Cartilage Healing and Repair

Zonal Architecture

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Articular cartilage is a specialized connective tissue with unique properties optimized for load bearing and joint articulation. Its composition and structure provide excellent mechanical function but severely limit intrinsic healing capacity.

Clinical Significance

Cartilage injuries are common, affecting up to 60% of patients undergoing knee arthroscopy. The inability of cartilage to heal spontaneously leads to progressive joint degeneration and osteoarthritis. Understanding cartilage biology is essential for rational treatment selection.

Historical Perspective

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

Cartilage Structure and Composition

Articular cartilage consists of chondrocytes embedded in an extensive extracellular matrix (ECM). The ECM comprises approximately 95% of tissue volume and contains:

Collagen (10-20% wet weight): Predominantly Type II collagen arranged in zone-specific orientations. Provides tensile strength and tissue architecture. Type IX and XI collagens are also present in smaller amounts.

Proteoglycans (5-10% wet weight): Aggrecan is the major proteoglycan, bound to hyaluronic acid. Glycosaminoglycans (chondroitin sulfate, keratan sulfate) create negative charge attracting water.

Water (65-80% wet weight): Trapped by proteoglycan charge. Provides compressive stiffness through fluid pressurization.

Zonal Organization

Why Partial Thickness Injuries Cannot Heal

Injuries confined to cartilage above the tidemark have no access to:

• Blood supply (no inflammatory cells)
• Bone marrow (no mesenchymal stem cells)
• Clotting factors (no fibrin scaffold)

Chondrocytes adjacent to injury have limited mitotic capacity and cannot migrate to fill defects. Proteoglycan depletion around the lesion rim leads to progressive degeneration.

Full Thickness Injury Response

When injury penetrates subchondral bone, the following sequence occurs:

1. Hemorrhage and clot formation - fibrin scaffold forms
2. Inflammatory response - macrophages and growth factors
3. MSC migration - marrow-derived stem cells populate defect
4. Fibrocartilage formation - cells differentiate into fibrochondrocytes
5. Type I collagen production - inferior repair tissue forms

This repair tissue is biomechanically inferior: less stiff, poor wear resistance, and tends to degenerate over time.

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

The management algorithm ends with "rehabilitation, graft integration and return-to-sport readiness", and the durability data above hinge on it — yet cartilage-repair rehabilitation is decisive and easily overlooked, because repair tissue matures slowly and is vulnerable to premature loading.

• The maturation timeline drives everything. Repair tissue (fibrocartilage after marrow stimulation, hyaline-like after ACI/MACI) is soft and disorganised at first and remodels over roughly 12 to 18 months; rehabilitation protects it while it matures.
• Continuous passive motion (CPM) and early protected ROM. Salter's work established that CPM nourishes chondral repair tissue and promotes a more hyaline-like result than immobilisation, so early protected motion is standard after most cartilage procedures (within joint-specific limits).
• Weight-bearing is governed by the LESION LOCATION:
  • Femoral condyle / tibial (weight-bearing) lesions — restricted/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/patella) lesions — weight-bearing in extension is usually allowed, but flexion is restricted with a brace to keep shear/load off the patellofemoral repair during the vulnerable phase.
• Staged 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 — because premature return is a leading cause of repair failure.

The single teaching point: match the weight-bearing and ROM restriction to the lesion location, and respect the long maturation window — a technically perfect repair fails if it is loaded too soon.

The OCA option above transplants fresh donor cartilage without HLA matching or immunosuppression — surprising for an allograft, and the reason ties straight back to this topic's central theme. Because articular cartilage is avascular, aneural and alymphatic, and its dense matrix physically shields the chondrocytes from the host immune system, the cartilage is relatively immunoprivileged and is not rejected the way a vascularised organ graft would be.

• Chondrocyte viability is the currency. The transplanted chondrocytes must survive to maintain the matrix, so graft viability declines with storage time — this is why fresh grafts are used within roughly 28 days, and a viability above about 70% is the commonly cited target for a usable graft.
• Screening, not matching. Donor grafts are screened for disease transmission and size/topography-matched to restore the joint contour, but they do not require blood-group/HLA matching or immunosuppression.
• What integrates and what does not. The bone portion is a non-living scaffold that the host revascularises and remodels by creeping substitution; the cartilage does not "heal in" but delivers immediate mature hyaline function — which is why OCA suits large or osteochondral defects, salvage and AVN, where the subchondral bone must also be replaced.

Selection Criteria

Microfracture: First-line for smaller defects, low cost, single stage.

OATS: Smaller defects where hyaline desired, single stage, limited by donor.

ACI/MACI: Larger defects, younger patients, willing to undergo two surgeries.

OCA: Large defects, salvage, AVN, requires fresh tissue availability.

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.

Articular cartilage has virtually no intrinsic healing capacity due to being avascular, aneural, alymphatic, and having chondrocytes with minimal mitotic activity. Partial thickness injuries (above tidemark) cannot heal—no blood supply means no inflammatory response or marrow-derived stem cells. Full thickness injuries penetrating subchondral bone access marrow elements and form fibrocartilage (Type I collagen), which is biomechanically inferior to native hyaline cartilage (Type II collagen). Surgical repair strategies aim to restore hyaline-like tissue: microfracture produces fibrocartilage, OATS transplants true hyaline, ACI/MACI aims for hyaline-like regeneration, and osteochondral allograft provides fresh hyaline cartilage for large defects. Cartilage is 65-80% water with chondrocytes comprising only 5% of tissue volume.