Discoid Lateral Meniscus

Discoid lateral meniscus is the most common congenital meniscal variant and the leading cause of mechanical snapping knee in children. Most discoid menisci are asymptomatic and discovered incidentally. The symptomatic ones bring clicking, early lateral compartment overload and progressive tearing, and the reason to recognise them early is that rim-preserving surgery protects the lateral compartment from premature osteoarthritis.

Who. Incidence is 3-5% in Western populations and up to 13-17% in East Asian cohorts. The lateral meniscus is affected much more often than the medial in Western practice, where a medial discoid meniscus is rare (1-2% of discoid menisci); the reverse is true in East Asian series. The variant is bilateral in 15-25% of cases, so image the contralateral knee when one is found. Symptoms present at 5-15 years, often first noticed with sport, and most series report a slight male predominance.

What it does to the knee. The snapping knee is the presenting complaint: an audible click with flexion and extension, lateral pain and swelling, an effusion after activity and an intermittent limp. Squatting, kneeling and pivoting sports become difficult, and the long-term cost is premature arthritis of the lateral compartment.

The theory that is still taught. The traditional account is that the fetal meniscus is a solid disc which normally undergoes central resorption, and that a discoid meniscus is that disc retained. It is memorable and widely repeated, and fetal morphometry does not support it: no discoid stage has been demonstrated in normal human development, and there is no resorption phase to fail.

What development actually shows. Across 41 human fetuses from 14 to 30 weeks and 14 adults, the proportion of the tibial plateau covered by the meniscus was consistently greater laterally than medially at every stage, and the layered collagen structure matured earlier in the lateral meniscus. The lateral meniscus is therefore normally the larger and the more variable of the two, which is a far better explanation for why discoid morphology is almost exclusively lateral than a resorption that never happens.

The tissue, which is what matters clinically. A discoid meniscus is structurally abnormal, not merely large. Its collagen is disorganised and the normal circumferential fibre architecture is deficient, so it cannot convert axial load into hoop stress properly: it transmits load centrally rather than circumferentially, sends higher contact stress to the lateral cartilage, degenerates within its substance and tears far more readily than a normal meniscus. Tears are found in 70 to 77% of symptomatic cases, and the degenerate central tissue is prone to horizontal cleavage.

Why a disc snaps. Thick central tissue catches between femur and tibia in extension. In the Wrisberg type, which lacks a posterior tibial attachment, the meniscus slides anteriorly and blocks terminal extension, producing the dynamic block and the classical clunk.

Instability is a separate problem from shape. Do not equate instability with the Wrisberg variant. The rim can be detached at its anterior, middle or posterior third, and the site recorded at arthroscopy is the subject of the stability check under Management.

The long-term consequences. Chronic overload marks the bone: a cupped lateral tibial plateau and squaring of the femoral condyle, and long-standing cases may develop valgus alignment from lateral compartment collapse. Even an untreated asymptomatic discoid meniscus accelerates lateral compartment wear, though the natural history in the absence of symptoms is usually benign, which is why the incidental finding is observed.

Why the rim heals and the centre does not. The whole rim-preservation and repair strategy rests on meniscal vascularity. Blood reaches the meniscus from the perimeniscal capillary plexus (geniculate branches) only at its periphery, which defines three zones:

• Red-red zone - peripheral, roughly the outer 3 mm, fully vascular; heals well and is ideal for repair
• Red-white zone - middle, junctional vascularity; variable healing
• White-white zone - inner third, avascular, nourished only by synovial diffusion; poor healing, and tears here are generally resected rather than repaired

That is why saucerisation resects the avascular central disc and keeps the vascular periphery as the rim, why a peripheral or Wrisberg-zone tear is repairable while a degenerate central horizontal cleavage usually is not, and why repair is favoured over resection in children, whose meniscus is relatively more vascular than an adult's.

Watanabe's 1969 system is the original arthroscopic classification and still the most widely cited. Ahn's modification is more clinically directed and adds the instability subtypes that decide whether reshaping alone will do. The two are complementary: Watanabe describes the shape, Ahn describes whether the rim is attached.

The Wrisberg type and the two meniscofemoral ligaments. The Wrisberg type is named after one of the two meniscofemoral ligaments, and the examiner will expect you to name both. They run from the posterior horn of the lateral meniscus to the medial femoral condyle, straddling the PCL: the ligament of Humphrey passes anterior to the PCL and the ligament of Wrisberg passes posterior to it ("Humphrey is in front, Wrisberg is at the rear"). They are accessory stabilisers of the lateral meniscus posterior horn; at least one is present in most knees, both in a minority.

Why reshaping alone fails. In the Wrisberg-variant discoid meniscus the normal posterior tibial (coronary/root) attachment is absent, so the posterior horn is anchored only by the ligament of Wrisberg. That leaves it free to translate anteriorly and snap, which is exactly why saucerisation alone leaves the meniscus hypermobile and posterior-horn reattachment is required.

History. The classic presentation is snapping, clicking or locking in a child aged 5-12. The child, or the parents, describe a knee that snaps, clicks or clunks, usually with flexion and extension, and there is no major trauma in most cases. Ask about:

• Intermittent locking (inability to fully extend) in fixed flexion, which the child may unlock with a twist; locking suggests a peripheral tear or an unstable Wrisberg variant
• Lateral knee pain worse with squatting, pivoting and stairs, and not painful at rest
• Effusion after activity and an intermittent limp
• Giving way, which points to an unstable Wrisberg variant

Examination. The snap is usually audible and may be visible, so watch and listen as the knee flexes and extends while palpating the lateral joint line, and check that the click reproduces the child's symptom. Expect a mild to moderate lateral compartment effusion and tenderness localised to the lateral joint line. Range of motion is usually full; a block to terminal extension suggests a Wrisberg variant or a peripheral tear.

Radiographs. Weight-bearing AP, lateral, skyline and tunnel (notch) views. Their job is to exclude other pathology and record baseline alignment; they occasionally raise suspicion, but they are often normal in early disease, so a normal film does not exclude the diagnosis and any child with mechanical lateral knee symptoms should proceed to MRI. Look for:

• Widened lateral joint space (greater than 5-6 mm)
• Cupping or sloping of the lateral tibial plateau
• Hypoplastic lateral femoral condyle
• Squaring of the lateral femoral condyle in long-standing cases

MRI is the definitive investigation: non-invasive, no radiation, and it defines the anatomy for surgical planning. The protocol is a standard knee MRI with sagittal, coronal and axial PD / T2 fat-saturated sequences. The criteria:

• Bow-tie sign: the meniscus appears as a continuous bow-tie on 3 or more consecutive sagittal slices, against only 2 for a normal meniscus. This is the most reliable criterion and reflects the meniscus wrapping continuously across the lateral compartment. It assumes 5 mm slices, so quote the slice thickness: the rule is really meniscal continuity across more than about 15 mm, and it fails on thin-slice sequences where a normal meniscus will span four or more slices
• Transverse width: minimal meniscal width greater than 15 mm on the coronal slice through the mid-body
• Ratio: meniscal width greater than 20% of the maximal tibial width on the same coronal image; some use meniscal-to-tibial coverage above 75%. Coverage of greater than 50% of the tibial plateau on the coronal view is supportive
• Posterior horn: an absent, truncated or anteriorly translated posterior horn suggests the Wrisberg variant
• Tears: high intrasubstance signal reaching the articular surface, or peripheral signal. Look for one rather than being surprised by it

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When the standard scan is equivocal. For a suspected Wrisberg variant or a complex tear, MR arthrography or a repeat MRI looks for anterior translation of the posterior horn and an absent posterior tibial attachment. It confirms the instability subtype and guides the need for stabilisation.

Two questions decide the pathway: is the child symptomatic, and is the peripheral rim attached. An incidental discoid meniscus is observed; a symptomatic stable one is reshaped; an unstable one is reshaped and stabilised.

Associated osteochondritis dissecans. A discoid lateral meniscus is a recognised association of osteochondritis dissecans of the lateral femoral condyle, in contrast to the more common medial-side OCD of the non-discoid knee; the abnormal thickness, poor load distribution and altered contact mechanics of the disc are thought to predispose the underlying condyle to a subchondral lesion. An unrecognised lesion changes the operation, because it may need drilling, fixation or grafting at the same arthroscopy, and its presence worsens the long-term prognosis. Scrutinise the lateral femoral condyle on the pre-operative MRI, and inspect it arthroscopically once the central disc has been saucerised and the condyle is exposed: the lesion is hidden until you lift the disc.

What predicts a good result. A stable Watanabe I or II meniscus with an isolated central disc, healthy articular cartilage, a motivated child and family, and a single-stage saucerisation.

What predicts a poor one. A Wrisberg variant missed at the index surgery, pre-existing cartilage damage, an unsalvageable circumferential tear, low-compliance rehabilitation, and a return to high-demand pivoting sport before adequate healing. The threshold that matters most is recognising and stabilising the Wrisberg variant at the first operation: missing instability is the commonest cause of reoperation and persistent symptoms.