Mankin, J Bone Joint Surg Am 1982 - The Response of Articular Cartilage to Mechanical Injury

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The Response of Articular Cartilage to Mechanical Injury

Mankin·J Bone Joint Surg Am·1982·1,229 citations·Review article

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Mankin reviewed how articular cartilage responds to mechanical injury and why its avascularity limits healing. Current Concepts Review of experimental evidence on three injury types: superficial laceration, deep injury penetrating subchondral bone, and blunt impact, plus the effect of postoperative motion.

Key Findings

Superficial lacerations confined to cartilage trigger a brief metabolic and mitotic response that subsides by 1 to 2 weeks. The defect never heals but remained stable without progression to osteoarthritis for at least 2 years.
Injuries penetrating subchondral bone recruit marrow-derived cells through a fibrin clot. The repair tissue is a fibrocartilage-hyaline mixture containing up to 20% type I collagen.
Osteochondral repair depended on defect size in an equine model: defects under 3 mm repaired completely by 3 months, whereas defects of 9 mm or more never repaired completely.
Impact strains of 40% or more killed chondrocytes, while strains of 10% or less caused no apparent injury. Repetitive subthreshold loading still produced about 20% hexosamine loss and 20% higher subchondral bone stiffness.
Significance: The review established that cartilage repair requires access to the vascular marrow, framed injury by depth and mechanism, and cited evidence that continuous passive motion yields more hyaline-like repair than immobilization.

Board PearlPartial-thickness chondral injuries do not heal because cartilage is avascular, whereas full-thickness injuries breaching subchondral bone heal with fibrocartilage rich in type I collagen.

The Response of Articular Cartilage to Mechanical Injury.

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The Response of Articular Cartilage to Mechanical Injury

Mankin·J Bone Joint Surg Am·1982·1,229 citations·Review article

|

Mankin reviewed how articular cartilage responds to mechanical injury and why its avascularity limits healing. Current Concepts Review of experimental evidence on three injury types: superficial laceration, deep injury penetrating subchondral bone, and blunt impact, plus the effect of postoperative motion.

Key Findings

Superficial lacerations confined to cartilage trigger a brief metabolic and mitotic response that subsides by 1 to 2 weeks. The defect never heals but remained stable without progression to osteoarthritis for at least 2 years.
Injuries penetrating subchondral bone recruit marrow-derived cells through a fibrin clot. The repair tissue is a fibrocartilage-hyaline mixture containing up to 20% type I collagen.
Osteochondral repair depended on defect size in an equine model: defects under 3 mm repaired completely by 3 months, whereas defects of 9 mm or more never repaired completely.
Impact strains of 40% or more killed chondrocytes, while strains of 10% or less caused no apparent injury. Repetitive subthreshold loading still produced about 20% hexosamine loss and 20% higher subchondral bone stiffness.
Significance: The review established that cartilage repair requires access to the vascular marrow, framed injury by depth and mechanism, and cited evidence that continuous passive motion yields more hyaline-like repair than immobilization.

Board PearlPartial-thickness chondral injuries do not heal because cartilage is avascular, whereas full-thickness injuries breaching subchondral bone heal with fibrocartilage rich in type I collagen.

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