Who cartilage repair is designed for

The short answer is: someone younger and active, with a specific patch of cartilage damage in an otherwise healthy joint, who has not found lasting relief through physiotherapy or conservative care. That profile — rather than age alone — is what specialist assessment is built around.

Four variables drive the candidacy decision more than any others: age and biological responsiveness, activity level and physical demand, lesion grade (classified on the ICRS scale), and lesion surface area. Younger, active patients tend to mount a stronger biological repair response and are better placed to complete the rehabilitation a procedure requires. Age works as a guide here, not a hard cut-off — a biologically responsive 55-year-old in good joint health may be a stronger candidate than a sedentary 35-year-old with multiple lesion sites.

The most important boundary is between focal and diffuse disease. Cartilage repair addresses a defined, isolated patch of damage in a joint that is otherwise structurally intact — stable ligaments, correct alignment, a single compartment affected. Where cartilage loss has spread across the joint surface, a localised repair cannot resolve joint-wide pain and deterioration, and a different pathway becomes appropriate.

Symptoms also need to cross a threshold: persistent, activity-limiting pain or mechanical symptoms that conservative management — physiotherapy, load adjustment, analgesia — has not resolved.

What the lesion assessment looks at

Once clinical candidacy looks likely, the next question is how the lesion itself measures up — and that requires imaging before any repair decision is made.

MRI provides the pre-operative map, showing location, depth, and approximate surface area of the defect. It is the gold standard for detecting cartilage problems, but intraoperative assessment at arthroscopy gives the definitive picture: grade and size can look different once the joint surface is inspected directly. Neither reading alone is sufficient; together they determine what repair is technically possible.

Lesion depth is classified on the ICRS scale. Grade 2 involves less than 50% of cartilage thickness — significant damage, but the deeper layers remain intact. Grade 3 extends beyond 50% of depth (further subdivided by how much of the surface area is involved), and Grade 4 penetrates through the subchondral bone entirely. Each step up signals how much structural cartilage remains and what biological environment the chosen repair will have to work with.

Surface area acts as a routing tool rather than a pass-or-fail gate. Defects under roughly 2 cm² are often suited to single-stage options or, where the lesion profile is appropriate, to an ultrasound-guided injectable collagen scaffold such as ChondroFiller injection in an outpatient setting. From around 2–4 cm² upward, cell-based techniques such as MACI or ACI become more appropriate; very large or posttraumatic defects may call for osteochondral allograft. The SUMMIT trial gives this a concrete anchor: lesions of 3 cm² or more achieved significantly better KOOS pain and function scores with MACI compared with microfracture at both two and five years. The conclusion is not that a larger defect excludes a patient — it is that it signals the need for a more substantial repair strategy.

When the window for repair has closed

The biology itself sets the boundary. Three anatomical realities make repair mechanistically impossible — not inadvisable, impossible.

When the bone surface beneath the cartilage has been exposed and worn smooth (eburnated bone), there is no biological substrate left for new tissue to anchor into. Microfracture, cell-based techniques, and scaffold approaches all depend on healthy underlying bone to integrate; bone-on-bone contact removes that foundation entirely.

Where degeneration has spread across multiple compartments of the joint, a localised repair patch addresses only a fraction of the damaged surface. Joint-wide friction and load imbalance continue unresolved; the repaired site cannot function in isolation from the surrounding tissue.

Severe, uncorrected malalignment or ligament instability presents a third limit. Mechanical forces that drove the original damage persist; repaired tissue cannot mature in an environment that abnormally loads it from day one. Advanced structural deformity combined with significant muscle wasting further reduces the biological responsiveness that tissue integration requires.

At this end of the spectrum, joint replacement is the clinically appropriate endpoint — not a sign that repair was withheld, but the correct answer given what the biology permits. For patients where alignment or instability is the primary concern rather than diffuse cartilage loss, the threshold shifts, and that distinction is addressed in the section that follows.

Joint problems that affect — but do not always end — candidacy

Many joints that arrive at a specialist consultation carry more than one problem at once. A cartilage defect may coexist with a meniscal tear, a degree of ligament laxity, or a mechanical alignment issue that has gradually shifted load onto the damaged compartment. Each of these, left uncorrected, would undermine any repair — but the critical point is that they can often be corrected concurrently, and doing so preserves candidacy rather than ending it.

Malalignment is the clearest example. Where the knee has drifted into varus or valgus, high tibial osteotomy (HTO) or distal femoral osteotomy (DFO) can redistribute load away from the damaged compartment. Combining alignment correction with a cartilage repair procedure in the same surgical episode is a clinically established approach for younger patients — it is not a complicating factor but a recognised part of the treatment plan.

Meniscal tears and ligament insufficiency follow the same principle. Addressing them at the same stage removes the mechanical environment that would otherwise accelerate failure of the repaired tissue; leaving them to a separate, later procedure raises recurrence risk without good clinical justification.

A patient who looks borderline on initial review — because several things in the joint need attention — may remain a genuine repair candidate once those concurrent issues are identified and addressed. Whether they do is determined by specialist assessment of the full joint environment, not by the presence of the additional problems alone.

How repair options are matched to the lesion

Technique choice follows lesion characteristics — once candidacy is established, three rough size bands provide a practical map of the options.

Smaller focal defects can be addressed without a theatre visit. The ChondroFiller injection delivers a liquid collagen scaffold directly into the defect under ultrasound guidance as an outpatient procedure; it gels in situ and recruits the patient's own progenitor cells through matrix-induced chondrogenesis. Where a single-stage surgical route is preferred for small-to-medium defects, AMIC (matrix-augmented microfracture, which places a resorbable scaffold over the marrow-stimulation site) and OATS/mosaicplasty (osteochondral autograft cylinders, typically for defects of 1–2 cm²) are established options; donor-site considerations are relevant with OATS.

Defects in roughly the 2–10 cm² range generally call for cell-based repair. MACI (autologous chondrocytes seeded onto a collagen membrane) and first-generation ACI are both two-stage procedures — biopsy first, implantation after a cell-culture interval — with solid mid-term evidence. The SUMMIT trial showed superior KOOS pain and function outcomes with MACI over microfracture for lesions of 3 cm² or more at both two and five years. Emerging single-stage ACI variants (sometimes referred to as STACI or next-generation ACI) aim to consolidate the two stages into one; published evidence here remains limited.

Very large or posttraumatic defects, especially where underlying bone is also involved, may require osteochondral allograft (OCA) — donor tissue that replaces both cartilage and bone in a single procedure.

Microfracture alone is no longer considered a modern first-line choice for most defects. Current evidence indicates fibrocartilage breakdown within two to three years and subchondral bone plate damage that can narrow future repair options.

Finding a cartilage specialist in the UK

Knowing roughly where a lesion sits — in size, depth, and joint environment — gives a patient a meaningful starting point for a first specialist conversation. The questions that matter most at that stage are whether the joint is structurally sound enough to support repair, whether any concurrent problems can be addressed at the same time, and which technique best matches the defect profile. No imaging report or online resource can answer those questions in place of a face-to-face assessment combining clinical history, examination, and specialist review of MRI findings.

Search MSK lists cartilage specialists across the UK, with filters for region, joint, and treatment type — a practical way to identify a consultant whose practice covers the full range of restorative options relevant to your situation.