Hip Pain

Yet hip pain is one of the most frequently mismanaged presentations in musculoskeletal practice, partly because the imaging findings most commonly encountered — degenerative changes, cam or pincer morphology, labral pathology — are poor predictors of pain and disability, and partly because the mechanical factors that drive the most common hip pain presentations are typically remote from the hip itself. The research on this has become increasingly clear over the last decade.

---

Gluteal Tendinopathy: It Is Compression, Not Degeneration, That Drives the Pain

For many years, lateral hip pain was attributed primarily to trochanteric bursitis — inflammation of the bursa overlying the greater trochanter. That model has been substantially revised.

A 2015 clinical commentary by Grimaldi and Fearon established the compression pathomechanics that now underpin clinical management of this condition. [1] The gluteal tendons — gluteus medius and minimus — insert onto the greater trochanter and pass over it in a manner that subjects them to compressive loading from the iliotibial band above. At zero degrees of hip adduction, the ITB exerts approximately 4 newtons of compressive force on the gluteal tendons. At 10 degrees of adduction — the kind of adduction that occurs simply when crossing the legs or allowing the pelvis to drop in single-leg stance — that load increases to 36 newtons. At 40 degrees, it reaches 106 newtons. [1]

The clinical consequence is that the positions and habits most likely to provoke lateral hip pain are not those involving direct contact with the painful area. They are positions that increase hip adduction: sitting with legs crossed, stretching the hip adductors or iliotibial band (which passively increases compressive tendon load), side-lying without a pillow between the knees, and walking with a narrow step width. These are the movements and postures that apply a sustained compressive load to tendons already sensitised by gluteal muscle weakness and altered abductor mechanics.

The landmark LEAP trial by Mellor and colleagues published in the BMJ in 2018 tested this understanding directly. [2] Across 204 participants with MRI-confirmed gluteal tendinopathy, an eight-week education and exercise program — specifically targeting load management and progressive hip abductor loading — was compared to corticosteroid injection and to a wait-and-see approach. At eight weeks, 77% of the exercise group reported global improvement, compared to 58.5% with corticosteroid injection and 29.4% with wait-and-see. At 52 weeks — one year later — the exercise group maintained superiority: 78.6% global success versus 57% for injection and 51.9% for wait-and-see. The advantage of injection had been entirely lost by the twelve-month mark. [2]

Gluteal tendinopathy is managed by progressively loading the gluteal tendons in positions that avoid compressive provocation — beginning with isometric abduction and progressing through kinetic chain loading — not by injecting the area or passively stretching the structures that are already compressing it. → Gluteal Tendinopathy

---

FAI Syndrome: Morphology Is Not Diagnosis

Femoroacetabular impingement — the constellation of cam and pincer morphology, labral pathology, and groin symptoms — is among the most over-imaged and over-interpreted diagnoses in musculoskeletal practice. The imaging findings of cam and pincer morphology are extremely common in the general population and in elite athletes, the majority of whom have no pain. Morphology alone is not a diagnosis.

The Warwick Agreement — an international multidisciplinary consensus statement involving 23 experts from nine countries and five clinical specialties — established a defining principle for FAI syndrome: it requires all three of the following to be present before the diagnosis applies. [3] Symptoms — typically groin or anterior hip pain, often activity-related. Clinical signs — specifically, reproduction of familiar symptoms with hip flexion, adduction, and internal rotation (the FADIR test) combined with restricted range of motion in flexion, particularly internal rotation. And imaging findings — cam or pincer morphology on plain film and/or CT, with or without labral pathology on MRI.

Imaging findings in the absence of corresponding symptoms and clinical signs do not constitute FAI syndrome and do not require treatment. This matters because the rates of asymptomatic cam morphology in the population — particularly in former footballers, hockey players, and anyone who loaded the hip heavily during adolescence when the femoral head is still developing — are high. Imaging-led management of asymptomatic morphology is not supported by the evidence.

The Warwick Agreement was explicit that the available evidence did not, at the time of publication, support surgery over conservative management for FAI syndrome. Hip-targeted rehabilitation — addressing stability, neuromuscular control, strength, and movement — remains the appropriate first-line approach for the majority of presentations. → FAI Syndrome

---

Proximal Hamstring Tendinopathy: A Load and Compression Story

Proximal hamstring tendinopathy is characterised by pain deep in the lower buttock, typically reproduced by sitting on hard surfaces, running — particularly uphill and at speed — and deep forward bending. It is frequently misdiagnosed as sciatica, piriformis syndrome, or lumbar referred pain. The distinguishing feature is localised ischial tuberosity pain, reproduced by resisted knee flexion and hip flexion combined, with a clear relationship to compressive loading at the ischial enthesis.

A 2025 clinical commentary by Rich, Cook, Hahne, and Ford outlines the clinical logic behind structured management. [4] The proximal hamstring tendon is compressed against the ischial tuberosity whenever the hip is flexed — the compressive load increases proportionally with hip flexion angle. Sitting, particularly on hard surfaces, provides sustained compressive load. Running applies cyclic compressive and tensile loads during the late swing phase. Hamstring stretching — the intuitive response to "tightness" in the posterior thigh — directly compresses the ischial enthesis and is contraindicated in the early and middle stages of rehabilitation.

The kinetic chain picture for proximal hamstring tendinopathy is consistent with the broader pattern seen across hip and lower limb conditions: gluteus medius, adductor magnus, and the triceps surae are commonly co-deficient alongside the hamstrings, and addressing the chain — not just the symptomatic tendon — is a core component of rehabilitation. [4] A proximal hamstring tendon that is progressively reloaded in the context of a hip that cannot control adduction and a calf that cannot absorb push-off load is a tendon that will continue to fail its load management. → Proximal Hamstring Tendinopathy

---

The Fascial Thread Through All Three

The gluteus maximus — the primary hip extensor and a critical compressive stabiliser of the sacroiliac joint — is a key anchor point of the posterior oblique myofascial sling, connecting through the thoracolumbar fascia to the contralateral latissimus dorsi. → The Posterior Oblique Sling Gluteal dysfunction therefore affects not just the hip, but the entire posterior chain from the ipsilateral lower limb to the contralateral shoulder.

The hamstrings and biceps femoris long head connect through the sacrotuberous ligament to the thoracolumbar fascia and erector spinae in the deep longitudinal sling. → The Deep Longitudinal Sling In this context, proximal hamstring tendinopathy is not just a local tendon problem — it is a dysfunction of the fascial chain that connects the foot to the lumbar spine, expressed at the ischial attachment point where load is concentrated by poor proximal mechanics.

Gluteal tendinopathy, FAI syndrome, and proximal hamstring tendinopathy all share a common thread: the hip's capacity to control adduction and manage compressive load is central to each presentation. Hip adductor tightness, restricted internal rotation, and inadequate gluteal activation are not independent findings — they are interrelated components of the same mechanical failure. Viewing them through a fascial lens means assessing the tissue quality of the hip's deep fascial investments, the gluteal and posterior compartment, and the proximal connections into the pelvis and lumbar spine, alongside the strength and movement patterning findings that more commonly guide assessment.

Our approach to hip pain begins with understanding what is creating the load — not just where the load is being expressed.

---

What Can You Do Right Now?

Avoid crossed-leg sitting for gluteal tendinopathy. This single postural change — eliminating hip adduction in sitting — can significantly reduce compressive load on sensitised gluteal tendons. Sit with hips level or slightly abducted, feet flat on the floor. When resting in a chair, a small wedge or rolled towel placed under the sit bones to tilt the pelvis anteriorly slightly reduces the compressive contact at the ischial tuberosity, which is relevant for proximal hamstring tendinopathy as well.

Don't stretch toward the pain. The instinct to stretch a painful posterior hip or thigh is common and usually counterproductive. Adductor stretching increases ITB compressive load on the gluteal tendons. Hamstring stretching compresses the ischial enthesis in proximal hamstring tendinopathy. In both cases, the tissue needs progressive loading — not lengthening into the painful position. Begin with isometric contractions: standing hip abduction against a wall for gluteal tendinopathy, bridge holds with mild hamstring load for proximal hamstring tendinopathy.

Strengthen the whole posterior chain. Hip abductor and external rotator capacity matters for every hip condition discussed here. Side-lying hip abduction, clamshells, and single-leg stance are the entry points. Romanian deadlifts and single-leg bridges, progressed appropriately, build the kinetic chain capacity that reduces compressive and tensile overload at the hip's vulnerable points.

Trust conservative management first. For FAI syndrome and gluteal tendinopathy, the evidence consistently shows that well-structured rehabilitation — targeting load management and progressive strengthening — produces outcomes at one year that are at least equal to, and often superior to, corticosteroid injection and surgical intervention. The time investment in conservative management is not a consolation prize — it is the evidence-supported first line.

---

Want to understand what's actually driving your hip pain?

Free 2-Week Rehab Program — request your copy

---