Osteochondral Defects of the Knee

Osteochondral defects of the knee involve damage to the articular cartilage and potentially underlying subchondral bone. Goals of treatment are pain relief, improved function, and prevention of osteoarthritis.

ICRS Classification

Grade I: Superficial softening, fibrillation Grade II: Partial thickness lesion (less than 50% depth) Grade III: Deep lesion (greater than 50% depth) or down to subchondral bone Grade IV: Full thickness with exposed subchondral bone

Grade III and IV are generally treated.

Location

Medial femoral condyle (MFC): Most common weight-bearing location for symptomatic lesions. Patellofemoral (patella/trochlea) lesions are next most frequent and behave differently — they tolerate microfracture poorly and ACI/MACI has historically had less reliable results here.

Differential Diagnosis of a Focal Knee Lesion

A focal cartilage/subchondral signal change on MRI is not always a treatable osteochondral defect. Distinguish the following before committing to a restoration procedure.

Articular (hyaline) cartilage is avascular, aneural and alymphatic, and adult chondrocytes have very limited mitotic capacity. Consequently a full-thickness chondral injury that does not reach the subchondral vascular bed mounts essentially no intrinsic repair and persists as a defect.

• Partial-thickness (chondral) injury — no access to marrow, no clot, no healing response; the defect remains and the rim degenerates over time.
• Full-thickness osteochondral injury — breaches the subchondral plate, allowing a marrow clot with mesenchymal stem cells to fill the defect. This heals with mechanically inferior fibrocartilage (Type I collagen) rather than true hyaline cartilage (Type II) — the biological basis of microfracture and its long-term deterioration.

Once cartilage is lost, increased peak contact stress accelerates degeneration of adjacent cartilage, and abnormal load transfer to subchondral bone produces marrow oedema and cysts — the substrate for progression toward focal then generalised osteoarthritis. Anything that raises focal contact stress (malalignment, meniscal deficiency, instability) magnifies this cascade, which is why concurrent pathology must be corrected.

• Symptoms: activity-related, often localised joint-line or anterior pain; effusion after activity; mechanical symptoms (catching, locking, giving way) suggest an unstable fragment or loose body.
• History: young/active patient, prior trauma, twisting injury, or insidious onset; ask about prior knee surgery (especially meniscectomy or ACL reconstruction) and any previous cartilage procedure.
• Examination: focal condylar or patellofemoral tenderness, effusion, possible crepitus; always assess limb alignment (varus/valgus, gait thrust), meniscal signs and ligament stability — these determine whether any cartilage procedure can succeed.
• Red flags against restoration: diffuse/bipolar pain, older age with established OA, inflammatory features.

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• Weight-bearing radiographs (AP, lateral, skyline, and a Rosenberg/45° flexion PA view) — assess joint space, exclude established OA, look for OCD or loose bodies.
• Long-leg standing alignment films — mandatory before any restoration procedure to quantify mechanical axis; uncorrected malalignment is a leading cause of failure.
• MRI — the key modality: maps cartilage lesion location, size and depth (ICRS grade), subchondral bone status (oedema, cysts), and concurrent meniscal/ligament pathology. Cartilage-sensitive sequences and quantitative mapping (e.g. T2/dGEMRIC) assess repair tissue on follow-up.
• Diagnostic arthroscopy — defines the true ICRS grade, lesion size, containment and shoulder quality, and is often the staging step (chondrocyte harvest) for ACI/MACI.

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Address Concurrent Pathology

Alignment: Varus/valgus malalignment must be corrected (HTO, DFO). Uncorrected alignment leads to failure.

Meniscus: Meniscal deficiency increases contact stress. Consider MAT if previous meniscectomy.

Ligaments: ACL deficiency causes abnormal kinematics. Reconstruct if unstable.

Patient Selection

• Young (typically under 40-50)
• Active, motivated
• Single compartment disease
• Focal lesion (not diffuse OA)
• Normal or correctable alignment
• Stable knee

The microfracture indications, the investigations section and the management algorithm all use "contained" lesion and healthy "shoulder" as selection criteria - the algorithm's decision node is literally "lesion size and containment" - but the concepts are never defined, and they decide which technique can work.

• Containment. A contained lesion is surrounded on all sides by an intact peripheral rim (wall) of healthy cartilage. That wall is what holds a marrow clot (microfracture/AMIC) or an ACI/MACI graft inside the defect - it is essential for those techniques to succeed.
• Uncontained lesions have a deficient rim - typically at the very edge of a condyle, at a bipolar ("kissing") lesion, or where the shoulder has broken down. A clot or cell graft cannot be retained, so marrow stimulation and cell therapy do poorly here; these lesions favour structural replacement that does not need a containing wall - OAT or osteochondral allograft, which bring their own bone and cartilage.
• Shoulder quality. The "shoulder" is the transition between the defect and the surrounding cartilage. A good shoulder is healthy, full-thickness cartilage firmly anchored to subchondral bone, so the surgeon can debride the lesion to stable vertical walls and create a well-contained defect. A poor shoulder (soft, fibrillated, delaminating or undermined cartilage) makes the "contained" appearance illusory - the walls will not hold a repair, which predicts failure of marrow stimulation and again favours OAT/OCA.
• Practical point: assess containment and shoulder quality at arthroscopy, together with size, before committing to a technique - a small lesion with a poor shoulder is not a good microfracture candidate.

The Controversies section flags "augmented marrow stimulation (scaffold-assisted / AMIC)" as the response to microfracture's declining reputation, but never explains what it is.

• AMIC = autologous matrix-induced chondrogenesis. It combines standard marrow stimulation (microfracture or drilling) with a collagen type I/III membrane (or scaffold) laid over the defect and sealed, usually with fibrin glue. The membrane protects and stabilises the marrow clot - which is otherwise prone to washout and uneven fill - and provides a three-dimensional scaffold that organises the marrow-derived mesenchymal cells as they differentiate.
• Why it exists. It targets microfracture's two weaknesses (an unstable clot with variable fill, and mechanically inferior fibrocartilage) while staying a single-stage, cell-culture-free, lower-cost procedure - unlike the two-stage, regulated and expensive ACI/MACI. It is therefore attractive where cell therapy is unavailable or unaffordable.
• Where it sits. Usually offered for medium (roughly 2 to 4 cm2) contained lesions where microfracture alone is unreliable but a two-stage cell therapy is not warranted or accessible; some surgeons extend it to larger contained defects.
• Evidence. Medium-term series report better and more durable defect fill than microfracture alone, but there is little high-level randomised evidence against MACI/ACI, so its precise place in the algorithm remains an area of active study - exactly the "augmented marrow stimulation" the controversies section refers to.

Procedure failure / persistent symptoms is the dominant concern — graft delamination, incomplete fill or progression to OA, ultimately leading to revision restoration or arthroplasty.

• Microfracture: subchondral bone overgrowth, intralesional osteophyte, subchondral cysts, and fibrocartilage breakdown with symptom recurrence at 2-5 years.
• OAT / mosaicplasty: donor-site morbidity, plug subsidence/proud plugs, surface incongruity, dead space between plugs ("valleys"), limited graft availability for large lesions.
• ACI / MACI: graft hypertrophy or delamination, periosteal patch overgrowth (older ACI), prolonged rehabilitation, two procedures and cost; possible incomplete integration.
• OCA: graft non-incorporation/collapse, immunologic and (rare) disease-transmission risk, dependence on chondrocyte viability that falls with storage time.
• General: infection, arthrofibrosis/stiffness, VTE, and accelerated degeneration if concurrent malalignment, meniscal deficiency or instability is left uncorrected.

Global Epidemiology

• Full-thickness chondral lesions are found in roughly 5-11% of knee arthroscopies, and some degree of cartilage damage in up to 60% — most are incidental, only a minority are symptomatic, focal and treatable.
• Symptomatic defects cluster in active patients in their 20s-40s; the medial femoral condyle is the most common symptomatic site, followed by the patellofemoral joint.
• Traumatic and sport-related chondral injury predominates in younger patients, while degenerative/diffuse lesions in older patients are not restoration candidates.

Side-by-Side Guidance

Registry & Outcome Notes

• Dedicated cartilage-repair registries are less mature than arthroplasty registries, but national joint registries (NJR, AJRR, AOANJRR, Swedish/Norwegian) capture the key downstream endpoint: conversion of a prior cartilage procedure to arthroplasty, informing real-world failure and survivorship.
• Long-term RCT data (Knutsen 2016) is more sobering than early single-arm series — both microfracture and first-generation ACI show substantial failure and radiographic OA at 14-15 years.

High- vs Limited-Resource Practice Variation

• Well-resourced settings: full menu available — microfracture/AMIC, OAT, two-stage MACI/ACI and fresh OCA, with combined osteotomy/MAT where indicated. Cell-therapy products (e.g. MACI) require regulatory approval and tissue-bank/lab infrastructure that is not universal.
• Limited-resource settings: marrow stimulation (microfracture/drilling) and OAT/mosaicplasty dominate because they are single-stage, low-cost and require no cell culture or allograft banking. Cultured-chondrocyte and fresh-allograft options are often unavailable, making patient selection and concurrent biomechanical correction even more important.

Exam Relevance (global)

• A core topic across FRCS (Tr & Orth), FRACS, EBOT/FEBOT, ABOS and DNB/MS curricula.
• Vivas test the ICRS/Outerbridge grading, the size-based treatment algorithm, and — most importantly — the principle that alignment, meniscal and ligament status must be assessed and corrected for any cartilage procedure to succeed.

• Does cartilage restoration prevent osteoarthritis? The honest answer is uncertain. The Knutsen 14-15 year RCT showed early radiographic OA in roughly half of survivors regardless of whether they had ACI or microfracture, and no difference in total knee replacement. Restoration improves symptoms but its disease-modifying claim is unproven — counsel patients accordingly.
• First-line for the 2-4 cm² "grey-zone" lesion. Microfracture, OAT and MACI all have advocates here. Microfracture is cheapest and single-stage but produces fibrocartilage; OAT gives true hyaline bone-cartilage but is donor-limited; MACI gives hyaline-like tissue but is two-stage and costly. No single technique is definitively superior across this whole range.
• Microfracture's declining reputation. Concerns about subchondral bone overgrowth, intralesional osteophytes and subchondral cysts after marrow stimulation have narrowed its indications toward truly small (under 2 cm²) contained lesions, and have driven interest in "augmented" marrow stimulation (scaffold-assisted / AMIC).
• Patellofemoral lesions remain the hardest subgroup. Historically poorer ACI results (Brittberg 1994) have improved with modern matrix techniques and concurrent patellofemoral realignment/unloading, but the evidence base is thinner than for the femoral condyle.
• OCA graft viability and access. Fresh osteochondral allograft depends on chondrocyte viability that falls with storage time, and availability/regulation of fresh allograft varies enormously between countries — a major practical determinant of which option a surgeon can actually offer.
• Biologics (PRP, BMAC, stem-cell injections). Widely marketed as cartilage "regenerators" but lacking high-level evidence for true cartilage restoration; current role is adjunctive symptom management at best.

Osteochondral defects involve damage to articular cartilage and underlying subchondral bone, with the medial femoral condyle (MFC) being the most common weight-bearing location. Treatment selection is size-dependent: microfracture for small lesions (less than 2cm²) produces fibrocartilage (Type I collagen), while MACI/ACI for larger lesions (greater than 2-4cm²) produces hyaline-like cartilage (Type II). OAT (mosaicplasty) transfers true hyaline cartilage with bone from non-weight-bearing areas. Critical principle: always address concomitant alignment, meniscal, and ligamentous pathology for successful outcomes.