Cartilage Healing and Repair

Imaging Gallery

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Imaging Gallery

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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.

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.

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.

TGA Regulation: MACI products require TGA approval and specialized facility certification. ACI services available at select centers with appropriate tissue culture facilities.

Registry Data: Cartilage procedures not captured in AOANJRR but outcomes tracked through individual institution databases and research registries.

PBS Considerations: Hyaluronic acid injections have limited PBS coverage. MACI is high cost and typically out-of-pocket or private insurance.

Clinical Practice: Microfracture remains first-line in many centers due to cost and simplicity. MACI available at tertiary sports medicine centers. Fresh allograft availability limited compared to North America.