The one boundary that rules out repair entirely

Patients searching for answers about cartilage repair usually arrive with a version of the same question: have I left it too long? In most cases the honest answer turns on one factor — not age, not weight, but the extent of cartilage loss across the joint.

When damage is generalised and the surfaces have worn through to bone, no currently available restorative procedure can help. Cartilage repair, transplantation, and injectable scaffold treatments all depend on the same precondition: a focal defect set within an otherwise intact joint. The Royal National Orthopaedic Hospital is explicit on this point — cartilage transplantation and stem cell therapy do not work once established osteoarthritis is present. Brigham and Women's Hospital states the same: once bone-on-bone arthritis has developed, repair is no longer an option. These are not conservative clinical opinions; they reflect a consistent limit across the evidence base.

The structural contrast matters. A focal 'pothole' — full-thickness loss confined to one area, surrounded by healthy cartilage — is precisely the scenario restorative techniques are designed to address. A joint where cartilage loss is diffuse and both articulating surfaces are compromised is a fundamentally different problem, and one that sits beyond the reach of repair. Everything that determines candidacy — age, body weight, defect size, alignment — applies only within this boundary, not past it.

Age and BMI — real risk factors, not automatic disqualifiers

The idea that turning 50 closes the door on cartilage repair is a common misconception — and one worth correcting plainly. Age matters, but it operates as a sliding scale rather than a switch.

Clinically, the optimal window sits below 40 years. Patients between 40 and 50 fall into a grey zone where each case is assessed individually. Above 50 to 55, failure rates for most traditional techniques tend to rise. Yet these figures are clinical heuristics, not hard thresholds. What specialists actually weigh is biological age: the condition of the surrounding cartilage, activity level, and overall joint health. A patient in their mid-fifties with a focal, isolated defect, well-preserved surrounding tissue, and a healthy body weight may still be a realistic candidate for repair.

It is worth noting that the evidence on outcomes in older patients is genuinely mixed — Brittberg et al. (2016) found conflicting results when reviewing the effect of advanced age on repair — which is precisely why individual clinical assessment carries more weight than any published age threshold.

Body weight operates as a separate, additive filter. An ideal BMI sits below 25 kg/m²; the range up to 30 is generally acceptable. BMI above 30 introduces two distinct problems: excess mechanical load bears down on newly repaired tissue before it can mature, and systemic low-grade inflammation associated with obesity actively hinders regeneration. These are independent mechanisms, not the same risk described twice. A patient in their early forties with a BMI of 33 may face greater barriers to a durable repair than a 54-year-old at a healthy weight — the joint biology, not just the birth year, determines the realistic options.

Defect size and containment — what the specialist is actually measuring

Once a specialist has established that the preservation window is open, the next set of questions shifts from eligibility to technique: how large is the defect, is it contained by a healthy cartilage rim, and what does the surrounding tissue look like? These characteristics — not just the presence of damage — determine which procedure is offered.

Small, contained, full-thickness lesions up to approximately 2 cm² have historically been treated with microfracture, which stimulates marrow cells to fill the void. However, microfracture's role has declined considerably. Current evidence shows it produces fibrocartilage — a mechanically inferior tissue — that tends to deteriorate within two to three years, and the procedure can damage the subchondral bone plate in ways that compromise future repair options. It remains a reference point in the clinical literature rather than a modern first-line choice, particularly for active patients who expect the repair to last.

Defects from roughly 2 cm² upward move toward techniques that generate or transfer hyaline-like cartilage. AMIC (matrix-augmented microfracture) bridges smaller defects where marrow stimulation is still viable but needs scaffolding support. OATS and mosaicplasty transplant small osteochondral plugs from a low-load donor site, typically suited to lesions up to around 2 cm² (or up to 4 cm² in mosaic configuration). ACI and MACI — cell-based implants seeded on a collagen membrane — are indicated for larger defects in the 2–10 cm² range. The SUMMIT trial demonstrated that for cartilage injuries of 3 cm² or more, MACI produced significantly better KOOS pain and function scores than microfracture at both two and five years. For extensive posttraumatic lesions where autograft supply is insufficient, fresh osteochondral allograft (OCA) is the appropriate option.

For suitable focal defects, ChondroFiller injection — an ultrasound-guided outpatient injectable collagen scaffold — offers an alternative pathway. Rather than requiring theatre-based surgery, the scaffold is placed image-guided and works via matrix-induced chondrogenesis, recruiting the patient's own progenitor cells to regenerate tissue within the defect site.

No single technique is universally superior; the match depends on defect size, containment, surrounding cartilage quality, and the patient's overall profile.

Malalignment and ligament instability — barriers that can sometimes be removed

A verdict of 'not suitable' sometimes conceals a more nuanced assessment: the problem is not the cartilage defect itself but a mechanical condition that is, in principle, fixable.

Uncorrected varus or valgus malalignment concentrates load across one compartment of the joint, overwhelming newly repaired tissue before it can mature. In such cases, a corrective osteotomy — typically a high tibial osteotomy (HTO) for varus alignment or a distal femoral osteotomy (DFO) for valgus — can redistribute force either before or alongside cartilage repair, converting a mechanically unsuitable joint into a viable one.

Ligament instability follows the same logic. An incompetent ACL allows abnormal shear forces across the repair site that disrupt graft integration. A 2025 multicentre study following 71 patients for five years found that cartilage repair performed concurrently with ACL reconstruction produced structurally equivalent repair tissue — measured by MOCART 2.0 and T2 mapping — to repair in a stable joint. That is a meaningful finding, but the same study showed patient-reported outcome scores remained significantly lower in the combined group at 60 months. The appropriate register here is 'structurally sound but not identical in clinical recovery' — a realistic basis for informed consent rather than a reason to exclude patients outright.

Anyone told they are unsuitable owing to alignment or ligament problems is worth asking one direct question: would correcting those issues change their candidacy?

Why timing matters — cartilage cannot heal itself

Underlying the candidacy criteria described above is a straightforward biological problem: cartilage has no blood supply. Without blood vessels, it cannot mount the inflammatory and regenerative response that other tissues use to close a wound. A cartilage defect does not scar over, fill in, or stabilise on its own — it simply persists, and under the repetitive mechanical loads of daily movement, tends to worsen.

The clinical significance of this becomes concrete at around 1 cm² of full-thickness loss. Below that threshold, defects may remain relatively stable; above it, the surrounding cartilage progressively breaks down as the lesion edges soften and the joint load redistributes onto already-compromised tissue. Left untreated, a focal 'pothole' can evolve into the diffuse, generalised loss that places a joint beyond the reach of repair.

There is some evidence that the pre-osteoarthritis state — where damage is present but not yet widespread — may be at least partially reversible with timely intervention. The trajectory without it is consistently in one direction.

None of this calls for alarm. Unexplained mechanical knee symptoms — catching, swelling, or deep aching after activity — are a reasonable prompt for specialist assessment, not a reason to assume the worst. The practical message is that prolonged watchful waiting carries a cost that earlier review does not.

Options when the preservation window has closed

Being past the cartilage repair window is not a clinical dead end. The pathway forward depends on how disease has distributed across the joint and on the patient's age, activity level, and the mechanical pattern driving deterioration.

For younger, active patients whose joint narrowing is principally driven by malalignment rather than global cartilage loss, osteotomy — high tibial (HTO) or distal femoral (DFO) — remains a meaningful joint-preservation option. By redistributing load away from the affected compartment, it can slow deterioration and, in some cases, defer joint replacement by years.

Where disease is more advanced, partial or total joint replacement is the established pathway. Outcomes at this stage are well-evidenced and reliably predictable. Partial replacement preserves native tissue where one compartment is predominantly affected; total replacement addresses the whole joint surface when loss is widespread.

Emerging biologics and tissue-engineering scaffolds are under active investigation as future routes beyond the current limits, but none yet offers a reliable path past established osteoarthritis. That position may shift with time; it has not shifted yet.

Identifying which of these pathways fits a specific situation requires specialist assessment. Search MSK lists joint-preservation and replacement surgeons across the UK, searchable by region and specialty.