Osteochondral Defects of the Knee

An osteochondral defect of the knee is damage to the articular cartilage and, potentially, to the subchondral bone beneath it. Treatment aims at pain relief, better function and the prevention of osteoarthritis.

Where. The medial femoral condyle (MFC) is the most common weight-bearing location for symptomatic lesions. Patellofemoral lesions, of the patella or trochlea, are next most frequent and behave differently: they tolerate microfracture poorly, and ACI/MACI has historically had less reliable results there.

ICRS grading. The ICRS grade classifies the cartilage damage by depth, and grades III and IV are generally the ones treated.

• 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

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

Depth decides the response.

• A partial-thickness (chondral) injury has no access to marrow, so no clot forms and there is no healing response; the defect remains and its rim degenerates over time.
• A full-thickness osteochondral injury breaches the subchondral plate, and a marrow clot carrying mesenchymal stem cells fills the defect. It heals with mechanically inferior fibrocartilage (Type I collagen) rather than true hyaline cartilage (Type II), which is the biological basis of microfracture and of its long-term deterioration.

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

The candidate. Cartilage restoration is for a focal lesion in a knee that is otherwise sound:

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

Treat the knee, not only the defect. Alignment, meniscal and ligament problems are addressed concurrently with the cartilage.

• Alignment. Varus or valgus malalignment must be corrected by osteotomy (HTO, DFO); uncorrected malalignment is a leading cause of failure.
• Meniscus. Meniscal deficiency increases contact stress. Consider meniscal allograft transplantation (MAT) after a previous meniscectomy.
• Ligaments. ACL deficiency causes abnormal kinematics. Reconstruct the ligament if the knee is unstable.

Containment and shoulder quality determine whether a marrow clot or a cell-based graft can stay stable in the defect. Assess both at arthroscopy, together with size, before committing to a technique, because the result may change the planned operation.

Containment. A contained lesion is surrounded on all sides by an intact peripheral rim (wall) of healthy cartilage. That wall holds a marrow clot (microfracture, AMIC) or an ACI/MACI graft inside the defect, and those techniques need it to succeed.

Uncontained lesions have a deficient rim, typically at the very edge of a condyle, in 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. These lesions favour structural replacement that needs no 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, which lets the surgeon 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. That predicts failure of marrow stimulation regardless of lesion size and again favours OAT or OCA, so a small lesion with a poor shoulder is not a good microfracture candidate.

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History. Expect a young or active patient with prior trauma, a twisting injury or an insidious onset. Ask about previous knee surgery, especially meniscectomy or ACL reconstruction, and about any previous cartilage procedure.

Symptoms. Pain is activity-related and often localised to the joint line or the front of the knee, with an effusion after activity. Mechanical symptoms (catching, locking, giving way) suggest an unstable fragment or a loose body.

Examination. Look for focal condylar or patellofemoral tenderness, an effusion and possibly crepitus. Always assess limb alignment (varus or valgus, a gait thrust), meniscal signs and ligament stability, because these determine whether any cartilage procedure can succeed.

Red flags against restoration. Diffuse or bipolar pain, older age with established osteoarthritis, and inflammatory features all count against a restoration procedure.

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

Radiographs. Weight-bearing films assess the joint space, exclude established osteoarthritis and look for OCD or loose bodies:

• AP
• Lateral
• Skyline
• Rosenberg (45° flexion PA)

Alignment films. Long-leg standing alignment films are mandatory before any restoration procedure, to quantify the mechanical axis.

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MRI is the key modality. It maps the lesion's location, size and depth (ICRS grade), the state of the subchondral bone (oedema, cysts) and any concurrent meniscal or ligament pathology. On follow-up, cartilage-sensitive sequences and quantitative mapping (for example T2 or dGEMRIC) assess the repair tissue.

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Arthroscopy. Diagnostic arthroscopy defines the true ICRS grade, lesion size, containment and shoulder quality, and the lesion can be measured directly with a probe. It is often also the staging step, the chondrocyte harvest, for ACI/MACI.

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Choosing by size. Treatment selection is size-dependent, and the zone matters too: a lesion in a weight-bearing area is one to treat.

• Small (less than 2 cm²) - microfracture, OAT
• Intermediate (2-4 cm²) - OAT, MACI
• Large (greater than 4 cm²) - MACI, osteochondral allograft (OCA)

Microfracture

Principle. Holes made in the subchondral bone let marrow elements (mesenchymal stem cells, blood) fill the defect, which heals with fibrocartilage. It is first-line for small lesions, less than 2 cm² and ideally less than 1.5 cm², contained with a healthy shoulder.

Technique. Debride the edges to stable margins, then create holes 3-4 mm apart and 3-4 mm deep. Stable vertical margins retain the marrow clot, and the spacing preserves bridges of subchondral bone and reduces tunnel convergence.

Outcome. Results are good in the short term (2-5 years) but deteriorate at 5+ years, since fibrocartilage is less durable than hyaline cartilage.

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ACI and MACI

Principle. Autologous chondrocyte implantation (ACI) and matrix-induced autologous chondrocyte implantation (MACI) repair the defect with the patient's own cultured chondrocytes, and produce hyaline-like cartilage (Type II collagen). It is a two-stage procedure:

1. Harvest chondrocytes arthroscopically
2. Culture and expand the cells (3-4 weeks)
3. Implant them, injected under a periosteal patch (ACI) or on a collagen membrane (MACI)

Indications. Larger lesions (greater than 2-4 cm²), failed microfracture and younger patients.

Bone loss. Where an osteochondral defect has lost bone, as in the trochlear defect below, autologous bone graft restores the subchondral plate before the MACI scaffold is placed cell-side toward bone and secured with fibrin glue. Bone and cartilage are addressed as separate reconstructive layers.

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Outcome. Good results are reported beyond 10 years, and MACI/ACI is better than microfracture for larger lesions. The trial behind that claim is SUMMIT, in which MACI was superior on pain and function at 2 and 5 years for defects 3 cm² or larger. At 14-15 years, however, first-generation ACI showed no advantage over microfracture (Knutsen), a result that cannot be transferred directly to MACI.

Osteochondral autograft transfer (OAT, mosaicplasty)

Principle. Osteochondral plugs are harvested from a non-weight-bearing area (trochlear edge, intercondylar notch) and transplanted into the defect in a single stage, bringing true hyaline cartilage with its bone. It suits small-to-moderate lesions (1-4 cm²) and is limited by donor-site morbidity.

Technique. Congruent plug height and minimal interplug gaps are critical; proud, recessed or widely spaced plugs increase contact stress. The example below is a small structural lateral femoral condyle defect replaced with two plugs.

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Osteochondral allograft (OCA)

Principle. A fresh allograft replaces bone and true hyaline cartilage together, like OAT, but without donor-site morbidity. It is used for large lesions (greater than 4 cm²) and is good for young patients with large defects. The price is disease-transmission risk, availability and cost.

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What it is. Autologous matrix-induced chondrogenesis (AMIC) augments marrow stimulation with a protective scaffold. Standard marrow stimulation (microfracture or drilling) is combined with a collagen type I/III membrane or scaffold laid over the defect and sealed, usually with fibrin glue.

What the membrane does. It protects and stabilises the marrow clot, which is otherwise prone to washout and uneven fill. It also provides a three-dimensional scaffold that organises the marrow-derived mesenchymal cells as they differentiate.

Why it exists. AMIC targets microfracture's two weaknesses, an unstable clot with variable fill and mechanically inferior fibrocartilage, while staying single-stage, cell-culture-free and lower-cost. ACI/MACI is two-stage, regulated and expensive, so AMIC is attractive where cell therapy is unavailable or unaffordable.

Where it sits. It is usually offered for medium (roughly 2-4 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.

Technique. Punctate bleeding appears across the prepared bed as irrigation pressure falls, confirming access to the subchondral vascular bed. The scaffold is secured with fibrin glue and then tested under wet arthroscopy; a stable construct should remain flush through joint motion without lifting at the edge. The patellar and trochlear defects below show the sequence.

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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.

Follow-up imaging. MRI after AMIC must assess both defect fill and the subchondral plate. Structural appearance can evolve despite durable clinical improvement, and it does not alone define success; the series below follows a medial femoral condyle defect to ten years.

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Failure is the dominant concern. Procedure failure with persistent symptoms (graft delamination, incomplete fill or progression to osteoarthritis) ultimately leads to revision restoration or arthroplasty. Each technique has its own ways of failing:

• 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 or 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 or collapse, immunological and (rare) disease-transmission risk, and dependence on chondrocyte viability that falls with storage time
• General - infection, arthrofibrosis or 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 fellowship curricula worldwide.
• 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.

Related pages: Articular Cartilage Injuries for the general treatment of chondral defects across joints, of which this page is the knee-specific case — the two share most of their evidence base because cartilage restoration trials are overwhelmingly knee trials; Osteochondritis Dissecans of the Knee for the subchondral-bone-driven lesion that presents in the same compartment and is managed differently; Osteochondral Lesion of the Talus for the same techniques applied where lesion access and containment differ; Cartilage Healing and Repair for why the tissue cannot restore itself and what fibrocartilage actually is; MRI Cartilage Assessment for the imaging that sizes and stages these defects; and ACL Injuries, Meniscal Transplant and Patellofemoral Instability for the instability, meniscal deficiency and maltracking that must be corrected or any cartilage procedure fails.

Does cartilage restoration prevent osteoarthritis? The honest answer is uncertain. In the Knutsen 14-15 year RCT roughly half of survivors had early radiographic osteoarthritis whether they had ACI or microfracture, and there was no difference in total knee replacement. Restoration improves symptoms, but its disease-modifying claim is unproven; counsel patients accordingly.

The 2-4 cm² grey zone. Microfracture, OAT and MACI all have advocates as first-line treatment here. Microfracture is cheapest and single-stage but produces fibrocartilage, OAT gives true hyaline bone and cartilage but is donor-limited, and 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. The same concerns have driven interest in augmented, scaffold-assisted marrow stimulation such as AMIC.

Patellofemoral lesions remain the hardest subgroup. Historically poorer ACI results (Brittberg 1994) have improved with modern matrix techniques and concurrent patellofemoral realignment or unloading, but the evidence base is thinner than for the femoral condyle.

Allograft access. Availability and regulation of fresh osteochondral allograft vary enormously between countries, a major practical determinant of which option a surgeon can actually offer.

Biologics (PRP, BMAC, stem-cell injections). These are widely marketed as cartilage "regenerators" but lack high-level evidence for true cartilage restoration. Their current role is adjunctive symptom management at best.