Why Knee Pain Is Rarely Just a Knee Problem: The Hip-Ankle-Knee Connection

The knee is a hinge joint. It sits between the hip and the foot, receiving force from both directions on every step, squat, jump, and landing. It has relatively limited frontal and transverse plane mobility of its own — it depends on the hip above and the ankle below to manage forces in those planes on its behalf. When either the hip or the ankle fails to do their job, the knee absorbs the shortfall. Not once, but thousands of times a day.

This is why the research on knee pain consistently points away from the knee. It points up to the hip, down to the foot, and across to the fascial system that ties them together.

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The Hip: The Single Biggest Driver of Knee Load

A 2010 clinical commentary by Powers in the Journal of Orthopaedic and Sports Physical Therapy synthesised the evidence on how hip mechanics drive knee injury across three of the most common presentations in clinical practice — patellofemoral pain syndrome, ITB syndrome, and ACL injury. [1]

The core finding: in weight-bearing tasks, the primary mechanism of patellofemoral pain is not the patella tracking laterally across the trochlea. It is the femur rotating internally beneath a patella that remains relatively stable. The distinction matters enormously. A patella that moves laterally requires a different intervention than a femur that rotates inward — but the two scenarios produce the same anterior knee pain and the same appearance on imaging.

What drives femoral internal rotation? Primarily: hip adduction in the frontal plane combined with insufficient hip external rotation control. The gluteus maximus, gluteus medius, and deep external rotators are the muscles responsible for resisting hip adduction and internal rotation during dynamic loading. When they are underperforming — through inhibition, fatigue, poor neuromuscular recruitment, or simple deconditioning from sustained sitting — the femur collapses inward on every loading cycle.

The load consequences are quantifiable. Powers found that a 10° increase in the Q-angle — which results directly from increased hip adduction and femoral internal rotation — produces a 45% increase in peak patellofemoral contact pressure. [1] That is not a marginal increase. It is the difference between a patellofemoral joint that manages its loads comfortably and one that is being repeatedly overloaded on every descent of a stair.

The hip abductor data for ITB syndrome tells a similar story. Runners with ITB syndrome demonstrate hip abductor strength deficits of 18–20% compared to pain-free controls. When those deficits are addressed with a six-week targeted hip strengthening programme, 92% return to pain-free running. [1] The intervention was not applied to the knee. The intervention was applied to the hip — because the hip was where the problem originated.

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The Foot: What's Below Matters Too

The hip is the dominant proximal driver of knee load, but it does not act in isolation. The foot and ankle contribute a consistent distal influence through the same rotational pathway — in the opposite direction.

Excessive foot pronation — flattening of the medial longitudinal arch during load — is accompanied by tibial internal rotation. Tibial internal rotation transmitted upward through a relatively rigid knee joint produces femoral internal rotation at the hip. The same kinematic cascade that begins at a weak hip can also begin at a pronating foot, and in many presentations both are operating simultaneously: a foot that pronates excessively into a hip that cannot resist the resulting internal rotation produces a knee that is being squeezed by mechanical inputs from two directions at once.

This is why knee pain assessment that stops at the knee misses the most actionable information available. The foot arch, the ankle dorsiflexion range, and the ankle stability profile are not optional extras in the knee assessment — they are part of the kinematic chain whose failure is expressing itself at the knee.

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The Fascia Lata and the ITB: Rethinking a Much-Misunderstood Structure

The iliotibial band is not a tendon. It is a thickening of the fascia lata — the deep fascial sleeve that invests the muscles of the thigh — running from the iliac crest and the tensor fasciae latae anteriorly, and from the gluteus maximus posteriorly, to the lateral tibial condyle (Gerdy's tubercle) below.

A landmark cadaveric and MRI study by Fairclough and colleagues fundamentally revised the understanding of how ITB syndrome develops. [2] Their finding: the ITB is firmly anchored to the distal femur by fibrous strands. It does not slide anteroposteriorly over the lateral epicondyle on the way many anatomy texts describe. The apparent movement is a tension shift between its anterior and posterior fibres as the knee passes through 30° of flexion — the position at which symptoms are most consistently provoked.

No bursa was identified in any of their cadaveric specimens at the classic compression point. What MRI showed instead was signal change in the richly innervated, vascularised fat pad that sits deep to the ITB at the lateral epicondyle — a structure containing Pacinian corpuscles and well capable of generating pain under compression. The correct model for ITB syndrome is fat pad compression, not friction of the band against bone.

What creates that compression? The same hip abductor weakness and consequent hip adduction in loading that increases femoral internal rotation at the patellofemoral joint. As the hip adducts in stance, the ITB is pulled taut proximally. The taut band compresses the fat pad against the lateral femoral condyle at the critical 30° flexion position. The compression, not the sliding, is the mechanism.

A 2025 randomised controlled trial by Ming and colleagues demonstrated that adding myofascial release to hip strengthening for ITB syndrome produced significantly greater reductions in both pain and measured ITB thickness — assessed on ultrasound — at four weeks, compared to hip strengthening alone. [3] This is direct evidence of fascial tissue change in response to manual intervention at the ITB — and it reinforces the picture of ITBS as a fascial compression problem with both structural and muscular contributors.

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Three Structures Through the Fascial Lens

Patellofemoral Pain Syndrome

PFPS is a diagnosis that encompasses multiple clinical subgroups — presentations driven by overuse and overload, by muscle performance deficits, by movement coordination impairments, and by mobility restrictions. What unifies them is that the patellofemoral joint is absorbing load it cannot distribute adequately — and the reason for that inadequate distribution almost always traces to the hip and, less frequently, the foot. The current clinical practice guideline provides Grade A evidence for combined hip and knee exercise therapy, with hip-targeted exercise targeting the posterolateral musculature preferred in early management. [4] PFPS is not self-limiting: over half of adolescents with the condition have persistent symptoms at two years. The stakes of getting the assessment right — and including the hip — are high. → Patellofemoral Pain Syndrome

ITB Syndrome

The runner who is told their ITB is "too tight" and needs stretching is receiving advice built on the friction model that Fairclough and colleagues dismantled in 2006. The ITB cannot be meaningfully lengthened by stretching — it is not a muscle. What can be changed is the compressive load applied to the fat pad beneath it, and that load is directly modifiable by improving hip abductor strength and control, reducing hip adduction during stance, and addressing fascial restriction within the fascia lata that increases lateral compartment tension. The evidence for fascial intervention specifically reducing ITB thickness — not just symptom scores — is now available. → ITB Syndrome

Patellar Tendinopathy

Patellar tendinopathy — jumper's knee — is a load management problem at its core. The patellar tendon's job is to transmit the quadriceps force from the thigh to the tibia during energy-storage tasks: jumping, landing, sprinting, change of direction. When the kinetic chain is operating well — hip extending powerfully, glutes loaded, trunk stiff and stable — the quadriceps contribution to landing and jump performance is distributed across the chain. When the proximal chain is underperforming, the quadriceps and patellar tendon carry a disproportionate share. Malliaras and colleagues are explicit on this: addressing the kinetic chain is not an adjunct to patellar tendinopathy rehabilitation — it is a core component. [5] A patellar tendon that is being progressively reloaded with a weak, poorly-coordinating hip above it is a tendon that will continue to fail its load management. → Patellar Tendinopathy

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The Fascial Thread Through All Three

The deep longitudinal sling — biceps femoris, sacrotuberous ligament, and erector spinae — runs from the foot to the lumbar spine and directly influences the hamstring loading environment around the knee. → The Deep Longitudinal Sling The fascia lata invests the entire thigh and transmits gluteal tension to the lateral knee. The quadriceps and patellar retinaculum are fascial as well as muscular structures — their tension balance determines how load is distributed across the patellofemoral joint.

Viewing knee pain through a fascial lens means assessing not just the tendons and joints of the knee but the tissue planes that connect the knee to everything above and below it: the density of the lateral fascial compartment of the thigh, the posterior chain mechanics running through the hamstrings and biceps femoris, the hip abductor and external rotator fascial investments, and the ankle-foot complex from which every loading cycle begins.

Our assessment of knee pain specifically includes the hip mechanics — abductor strength, external rotation control, and the fascial status of the gluteal and iliotibial region — as well as the ankle and foot, because the problem presenting at the knee is almost always a story that began elsewhere.

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What Can You Do Right Now?

Develop your hip abductor and external rotator capacity. Side-lying hip abduction, clamshells, banded lateral walks, and single-leg Romanian deadlifts are not just generic "glute exercises" — they are the specific mechanism by which the femur is prevented from collapsing inward during loading. For a runner with lateral knee pain, this is the most directly evidence-supported intervention available.

Observe your knee position during single-leg tasks. Stand in front of a mirror and perform a single-leg squat. Does your knee collapse inward as you descend? Does your pelvis drop on the non-stance side? These are visible signs of the hip adduction and abductor weakness patterns that load the knee in the patterns described above. The observation costs nothing and tells you more than most imaging.

Don't neglect the foot. If you pronate significantly — your medial arch collapses substantially under load — that is transmitting tibial and femoral internal rotation upward into your knee on every step. Supportive footwear, orthotics, and foot-intrinsic strengthening (single-leg calf raises, toe spread drills, short-foot exercises) address the distal contribution to knee load.

Manage load, not absence. For patellar tendinopathy in particular, complete rest degrades tendon capacity and makes reloading harder. Isometric quadriceps loading (wall sits, leg press holds) provides tendon stimulus with lower compressive load and is well tolerated in irritable presentations. The goal is continued loading at an appropriate level — not stopping entirely.

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