case study: the surgically repaired tendon tear

• Woman ≥ 55-65 years with chronic GTPS, conservative failure ≥ 6 months;
• Marked, persistent abductor weakness (positive Trendelenburg) despite rehabilitation;
• MRI showing a high-grade partial or full-thickness tear of the gluteus medius tendon.

1. Focused shockwave therapy : where symptoms dominate but there is no complete tear. The Harding 2024 meta-analysis (Musculoskeletal Care) confirms a significant benefit on pain versus placebo in GTPS.⁴
2. PRP (Fitzpatrick 2019, AJSM) : RCT n=80, superiority at 2 years over corticosteroids for function and pain.⁵
3. Endoscopic tendon repair surgery (Walker-Santiago 2020, systematic review): arthroscopic reattachment of the gluteus medius and minimus. Progressive restoration of strength and resolution of pain in the majority of cases at 1-2 years after surgery, but it demands rigorous post-operative rehabilitation (8-12 months).⁶
4. Special cases after total hip replacement : persistent trochanteric pain after hip arthroplasty → look for a local mechanism (implant impingement, an intra-articular fragment, low-grade infection); do not settle for a diagnosis of “secondary GTPS”.

7.1. When, and to which other health professionals, should you refer?

• Red flags (see chapter 1): recent history of cancer, severe non-mechanical night pain, fever, unexplained weight loss, progressive neurological deficit, high-energy trauma, suspected stress fracture.
• Failure of well-conducted conservative treatment at ≥ 8-12 weeks → see a doctor to discuss shockwave therapy / PRP / imaging / injection.
• Suspected complete tendon tear (major Trendelenburg, marked abductor weakness) → hip MRI + orthopaedic opinion.
• Significant psychiatric comorbidities (major depression, disabling anxiety disorders) → referral to a psychologist or to the GP.
• Suspected systemic disease (spondyloarthritis, rheumatoid arthritis, fibromyalgia) → rheumatologist.
• Progressive, symmetrical bilateral GTPS → full rheumatological work-up.

• The GP : for a short NSAID prescription if needed, test requests, specialist referral.
• Sports physician / rehabilitation physician : for recreational and competitive athletes, shockwave therapy, PRP.
• Rheumatologist : suspected inflammatory disease, rheumatological comorbidities.
• Orthopaedic surgeon : suspected tendon tear, prolonged conservative failure.
• Dietitian / nutritionist : high BMI (one of the major modifiable risk factors).
• Clinical psychologist / pain specialist : kinesiophobia, catastrophising, anxiety and depressive comorbidities, signs of central sensitisation.

7.2. How do you measure outcomes and overcome the barriers to implementation?

• VISA-G (Victorian Institute of Sport Assessment - Gluteal): 8 items, validated specifically for gluteal tendinopathy, with demonstrated responsiveness to change.²
• HOOS (Hip disability and Osteoarthritis Outcome Score): a generic hip measure, 5 subscales (pain, symptoms, activities of daily living, sport, quality of life).
• Numerical Pain Rating Scale (NPRS) 0-10 : simple, validated.
• GROC (Global Rating of Change): the patient's own perceived rating of change (-7 to +7), used in LEAP.
• FABQ (Fear-Avoidance Beliefs Questionnaire): screening for kinesiophobia.

• Present the 3 evidence-based options to the patient: (1) education + exercise (1^st line, long-term success but requires commitment), (2) corticosteroid injection (fast but transient), (3) watchful waiting alone (an option if the acute episode is not very disabling).
• Explain the real figures (LEAP 2018) in language the patient can understand.
• Identify the values and preferences of the patient (do they prefer immediate relief or a lasting solution? Which activities do they want to get back to?).
• Build together the treatment plan, with concrete goals and criteria for reassessment.