Why defect size alone rarely settles the question

When a surgeon raises both osteochondral allograft (OCA) and matrix-induced autologous chondrocyte implantation (MACI) as possible routes for a large knee cartilage defect, the natural question is: what tips the decision one way or the other? The short answer is that defect size does most of the initial filtering — both procedures are designed for lesions that have grown beyond what microfracture or an osteochondral autograft (OATS) can reliably address, broadly above the 2–4 cm² range. But size alone rarely closes the argument.

The more decisive variable is depth: specifically, whether the lesion stays within the cartilage layer or breaches the subchondral bone beneath it. A medium-sized defect of 4–5 cm² with an intact bone plate may be well suited to MACI; the same surface area with underlying bone damage often is not. OCA replaces both the cartilage and the bone in a single procedure, which gives it a structural advantage when the deeper layer is compromised.

Thinking of this as a clinical ladder — rather than a binary either/or — is more useful. Area sets the shortlist; depth, bone quality, prior treatment history, and patient age then determine which rung of that ladder applies to a given case. The sections that follow work through each of those variables in turn.

The size range where OCA and MACI overlap

Three centimetres squared is a useful reference point — but not for the reason patients sometimes assume. The SUMMIT randomised trial established that defects of 3 cm² or more achieved meaningfully better KOOS pain and function scores with MACI than with microfracture at both two and five years. That threshold marks where MACI demonstrably outperforms marrow stimulation; it does not mark the point at which OCA becomes necessary.

Real-world practice confirms MACI is routinely applied well into mid-to-large defect territory. A database of 2,690 patients found a mean defect area of 5.64 cm², with 70% of cases falling between 3 cm² and 10 cm². Clinical trial populations tended toward somewhat smaller lesions, underlining that surgeons in everyday practice regularly extend MACI to defects considerably larger than the original approval evidence covered.

OCA's cited therapeutic range begins at roughly 2 cm² and extends to 8 cm² or beyond, meaning both procedures share considerable common ground — broadly across the 3–8 cm² band. Each has a documented clinical evidence base within that zone, and both are technically feasible. A defect of 5 cm², for example, does not fall naturally into one column or the other on area measurement alone.

That shared territory is precisely where size stops being the primary arbiter and where the structural character of the lesion — how far it extends below the cartilage surface — becomes the more informative variable.

When bone loss makes MACI the wrong tool

MACI is, in structural terms, a surface repair. The cell-seeded collagen membrane bonds to existing tissue at the base of the defect — which means that tissue needs to be there. When trauma, avascular necrosis, a large osteochondritis dissecans (OCD) lesion, or a bone cyst has eroded the subchondral plate, MACI has no adequate substrate to anchor to. Placing the membrane over a compromised or absent bone foundation does not restore the joint; it leaves the biological repair unsupported from below.

OCA bypasses this problem entirely by transplanting a plug of donor bone and overlying cartilage together in a single stage. The structural deficit is addressed at the same time as the articular surface.

The clinical evidence bears this out. A retrospective cohort of 148 patients — 82 treated with ACI and 66 with OCA — found no significant difference in KOOS JR or IKDC scores between the two procedures when bone loss was excluded from the analysis. On cartilage-only lesions with an intact subchondral plate (broadly ICRS Grade 3–4 without bone breach), the two approaches perform comparably over a mean follow-up of 6.7 years. The same study noted that when significant subchondral bone damage or loss was present, OCA may hold an advantage — because it restores the osseous layer that cell-based repair cannot.

In practical terms, the threshold at which bone involvement consistently tips the choice toward OCA sits at roughly 4 cm² combined area with demonstrable subchondral damage, though that figure is a rule of thumb rather than a firm cut-off. MRI is the primary pre-operative tool for assessing depth; direct intraoperative inspection at arthroscopy often refines the picture further. A lesion that looks manageable on imaging can reveal more extensive bone involvement once the surgeon has a direct view — which is one reason the area measurement alone rarely finalises the decision in advance.

Salvage after failed microfracture or ACI

For patients who have already been through a cartilage procedure — most often microfracture — the treatment landscape shifts in ways that are not always explained clearly at the time of re-referral.

Microfracture has a well-established historical role as a first response to smaller focal defects, and for many years it was the default starting point. The difficulty is that the fibrocartilage it generates tends to break down within two to three years, and the drilling process itself can leave residual scarring and disruption of the subchondral bone plate. That damaged bone bed is not simply a surface problem: it compromises the structural foundation on which any subsequent repair must rest.

This matters directly for the OCA versus MACI question. A cell-seeded membrane — whether first-generation ACI or MACI — depends on a healthy, vascularised subchondral substrate to integrate and survive. When the bone plate has been disrupted by prior marrow stimulation and subsequent fibrocartilage failure, that substrate may no longer be adequate. In these cases, failed microfracture is an independent clinical trigger for OCA rather than a second attempt at cell-based repair.

The same logic applies, though less commonly, after a failed first-generation ACI. Where prior cell-based treatment has not held and the tissue environment is compromised, OCA offers structural salvage by replacing both the cartilage layer and the bone beneath it — addressing the deficit that a membrane-based approach could not resolve alone.

Age, graft survival, and practical trade-offs

Even when size and depth point in the same direction, a handful of practical factors tend to surface in the consultation room — and they are worth understanding before that conversation happens.

Age is one of the more visible. In comparative cohorts, patients treated with ACI or MACI averaged around 31 years at the time of surgery, roughly six years younger than those who received OCA (mean 37.7 years). This gap reflects how surgeons already weigh biological age against anticipated joint demands: MACI is FDA-approved for patients aged 18–55 and is contraindicated where cartilage loss is diffuse rather than focal. Patients who fall outside that profile — whether older, or with broader joint involvement — move toward OCA by default rather than by preference.

OCA's graft longevity gives some reassurance for that decision. Published series report survival rates of 59–91% at 10–25 years, with approximately 90% of grafts functioning at the 10-year mark and around 70% retained at 20–25 years. For a younger active patient who needs decades of joint function, that track record is a meaningful consideration.

Two practical constraints pull in the other direction. MACI requires two separate procedures — a biopsy to harvest chondrocytes, followed weeks later by implantation — which adds both surgical exposure and recovery time. OCA is single-stage, but depends on donor tissue availability, and carries a small risk of disease transmission inherent to any allograft; thorough tissue banking protocols reduce but do not eliminate that risk. Neither factor overrides size or depth as the primary decision driver, but both belong in an informed discussion with a specialist.

Evidence gaps and how to find the right specialist

Direct head-to-head trial evidence for OCA versus MACI in large defects — specifically those exceeding 6 cm² with measurable subchondral bone loss — does not yet exist. Most of the comparative data covered in this article come from retrospective cohorts or indirect trial findings. The SUMMIT RCT established that MACI outperforms microfracture for defects of 3 cm² or more, but it did not place OCA as the comparator, leaving that specific question unanswered in the published literature.

In practice, the surgical assessment is designed to fill precisely this gap. Surgeons draw on MRI, weight-bearing imaging, and intraoperative depth evaluation together to determine whether the subchondral plate is involved — the variable that an area measurement alone cannot capture. Patients who work with a surgeon experienced in both procedures are better placed to have that individualised conversation. Search MSK lists specialists across the UK who offer both OCA and MACI; filtering by region and specialty is a practical starting point for identifying someone with relevant large-defect experience.

The clearest summary the evidence supports: where the bone plate is intact, MACI is the default for large focal cartilage defects; where it is compromised — through depth of injury, prior failed repair, or frank bone loss — OCA addresses what a cell-seeded membrane cannot.