Why the size of a cartilage defect changes everything

A number on your MRI report — the area of the cartilage defect, measured in square centimetres — does more to determine your treatment options than almost any other single finding. That figure is not just a description of how much cartilage is affected; it is effectively a routing decision for the type of repair that is biologically and technically feasible.

Clinicians grade these lesions using the ICRS (International Cartilage Repair Society) or Outerbridge scale, running from a surface softening at grade I through to a full-thickness hole exposing bare bone at grade III–IV. It is at those higher grades that active repair becomes relevant, and it is the lesion's measured area at that depth that shapes what is realistically on the table.

Three broad size bands map to three different procedural approaches. Defects under roughly 2 cm² can be addressed with marrow-stimulation techniques or a single-plug autograft transfer. Between 2 cm² and 4 cm², mosaicplasty — tiling several smaller autograft plugs side by side — extends coverage without requiring a second operation or donor tissue. Beyond 4 cm², or where significant bone loss is also present, the available supply of harvestable autograft runs out, and a different category of intervention is required altogether.

Size does not act in complete isolation. A 3 cm² defect accompanied by underlying bone damage can behave clinically like a considerably larger lesion and may therefore need treatment from a higher band. The goal across all three bands remains the same: restoring durable, load-bearing tissue — not simply reducing symptoms in the short term. The sections that follow work through each band in detail.

Microfracture: its historical role and why smaller defects still need a closer look

Microfracture has been the most widely used cartilage procedure for two decades, largely because it is technically straightforward: fine picks perforate the subchondral bone beneath the defect, allowing marrow-derived stem cells to migrate upwards and fill the cavity with a repair clot. The tissue that forms is fibrocartilage — not the true hyaline cartilage that lines a healthy joint. Fibrocartilage is structurally softer and less resistant to wear, and under repetitive loading it tends to break down within two to three years, particularly in active patients.

There is a second concern that matters for anyone who may need further treatment in future. The perforations damage the subchondral bone plate — the dense layer sitting just below the cartilage surface — and that damage can reduce the likelihood of success for any subsequent repair procedure. For younger patients especially, preserving that plate is worth factoring into the decision early.

The 2021 Cartilage Book — a standard orthopaedic reference text used across surgical practice — still lists microfracture alongside mosaicplasty as a reasonable option for lesions under approximately 2 cm², particularly in lower-demand or older patients. That reflects the reality that microfracture retains a role in a specific, narrow window. But as alternatives have matured, the threshold at which clinicians reach for it first has continued to narrow. For younger, more active patients, the outcome gap between mosaicplasty and microfracture becomes visible even below 2 cm² when follow-up extends to a decade.

OATS and mosaicplasty: matched hyaline cartilage for the one-to-four centimetre range

The distinction between OATS and mosaicplasty is spatial. OATS — osteochondral autograft transfer — takes a single cylindrical plug, typically 8–10 mm in diameter, of the patient's own cartilage together with its underlying bone from a lower-load region of the same knee, and seats it precisely into the prepared defect. One plug, one hole. That makes it well-matched to compact focal lesions up to roughly 2 cm².

Mosaicplasty follows the same biological logic but tiles two or more smaller plugs side by side, filling a larger area in a mosaic pattern. This extension of coverage pushes the technique's upper reach to approximately 4 cm² — still within a single operation, without a second-stage procedure, cell-culture step, or donor tissue from another person.

What both approaches share matters more than how they differ from each other: the transplanted material is mature hyaline cartilage already bonded to its subchondral bone plate. This is structurally the same tissue as the original surface, not the fibrocartilage substitute that forms after marrow stimulation. The 2021 Cartilage Book notes that mosaicplasty shows higher clinical scores than microfracture at long-term follow-up in this size range — a finding consistent with the mechanical difference between the two repair tissues over years of loading.

Donor-site morbidity — discomfort or mild weakness at the harvest site on the peripheral femoral condyle — is a genuine consideration in the planning conversation, not a reason to avoid the procedure in well-selected patients. The benefit-to-risk balance shifts, however, as defect size grows: harvesting sufficient autograft for defects much above 4 cm² requires removing tissue at a scale that can cause lasting problems at the donor site itself. That practical ceiling is where autograft-based repair stops and other options begin.

What the long-term outcome evidence shows — and where it is still limited

The evidence base splits cleanly along one axis: activity demand. In athletes specifically, published data from the London Cartilage Clinic reports approximately double the rate of good or excellent outcomes — and a comparable gap in return-to-sport rates — with OATS or mosaicplasty compared with microfracture over a ten-year horizon. Pareek et al.'s 2016 systematic review, examining 10-year follow-up data across published OATS series, found that both IKDC and Lysholm scores rose significantly from pre-operative baseline and held those gains at the decade mark.

The picture looks different in general populations. The Ulstein 2014 prospective RCT — the most directly comparable controlled trial available — followed 25 patients with ICRS grade 3–4 lesions over a median of 9.8 years and found no statistically significant difference between microfracture and OAT mosaicplasty in Lysholm score, KOOS, isokinetic muscle strength, or radiographic osteoarthritis appearances. Mean Lysholm scores were 69.7 for microfracture versus 62.6 for mosaicplasty — a numerical gap that did not reach significance.

The reconciliation lies in the tissue, not in a contradiction. Fibrocartilage tolerates moderate, variable loading reasonably well; it degrades under the repetitive high-load cycles that characterise athletic activity. Differences that are invisible in a mixed-activity cohort become apparent — and widen — in sport-specific populations followed over the same period.

One important caveat: with only 25 participants, the Ulstein trial carries limited statistical power. Its null result should be read as inconclusive, not as evidence that the techniques are equivalent across all patient types. There is also, to date, no published head-to-head RCT comparing OATS or mosaicplasty with osteochondral allograft — a gap that consultants navigate through cohort data and individual case assessment.

When defects exceed the autograft limit: OCA and MACI as the step-up

The ceiling established by donor-site supply — roughly 4 cm² for mosaicplasty — is where two distinct alternatives take over, each suited to a different clinical picture.

Fresh osteochondral allograft (OCA) provides a size-matched cylinder of donor cartilage together with its underlying subchondral bone, making it the appropriate step when a defect exceeds approximately 4 cm² (some series extend to 6–9 cm²), involves significant bone loss, affects both opposing joint surfaces, or arises in a revision setting where prior procedures have already disturbed the bone plate. Because the tissue comes from a donor rather than the patient's own knee, the supply constraint that caps mosaicplasty does not apply.

MACI — matrix-induced autologous chondrocyte implantation — occupies a parallel niche for larger defects where the bone itself remains essentially intact. The SUMMIT trial found that at this size threshold (≥3 cm²), KOOS pain and function scores were substantially better with MACI than with microfracture at both two and five years — evidence that marrow stimulation becomes an inadequate repair strategy as defect area grows. MACI does, however, require two separate procedures: a biopsy to harvest chondrocytes, followed by reimplantation of cells cultured on a collagen membrane.

Neither pathway competes with mosaicplasty in its core 1–4 cm² range; they complete the size ladder above it.

Getting an accurate assessment and planning the right repair

The size ladder described across this article — microfracture under 2 cm², OATS and mosaicplasty from 1 to 4 cm², OCA and MACI beyond that — is a clinical framework, not a rigid formula. Age, activity demand, defect geometry, bone involvement, and revision history all shift where a given patient sits on that ladder. A young athlete with a 1.8 cm² lesion and mild varus malalignment faces a different surgical calculation than an older patient with an apparently identical MRI finding.

Accurate measurement is the prerequisite. Weight-bearing X-rays, high-field or Open MRI, and clinical assessment together define defect size, depth, and bone involvement — the variables that most reliably determine procedural fit. Where malalignment is a contributing factor, objective biomechanical evaluation — MAI Motion® markerless motion capture provides one such measure — can inform both surgical planning and postoperative loading strategy.

The clearest conclusion to draw from the evidence reviewed here is that matching the repair to the defect — rather than defaulting to the most technically familiar procedure — is what the long-term outcome data consistently reward.

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