Why Cartilage and Chondral Defects of the Knee Rarely Heal Naturally
Articular cartilage defects larger than 2-4 mm in diameter rarely heal naturally because cartilage is avascular, lacks lymphatic drainage, has no neural elements, and is immunologically isolated by its extracellular matrix, fundamentally preventing the inflammatory and reparative processes required for tissue healing. 1
Fundamental Biological Barriers to Natural Healing
Absence of Vascular Supply
- Articular cartilage is completely avascular, which prevents delivery of inflammatory cells, growth factors, and mesenchymal stem cells necessary for tissue repair. 1, 2
- Without blood supply, the typical wound healing cascade (inflammation, proliferation, remodeling) cannot occur in superficial or partial-thickness cartilage defects. 3
- Only when defects penetrate the subchondral bone plate can hematoma formation and stem cell migration occur, but this produces inferior fibrocartilage rather than native hyaline cartilage. 3
Structural and Cellular Limitations
- Cartilage lacks lymphatic drainage and neural elements, further isolating it from systemic repair mechanisms. 1
- The dense extracellular matrix surrounding chondrocytes shields them from immunological recognition and prevents cellular migration into defect sites. 1
- Chondrocytes have limited proliferative capacity and cannot adequately repopulate defect areas, particularly in larger lesions. 3
Size-Dependent Healing Potential
Critical Defect Size
- Defects smaller than 2-4 mm may have some limited healing potential, but lesions exceeding this threshold demonstrate virtually no spontaneous repair. 1
- The American Academy of Orthopaedic Surgeons recognizes this size threshold in treatment algorithms, recommending surgical intervention for defects ≥2 cm². 4
Quality of Repair Tissue
- When healing does occur (typically only in full-thickness defects penetrating subchondral bone), the repair tissue is fibrocartilage rather than hyaline cartilage. 3, 5
- Fibrocartilage is biomechanically inferior to native hyaline cartilage and provides only transient, inadequate replacement that degenerates over time. 3
Integration Failure at Defect Margins
Barriers to Lateral Integration
- Even when repair tissue forms, it fails to integrate laterally with surrounding native cartilage due to chondrocyte cell death at wound edges, the dense collagenous and proteoglycan networks that resist cellular migration, and lack of vascular ingrowth to support tissue bridging. 3
- This integration failure leads to mechanical instability of repair tissue and poor long-term prognosis. 3
Clinical Implications
Progression to Osteoarthritis
- The poor intrinsic healing capacity of cartilage means untreated defects typically progress to disabling pain and early osteoarthritis. 5
- The American Academy of Orthopaedic Surgeons emphasizes that long-term monitoring is important as chondromalacia may progress to osteoarthritis if not properly managed. 6
Hostile Joint Environment
- The mechanical loading and shear forces in weight-bearing joints like the knee create a hostile environment that further impedes any limited healing attempts. 5
- This mechanical stress accelerates degeneration of any fibrocartilage that does form in penetrating defects. 5
Common Pitfalls in Understanding Cartilage Healing
- Do not assume that bleeding into a defect (from penetrating subchondral bone) represents adequate healing—the resulting fibrocartilage is structurally and functionally inferior to hyaline cartilage. 3
- Do not expect superficial or partial-thickness defects to heal at all—without penetration to vascularized bone, no repair response occurs. 3, 1
- Recognize that the avascular nature of cartilage is the fundamental barrier; all other factors (lack of stem cells, poor integration, mechanical stress) are downstream consequences of this primary limitation. 1, 2