Knee and Leg

Part 3 · The lower limb

The knee joint, menisci and cruciates, and the compartments of the leg

The joint that was asked for everything

The knee has to do two incompatible things. It must permit a large sagittal range — around 140° — so that we can squat, sit, climb and run. And it must be stable under loads of several times body weight, in a joint whose articular surfaces are two convex femoral condyles sitting on a nearly flat tibial plateau.

There is almost no bony congruence. Every bit of stability is bought from ligaments, menisci and muscle. That is the whole explanation for the knee’s clinical profile: the highest ligament injury burden of any joint, the highest meniscal injury rate, and one of the highest rates of symptomatic osteoarthritis.

Learning outcomes

• Describe the tibiofemoral and patellofemoral joints, their surfaces, capsule and bursae.
• Describe the menisci in detail — attachments, blood supply, function and injury patterns.
• Describe the cruciate and collateral ligaments and the posterolateral and posteromedial corners.
• Explain the screw-home mechanism and its clinical importance.
• Describe the arthrokinematics of the knee and the changing instantaneous axis of rotation.
• Describe the popliteal fossa, its boundaries and contents.
• Describe the four compartments of the leg with muscles, nerves, vessels and actions.
• Describe the course of the tibial and common fibular nerves and predict lesion effects.
• Explain ACL injury, meniscal tears, patellofemoral pain, medial tibial stress syndrome, Achilles pathology and DVT, with rehabilitation implications.
• Perform and interpret the principal knee tests with their known accuracy.

The tibiofemoral joint

Figure 1 · The knee joint

Articular surfaces

• Femoral condyles: convex in both planes; the medial condyle is longer, narrower and more curved, extending further distally and posteriorly; the lateral condyle is wider and flatter and projects further anteriorly (helping to resist lateral patellar dislocation).
• Tibial plateau: the medial surface is concave and larger; the lateral is convex and smaller — which is why the lateral meniscus is more mobile and why the lateral compartment permits more rotation.
• Posterior tibial slope ~7–10°, which produces an anterior shear component under axial load and is a recognised ACL injury risk factor when steep.
• The condyles are separated by the intercondylar eminence and its tubercles, and by the intercondylar fossa of the femur.

The joint is classified as a modified hinge (bicondylar) synovial joint with two degrees of freedom: flexion–extension, and axial rotation (available only in flexion).

Capsule, synovium and bursae

The capsule is deficient anteriorly, where the quadriceps tendon, patella and patellar ligament replace it, and is reinforced by the medial and lateral patellar retinacula.

The synovial membrane is the most extensive in the body and has an unusual arrangement: it invaginates from behind to cover the cruciates, so the cruciate ligaments are intracapsular but extrasynovial.

The infrapatellar (Hoffa’s) fat pad deserves separate mention: it is one of the most densely innervated structures in the knee, a genuine and under-recognised source of anterior knee pain, and it is impinged in extension when swollen or when the knee hyperextends.

Movements

Close-packed position: full extension with lateral rotation of the tibia. Resting position: ~25° flexion. Capsular pattern: flexion grossly more limited than extension (e.g. a knee losing 90° of flexion may lose only 10° of extension).

The screw-home mechanism

In the last ~20–30° of extension, the tibia rotates laterally ~10° on the femur (or, in weight bearing, the femur rotates medially on a fixed tibia). This is an automatic, obligatory, passive movement — not under voluntary control.

Why it happens — three contributing mechanisms: 1. The medial femoral condyle’s articular surface is longer than the lateral. As extension proceeds, the lateral compartment runs out of surface first, and continued extension forces the tibia to spin laterally around the medial condyle. 2. The anterior cruciate ligament tightens in extension, drawing the tibia into lateral rotation. 3. The lateral pull of the quadriceps contributes.

What it achieves: in full extension the joint is close-packed, the collaterals and cruciates are taut, the menisci are maximally congruent, and the knee is locked — allowing prolonged standing with minimal quadriceps activity, which is metabolically essential.

Unlocking requires popliteus, which internally rotates the tibia (or externally rotates the femur in weight bearing) at the start of flexion. Popliteus is a small muscle with a disproportionately important job, and it also retracts the lateral meniscus and acts as a posterolateral stabiliser.

Clinically: a knee that cannot achieve full extension cannot lock, so the quadriceps must work continuously in standing — which is fatiguing, painful and one reason that restoring full extension is the first priority after knee injury or surgery, ahead of flexion. A flexion contracture of even 10° imposes a substantial and continuous quadriceps demand.

Arthrokinematics

• Open chain (tibia moving on femur): during extension the concave tibia glides anteriorly as the tibia extends anteriorly — concave-on-convex, same direction (Chapter 1).
• Closed chain (femur moving on tibia): during extension the convex femur glides posteriorly while rolling anteriorly — convex-on-concave, opposite directions.
• Roll and glide combine. In pure rolling, the femur would roll off the back of the tibia within about 20° of flexion; the accompanying glide keeps it centred. The cruciates are the mechanism: the four-bar linkage of the ACL, PCL and their tibial and femoral attachments dictates the ratio of roll to glide through the range.
• The instantaneous axis of rotation migrates posteriorly with flexion, tracing a J-shaped evolute — which is why no single-axis brace hinge tracks the knee exactly, and why quadriceps and hamstring moment arms change with angle.

The menisci

Two semilunar fibrocartilaginous wedges, triangular in cross-section, thick peripherally and thin centrally, covering ~60–70% of the tibial plateau surface.

Functions

• Load transmission and distribution — the menisci transmit approximately 50% of load in extension and up to 85–90% of load in the lateral compartment in deep flexion. Total meniscectomy increases peak contact stress by two- to three-fold.
• Increase congruence between convex femur and flat tibia.
• Shock absorption — meniscectomised knees show measurably reduced shock absorbing capacity.
• Secondary stability — the posterior horn of the medial meniscus is an important secondary restraint to anterior tibial translation, which is why medial meniscal tears accompany chronic ACL deficiency.
• Lubrication and proprioception — the peripheral third contains mechanoreceptors.

Structure and blood supply

Collagen fibres are predominantly circumferential, converting compressive load into hoop stress resisted at the anterior and posterior root attachments, with radial “tie” fibres preventing longitudinal splitting.

The root tear. If a meniscal root is avulsed, hoop stress can no longer be contained, the meniscus extrudes peripherally, and the joint behaves as though the meniscus were absent. A root tear is biomechanically equivalent to a total meniscectomy — which is why root repair is now pursued aggressively rather than treated as a degenerative finding.

Vascular zones (Arnoczky and Warren):

Vascularity declines with age: the whole meniscus is vascular at birth, and only the peripheral 10–30% remains so in adulthood.

Tear patterns and management

Longitudinal, bucket-handle (a displaced longitudinal tear producing a springy block to extension — a locked knee), radial, horizontal cleavage (typically degenerative), flap, complex, and root tears.

A crucial distinction in management:

• Traumatic tears in young patients, especially peripheral, repairable tears and displaced bucket-handle tears causing true locking — these warrant surgical consideration.
• Degenerative meniscal tears in middle-aged and older patients — multiple high-quality randomised trials (METEOR, FIDELITY, ESCAPE and others) show that arthroscopic partial meniscectomy is no better than exercise therapy, and no better than sham surgery, for degenerative tears with or without mild osteoarthritis. Exercise therapy is first-line.

This is one of the clearest examples in musculoskeletal medicine of imaging findings driving unnecessary surgery, and it is worth being able to explain to patients who arrive with an MRI report and an expectation.

The ligaments

Figure 2 · What holds the knee together

The cruciates

Named for their tibial attachments, and crossing each other like the limbs of an X.

ACL rupture produces an immediate haemarthrosis within 2 hours (the ligament is vascular and intracapsular), a “pop”, and giving way on pivoting. The Lachman test (30° flexion) is the most accurate single test (sensitivity ~85%, specificity ~94%); the pivot shift is the most specific (~98%) but hardest to perform in an acute knee; the anterior drawer at 90° is the least accurate.

Why the ACL does not heal: intra-articular position, synovial fluid preventing fibrin clot formation, and poor vascularity (Chapter 7). Hence reconstruction rather than repair — though non-operative management with structured rehabilitation is a legitimate option for many patients, and the decision is now framed around activity demands rather than automatic surgery.

Female ACL injury risk is 2–8 times that of males in comparable sports, attributed to a combination of anatomical (wider pelvis, greater Q angle, narrower intercondylar notch, steeper tibial slope), hormonal, and — most importantly, because it is modifiable — neuromuscular factors (dynamic valgus on landing, quadriceps-dominant strategies, reduced hamstring co-activation). Neuromuscular training programmes reduce ACL injury incidence by roughly 50%, and by more in females, making prevention one of the highest-value interventions in sports physiotherapy.

The collaterals and the corners

The “unhappy triad” (O’Donoghue) — ACL + MCL + medial meniscus — from a valgus, externally rotating force on a planted foot. Modern imaging shows the lateral meniscus is in fact more often torn in acute ACL injuries, so the classical triad is taught as history rather than as current fact.

Knee ligament examination

Ottawa knee rules determine the need for radiography after acute knee injury: age ≥55, isolated patellar tenderness, fibular head tenderness, inability to flex to 90°, or inability to weight-bear four steps both immediately and in the department.

The popliteal fossa

A diamond-shaped space behind the knee.

Contents, from superficial to deep — the order matters and is examinable:

• Tibial nerve (most superficial and most medial in the upper fossa)
• Common fibular nerve (along the medial border of biceps femoris, heading laterally)
• Popliteal vein
• Popliteal artery (deepest, lying directly on the joint capsule)

Plus the small saphenous vein, popliteal lymph nodes, and the posterior femoral cutaneous nerve.

Clinical: because the artery is the deepest structure and lies against the capsule, it is vulnerable in supracondylar femoral fractures and knee dislocation — popliteal artery injury complicates up to a third of knee dislocations, and a knee dislocation is therefore a limb-threatening emergency requiring vascular assessment (ankle–brachial index and often CT angiography) regardless of palpable pulses. The popliteal artery is also the second commonest site of peripheral aneurysm.

Popliteal (Baker’s) cyst: distension of the semimembranosus–gastrocnemius bursa, usually secondary to an intra-articular problem in adults (meniscal tear, osteoarthritis, inflammatory arthritis). Rupture produces acute calf pain and swelling that closely mimics DVT — and it is the physiotherapist who often sees it first.

The leg: four compartments

Figure 3 · Compartments of the leg

Divided by the interosseous membrane, the anterior and posterior intermuscular septa, and the transverse intermuscular septum.

Key muscles in detail

The calcaneal (Achilles) tendon — the thickest and strongest tendon in the body, formed from gastrocnemius and soleus, spiralling ~90° as it descends (which contributes to the stress concentration in its watershed zone, 2–6 cm above the insertion). It withstands loads of 6–12 × body weight in running.

The plantaris — small, with a very long tendon; absent in 7–20% of people; commonly harvested for graft; its rupture is one differential for acute calf pain.

Nerves and vessels of the leg

Figure 4 · Cross-section of the leg and the popliteal fossa

Tibial nerve (L4–S3)

Passes vertically through the popliteal fossa, deep to the soleal arch (a potential entrapment point) into the deep posterior compartment, and runs with the posterior tibial vessels to pass behind the medial malleolus in the tarsal tunnel, dividing into medial and lateral plantar nerves.

• Motor: all of the superficial and deep posterior compartments; via its plantar branches, all intrinsic foot muscles except extensor digitorum brevis.
• Sensory: the sural nerve (with a contribution from the common fibular) to the posterolateral leg and lateral foot; the medial calcaneal branch to the heel; the sole via the plantar nerves.
• Lesion: loss of plantarflexion, inversion and toe flexion, with calcaneovalgus deformity and loss of sole sensation — functionally devastating for gait push-off. Tarsal tunnel syndrome produces burning sole pain and paraesthesia, worse with standing and walking.

Common fibular nerve (L4–S2)

Runs along the medial border of biceps femoris, crosses the lateral head of gastrocnemius, and winds subcutaneously around the neck of the fibula — where it is the most commonly injured nerve in the lower limb. It divides within fibularis longus into:

• Superficial fibular nerve — the lateral compartment (fibularis longus and brevis) and sensation over most of the dorsum of the foot.
• Deep fibular nerve — the anterior compartment and sensation over the first web space only (its autonomous zone).

Common fibular nerve palsy produces:

• Foot drop with a high-stepping (steppage) gait and foot slap
• Loss of eversion
• Sensory loss over the anterolateral leg and dorsum of foot
• Inversion is preserved (tibialis posterior, tibial nerve) — which is how it is distinguished from an L5 radiculopathy, in which hip abduction (gluteus medius) and inversion are also weak

Causes: fibular neck fracture, tight plaster or bandage, prolonged squatting or leg crossing, positioning during surgery or in the unconscious patient, ganglion, and weight loss (loss of protective fat). Every physiotherapist positioning or splinting a limb must know this.

Vessels

The popliteal artery divides at the lower border of popliteus into:

• Anterior tibial artery — passes above the interosseous membrane into the anterior compartment, descends on it with the deep fibular nerve, and becomes the dorsalis pedis anterior to the ankle (palpable lateral to the EHL tendon).
• Posterior tibial artery — descends in the deep posterior compartment with the tibial nerve, palpable behind the medial malleolus, and divides into the medial and lateral plantar arteries. It gives the fibular (peroneal) artery, which supplies the lateral compartment.

Venous return depends on the calf muscle pump acting on the deep veins within their fascial envelope, with valves directing flow proximally and from superficial to deep via perforators. Immobility, valve incompetence and hypercoagulability form Virchow’s triad.

Deep vein thrombosis — what a physiotherapist must know

Presentation: unilateral calf pain, swelling (measure calf circumference 10 cm below the tibial tuberosity — a difference >3 cm is significant), warmth, erythema, and tenderness along the deep venous system. Homans’ sign is unreliable and should not be used to rule DVT in or out.

Use the Wells score and refer for D-dimer and ultrasound rather than relying on clinical signs. Differentials include ruptured Baker’s cyst, calf muscle tear, cellulitis and superficial thrombophlebitis.

If DVT is suspected, do not massage, do not perform vigorous passive movement, and do not apply compression until it has been excluded or treated — the risk is pulmonary embolism. Once anticoagulation is established, early mobilisation is safe and is recommended.

Clinical conditions

Patellofemoral pain

The commonest knee complaint in adolescents and young adults, and in runners.

• Presentation: diffuse anterior or retropatellar pain, aggravated by activities that load the flexed knee — stairs, squatting, running, and prolonged sitting (the “theatre sign”). This is the patellofemoral joint reaction force curve made clinical (Chapter 13): PFJ force rises steeply with knee flexion under load.
• Contributing factors: quadriceps weakness (particularly eccentric), hip abductor and external rotator weakness with dynamic valgus, reduced hip and ankle flexibility, altered running mechanics, training load error, and increased body mass.
• Management (the 2018 international consensus): exercise therapy is the core, combining hip-targeted and knee-targeted exercise (hip-targeted work produces earlier pain reduction), with load management, gait retraining and foot orthoses in selected cases. The old model of “VMO weakness causing lateral maltracking” as the universal explanation is not supported — selective VMO activation training has not been shown to be superior to general quadriceps work.
• Note that imaging is unhelpful and that the term “chondromalacia patellae” describes a cartilage finding, not this clinical syndrome.

Patellar tendinopathy (“jumper’s knee”)

Pain at the inferior pole of the patella, in jumping and change-of-direction athletes; a load-related tendinopathy following the continuum model (Chapter 7). Managed with isometrics for pain, then progressive heavy slow resistance or eccentric decline squats, plus jump-landing mechanics and load management. Deep knee flexion under load compresses the tendon against the patella — so, as with other insertional tendinopathies, deep painful loading early is counterproductive.

Iliotibial band syndrome

Lateral knee pain, classically in runners and cyclists, at around 30° of knee flexion where the ITB is closest to the lateral femoral epicondyle.

• The mechanism is compression, not friction: MRI shows a richly innervated fat pad deep to the ITB, and the ITB is firmly anchored to the femur, so it cannot literally “flick” back and forth. The ITB cannot be meaningfully stretched or “released” — it has a modulus close to that of soft tissue steel-work, and foam rolling produces neurophysiological, not structural, effects.
• Management: load modification, hip abductor and external rotator strengthening, running gait modification (increasing step width and cadence, reducing hip adduction), avoiding compressive positions early.

Medial tibial stress syndrome (“shin splints”)

Exercise-induced pain along the posteromedial tibial border, over a length of ≥5 cm, in runners and military recruits.

• Pathology: a bone stress reaction of the tibia with periosteal involvement — increasingly viewed as part of the bone stress injury continuum rather than a traction periostitis.
• Must be distinguished from: tibial stress fracture (focal tenderness <5 cm, pain at rest and at night — and note that the anterior tibial cortex is a high-risk site with a poor prognosis, the “dreaded black line”), chronic exertional compartment syndrome (predictable onset at a set distance, tightness and paraesthesia, resolving within minutes of stopping — confirmed by intracompartmental pressure testing), and popliteal artery entrapment.
• Management: load reduction with maintained cardiovascular training, gradual return, addressing training error, calf and foot strengthening, cadence adjustment, and bone health screening including RED-S where indicated.

Achilles tendinopathy and rupture

The Thompson (Simmonds’ calf squeeze) test is the single most useful bedside test and is often the only one needed. Around 20–25% of Achilles ruptures are missed at first presentation, usually because some plantarflexion is preserved by the deep posterior compartment muscles and the examiner is reassured by it.

Where students consistently go wrong

• Naming the cruciates by their femoral attachments. They are named for their tibial attachments.
• Forgetting the cruciates are intracapsular but extrasynovial.
• Saying the MCL is not attached to the meniscus. The deep layer is — hence combined injuries.
• Attributing the medial meniscus’s higher injury rate to size. It is tethering, not size.
• Missing the screw-home mechanism’s clinical point. Full extension must be restored first.
• Forgetting popliteus unlocks the knee.
• Putting the popliteal artery superficial. It is the deepest structure and is at risk in knee dislocation.
• Recommending arthroscopy for a degenerative meniscal tear. The trials say exercise.
• Relying on Homans’ sign for DVT. Use the Wells score.
• Stretching or “releasing” the ITB. It is a compression problem and the band cannot be lengthened.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 15 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 16 — Ankle and Foot: the ankle mortise, its ligaments, and the arches of the foot.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents