Cartilage Healing and Repair

Articular cartilage is a specialised connective tissue built for load bearing and joint articulation. The composition and structure that give it excellent mechanical function also leave it with virtually no intrinsic healing capacity.

Why it matters. Cartilage injuries are common, affecting up to 60% of patients undergoing knee arthroscopy. Because the tissue cannot heal spontaneously, injury leads to progressive joint degeneration and osteoarthritis, and understanding its biology is essential for choosing a treatment rationally.

Hunter's warning. Hunter's 1743 statement that "ulcerated cartilage is a troublesome thing, once destroyed it is not repaired" remains relevant. Modern surgical techniques try to overcome this biological limitation through a range of regenerative strategies.

The matrix. Articular cartilage consists of chondrocytes embedded in an extensive extracellular matrix (ECM), which makes up about 95% of tissue volume; the chondrocytes are only 5%. By wet weight the matrix is:

• Water, 65-80%, trapped by the charge of the proteoglycans, which gives compressive stiffness through fluid pressurisation
• Collagen, 10-20%, predominantly Type II, arranged in zone-specific orientations to provide tensile strength and the tissue's architecture, with smaller amounts of Types IX and XI
• Proteoglycans, 5-10%, chiefly aggrecan, bound to hyaluronic acid; glycosaminoglycans (chondroitin sulphate, keratan sulphate) create the negative charge that attracts water

The zones. Collagen orientation, cell shape and function change with depth from the surface, down to a calcified layer that makes the transition to subchondral bone.

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Nothing arrives to repair it. Articular cartilage is avascular, aneural and alymphatic, and adult chondrocytes have minimal mitotic activity. With no blood supply there is no inflammatory response and no marrow-derived stem cells. Nutrition reaches the chondrocytes only by diffusion from synovial fluid, and matrix turnover is extremely slow.

Partial-thickness injury. An injury confined to cartilage above the tidemark has no access to:

• Blood supply, so no inflammatory cells
• Bone marrow, so no mesenchymal stem cells
• Clotting factors, so no fibrin scaffold

The chondrocytes beside the injury have limited mitotic capacity and cannot migrate to fill the defect. Proteoglycan is depleted around the rim of the lesion, and that leads to progressive degeneration.

Full-thickness injury. When the injury penetrates subchondral bone, marrow elements reach the defect and a repair sequence follows:

1. Haemorrhage and clot formation, which lays down a fibrin scaffold
2. An inflammatory response, with macrophages and growth factors
3. Migration of marrow-derived stem cells (MSCs) into the defect
4. Differentiation of those cells into fibrochondrocytes, forming fibrocartilage
5. Production of Type I collagen, and an inferior repair tissue

What that repair is worth. The result is fibrocartilage, made of Type I collagen, in place of hyaline cartilage made of Type II. It is less stiff in compression, resists wear poorly and tends to deteriorate over time under load.

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A diagnosis of exclusion. A focal chondral defect is a clinical diagnosis of exclusion. Several conditions mimic its presentation of mechanical knee pain, effusion and catching, and they must be distinguished because management differs entirely.

Defining the lesion. MRI localises a focal osteochondral lesion and its subchondral response, which distinguishes a contained repair target from diffuse cartilage loss. Direct arthroscopic inspection defines lesion size, containment and unstable tissue more accurately than surface imaging alone, and associated findings such as a loose body or tibial damage also change the repair plan.

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The goal. Every surgical option aims to restore hyaline-like tissue. Microfracture produces fibrocartilage; osteochondral autograft (OATS) and fresh osteochondral allograft (OCA) transplant true hyaline cartilage; autologous chondrocyte implantation (ACI/MACI) aims for hyaline-like regeneration, with variable success.

Marrow StimulationOsteochondral AutograftCell-Based Therapies

Microfracture. Microfracture is the most commonly performed cartilage repair procedure, and widely used because it is simple and cheap. Holes of 3-4mm are made in the subchondral bone at 3-4mm intervals, and marrow bleeding into the defect supplies MSCs, growth factors and a fibrin scaffold for the repair tissue, which is fibrocartilage.

Indications. It suits smaller defects, under 2-4 cm², that are contained with stable shoulders, and many centres use it as first-line treatment.

Outcomes. Short-term results are good, but they deteriorate at 5-8 years as the fibrocartilage degenerates under load.

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OATS. Cylindrical plugs of hyaline cartilage with their underlying bone are transferred from non-weight-bearing areas into the defect. Donor sites are the lateral trochlear ridge and the margins of the intercondylar notch. The operation transplants mature, functional hyaline cartilage rather than attempting to regenerate it.

Mosaicplasty. The defect is measured, cylindrical grafts are harvested from a low-load region, recipient sockets are prepared, and the plugs are tamped flush to restore a congruent hyaline-cartilage surface.

Strengths and limits. It gives true hyaline cartilage and immediate structural restoration in a single stage. Against that are donor-site morbidity, limited graft availability (under 3-4 cm²) and the difficulty of matching the convexity or concavity of the recipient surface.

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Autologous chondrocyte implantation. A two-stage procedure: cartilage is harvested and the chondrocytes cultured, then the cells are reimplanted, where they produce hyaline-like matrix in the defect. The technique has passed through three generations:

• First: cells injected under a periosteal patch
• Second: a collagen membrane cover
• Third (MACI): matrix-assisted, with cells seeded on a scaffold

Indications and results. ACI is indicated for larger defects of 2-10 cm², in young, active patients, and after failed microfracture. Biopsies show hyaline-like tissue in 70-80%, and medium-term clinical results are good.

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Emerging therapies. These continue to evolve rapidly:

• Stem cell approaches: bone marrow aspirate concentrate (BMAC) and adipose-derived stem cells
• Scaffolds: various synthetic and biological matrices, including hyaluronic scaffolds for matrix-assisted techniques
• Growth factors: BMP-7, TGF-beta and IGF-1, under investigation

Why it is not rejected. Fresh osteochondral allograft transplants donor cartilage without HLA matching or immunosuppression, which is surprising for an allograft. Because cartilage is avascular, aneural and alymphatic, and its dense matrix physically shields the chondrocytes from the host immune system, it is relatively immunoprivileged and is not rejected the way a vascularised organ graft would be. Donor grafts are screened for disease transmission and matched for size and topography to restore the joint contour, but need no blood-group or HLA matching.

Viability is the currency. The transplanted chondrocytes must survive to maintain the matrix, and viability declines with storage time. Fresh grafts are therefore used within roughly 28 days, and a viability above about 70% is the commonly cited target for a usable graft.

What integrates. The bone is a non-living scaffold that the host revascularises and remodels by creeping substitution. The cartilage does not "heal in" but delivers mature hyaline function from the start, which is why OCA suits large (over 4 cm²) or osteochondral defects, salvage and AVN, where the subchondral bone must also be replaced.

Technique. Planning and implantation rest on four points:

• Weight-bearing radiographs, long-leg alignment and MRI define the defect dimensions, bone loss, joint-space condition and mechanical environment before a structural graft is selected
• The donor cartilage-bone segment is cut to final dimensions and trialled against the recipient template so that contour, thickness and orientation match before implantation
• The diseased osteochondral unit is reamed to a stable bed of known depth, allowing a press-fit graft without proud or recessed cartilage edges
• The graft is inserted in its planned orientation and tamped flush with the surrounding cartilage, minimising step-off and shear at the host-graft interface

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Beyond defect size. The size ranges in the table overlap, and the rest of the choice turns on these:

• Microfracture: first-line for smaller defects, low cost, single stage
• OATS: smaller defects where hyaline cartilage is wanted in a single stage, limited by donor tissue
• ACI/MACI: larger defects in younger patients willing to undergo two operations
• OCA: large defects, salvage and AVN, and it requires fresh tissue to be available

Is there a size threshold? The historical 2 cm² cut-off between microfracture and ACI is not firmly evidence-based. The SUMMIT trial used 3 cm², while registries suggest microfracture underperforms even below 2 cm² in high-demand patients. The true threshold is patient- and lesion-specific, not a fixed number.

Does microfracture do harm? Perforating the subchondral plate can produce intralesional osteophytes, subchondral cysts and bony overgrowth, and may compromise later procedures. Some surgeons now prefer subchondral-sparing nanofracture or microdrilling, with smaller-diameter, deeper channels, to reduce thermal necrosis and plate damage, but high-level comparative data remain limited.

Biological augmentation. Platelet-rich plasma (PRP) and bone marrow aspirate concentrate (BMAC) are widely used to "augment" marrow stimulation, but the evidence is heterogeneous and largely low-level. No standardised preparation exists, and robust RCT data do not yet support routine use.

Repair versus natural history. Many small, asymptomatic chondral lesions found incidentally at arthroscopy may never become symptomatic, so over-treatment is a genuine risk. The decision to intervene should be driven by symptoms attributable to the lesion, not by its mere presence on MRI.

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Why it decides the result. Rehabilitation after cartilage repair is decisive and easily overlooked, and the durability data above hinge on it. Repair tissue matures slowly and is vulnerable to premature loading.

The maturation window. Repair tissue, fibrocartilage after marrow stimulation or hyaline-like tissue after ACI/MACI, is soft and disorganised at first and remodels over roughly 12 to 18 months. Rehabilitation protects it while it matures.

Early motion. Salter's work established that continuous passive motion (CPM) nourishes chondral repair tissue and promotes a more hyaline-like result than immobilisation. Early protected motion is therefore standard after most cartilage procedures, within joint-specific limits.

Weight-bearing follows the lesion location.

• Femoral condyle or tibial (weight-bearing) lesions: restricted or protected weight-bearing, touch or partial, for about 6 to 8 weeks with early full range of motion, so the repair is moved but not compressed
• Patellofemoral (trochlea or patella) lesions: weight-bearing in extension is usually allowed, but flexion is restricted with a brace to keep shear and load off the repair during the vulnerable phase

Return to sport. Impact and pivoting sport are resumed deliberately late, commonly around 6 to 9 months after microfracture and 9 to 18 months after ACI/MACI or osteochondral procedures. Premature return is a leading cause of repair failure.

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Global Epidemiology

Focal chondral or osteochondral lesions are found in roughly 60% of knee arthroscopies, with full-thickness (ICRS grade III-IV) lesions in around 5-11%. They are most common in active patients in the third and fourth decades, and a substantial minority are associated with concurrent ligament or meniscal injury — reinforcing that cartilage damage is rarely an isolated problem.

Side-by-Side Guidance

Registry & Resource Notes

• Dedicated cartilage registries (e.g. the German Cartilage Registry / KnorpelRegister DGOU and national procedure registries) track repair outcomes; unlike arthroplasty, cartilage procedures are not consistently captured in joint-replacement registries.
• High-resource settings: full menu available — matrix-assisted ACI, fresh osteochondral allograft, and biologic augmentation in specialist centres.
• Limited-resource settings: marrow stimulation (microfracture/microdrilling) and osteochondral autograft dominate because they are single-stage, low-cost and need no cell-culture facility or tissue bank. Fresh allograft availability is constrained by tissue-banking infrastructure and short chondrocyte viability windows.