Greater Trochanteric Pain Syndrome

Hip & Groin

Overview

Greater trochanteric pain syndrome (GTPS) is the current preferred term for lateral hip pain arising from the peritrochanteric structures - principally gluteal tendinopathy and trochanteric bursitis. It replaces the older "trochanteric bursitis" term, which incorrectly implied bursal inflammation as the primary pathology. Current evidence shows gluteal tendinopathy (particularly of gluteus medius and minimus) is the primary driver in most cases, with bursitis often a secondary or incidental finding. GTPS is common, especially in women aged 40-60, and is the commonest cause of lateral hip pain. It is frequently misdiagnosed as hip OA or lumbar referred pain and commonly coexists with both, particularly in older patients.

Anatomy & Pathophysiology

The greater trochanter is the lateral bony prominence of the proximal femur, serving as the attachment site for the gluteal tendons and surrounded by several bursae.

Key structures:

  • Gluteus medius is the primary hip abductor, inserting onto the lateral and superoposterior facets of the greater trochanter. Its tendon is the most commonly affected structure in GTPS - analogous to the supraspinatus of the shoulder, with GTPS termed the "rotator cuff tear of the hip"
  • Gluteus minimus inserts onto the anterior facet of the greater trochanter and is frequently involved alongside gluteus medius, with a key stabilising role during gait
  • The iliotibial band passes over the greater trochanter. Compression of the gluteal tendons between the ITB and trochanter during hip adduction is a recognised pathological mechanism
  • Trochanteric bursae (the subgluteus maximus / trochanteric bursa) lie between the greater trochanter and the gluteus maximus / ITB. Bursitis is usually secondary to tendinopathy and rarely the primary isolated pathology
Greater trochanteric pain syndrome: gluteal tendinopathy (medius and minimus insertion) is the dominant pathology. Trochanteric bursitis is usually secondary, not the primary diagnosis.

Pathological mechanism - compressive tendinopathy: GTPS is understood as a compressive tendinopathy of the gluteal tendons. The gluteus medius and minimus tendons are compressed against the greater trochanter, particularly during hip adduction (crossing legs, lying on the affected side, hip-hitched standing), single-leg stance, stairs, walking, and running (especially on cambered surfaces). The pathology mirrors rotator cuff tendinopathy - reactive tendinopathy through dysrepair to degenerative tendinopathy, with potential partial or complete tears in older women. Reducing compressive loads is as important as strengthening.

Hormonal factors: oestrogen has a protective effect on collagen synthesis and tendon health. The peak incidence in peri- and post-menopausal women is linked to declining oestrogen levels. In recalcitrant cases in this demographic, discussion regarding HRT with the patient's GP may be a useful adjunct.

Risk factors: female sex (strongest demographic factor), age 40-60, obesity, sedentary lifestyle, rapid increase in walking or running load, contralateral hip or knee pathology, lumbar spine pathology (L5 radiculopathy causing gluteus medius weakness), leg length discrepancy, and previous hip or knee surgery.

Clinical Pearl

GTPS is NOT primarily bursitis - gluteal tendinopathy (gluteus medius with or without minimus) is the primary pathology. Think rotator cuff tear of the hip. The compressive mechanism is central: gluteal tendons are compressed against the trochanter during hip adduction. Reducing compressive loads is as important as strengthening.

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