Articular Cartilage Injuries

Articular cartilage is avascular, aneural and alymphatic. It takes its nutrition by diffusion from synovial fluid, and without a blood supply there is no inflammatory healing response. Every repair on this page works around that fact: either a channel is opened to the marrow (microfracture) or cells are brought in from outside (ACI). The zonal architecture is set out in articular cartilage structure, and the reasons the tissue cannot regenerate itself in cartilage healing and repair.

Who. Cartilage damage is seen in 60% of knee arthroscopies. Peak incidence is between 10 and 50 years, males are more commonly affected, and sports injuries are a common cause. Defects are traumatic or degenerative, and the distinction shapes who is a candidate for repair (see Clinical Assessment).

Natural history. Full-thickness defects do not heal; partial-thickness defects may not progress. Size correlates with symptoms, the surrounding cartilage is at risk, and an untreated defect leads to osteoarthritis.

The zones. Hyaline cartilage is layered, and the collagen orientation and the load resisted differ by zone:

• Superficial (tangential) zone - Type II collagen parallel to the surface; resists shear
• Middle (transitional) zone - oblique collagen; resists compressive forces
• Deep (radial) zone - perpendicular collagen; anchors to the tidemark
• Calcified cartilage - above the subchondral bone; the tidemark separates it from the deep zone

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Composition. Water is 65-80% of wet weight and is biphasic with the solid matrix. Type II collagen is 10-20% of wet weight and provides tensile strength. Proteoglycans (aggrecan) carry a negative charge that attracts water, and that is what resists compression. Chondrocytes occupy only 1-5% of the volume; they maintain the matrix and do not divide.

Biomechanics. Compressive strength comes from the proteoglycan-water interaction and tensile strength from the collagen network. Lubrication is boundary and fluid film, and the coefficient of friction is 0.001-0.01, lower than ice on ice.

Grade the lesion with ICRS, and know Outerbridge because it is older and less commonly used now but may appear in exam questions. The size grouping that chooses the operation is in Management.

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History. Establish whether the onset was acute trauma or insidious, and whether the pain is activity-related with mechanical symptoms. Locking or catching raises the question of a loose body. Ask about the pattern of swelling (the effusion) and about previous surgery, which may represent a failed treatment.

Examination. An effusion is common after an acute injury, and tenderness is focal at the joint line. Range of motion is usually preserved unless the knee locks. Assess alignment for varus or valgus, and stability with ACL and meniscal tests.

Traumatic or degenerative. A traumatic defect is single and contained, with healthy surrounding cartilage, and is a good candidate for a restorative procedure. A degenerative defect is one of multiple lesions with poor surrounding cartilage, and kissing lesions are common; it is a poor candidate for isolated cartilage surgery, and arthroplasty or osteotomy should be considered instead.

MRI is the gold standard for cartilage evaluation. Proton density sequences, T2 mapping and dGEMRIC are used, and the assessment covers location, size, depth and bone oedema. Kissing (bipolar) lesions carry a worse prognosis, and the quality of the surrounding cartilage affects surgical planning.

Radiographs are taken weight-bearing:

• Standing AP - joint space narrowing
• Rosenberg view (45° flexion PA) - more sensitive
• Long leg alignment films - the mechanical axis, before any osteotomy
• Lateral - the patellofemoral joint and trochlear dysplasia

Arthroscopy is the definitive assessment. The probe detects softening and depth, size is measured with a calibrated probe or ruler, the rim is assessed for stability if ACI is being considered, and a biopsy is taken if proceeding to ACI.

The decision. Size is the primary determinant of treatment, and it must be combined with patient age, activity, location, depth and concomitant pathology rather than used in isolation.

Algorithm

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Debridement is the first step of the ladder: it removes loose fragments.

Which size. Every number above is useless without knowing what is being measured, and this is where the algorithm is most often misapplied. The size that decides the operation is the defect measured arthroscopically after debridement back to stable, vertical, healthy cartilage walls, not the size reported on MRI. The two differ systematically and in one direction: the debrided defect is larger, because undermined and delaminated cartilage at the rim looks intact on MRI and is removed once probed. A lesion reported as 1.8 cm² can comfortably become 2.5 cm² on the table, which moves it out of marrow-stimulation territory and into a graft or cell-based procedure. Three practical consequences follow:

• Consent for the range, not the plan. A patient booked for microfracture on an MRI measurement should be consented for the possibility of a larger procedure, or for a staged approach with a biopsy taken at the index arthroscopy if cell therapy is a realistic destination.
• Measure it properly. Use a calibrated arthroscopic probe, and record the defect in two perpendicular dimensions after debridement rather than estimating an area by eye.
• The thresholds were derived against durability, not early pain relief. Marrow stimulation performs respectably at one to two years across a wide range of defect sizes; what deteriorates with time and with increasing size is the durability of the fibrocartilage fill. A threshold quoted without that context invites the wrong conclusion when a large defect appears to do well at first review.

Microfracture (under 2cm²). Marrow stimulation is single-stage and low-cost, the first line for small lesions and best for a contained defect on the femoral condyle. Penetrating the subchondral plate gives the marrow elements access to the defect, and the repair tissue they form is fibrocartilage.

OATS / mosaicplasty (2-4cm²). Osteochondral autograft transfer moves cylindrical plugs of true hyaline cartilage, with their bone, from a non-weight-bearing area into the defect. The ceiling is the donor: availability and donor-site morbidity limit how many plugs can be taken, and therefore how large a defect can be resurfaced.

ACI / MACI (over 4cm²). Cultured autologous chondrocytes are implanted at a second operation, so the procedure is two-stage and expensive, and it requires an intact cartilage rim (shoulders). It gives the best long-term hyaline-like restoration for large lesions.

Fresh osteochondral allograft (large with bone loss). A single graft replaces both cartilage and subchondral bone, which makes it the option when the lesion involves the subchondral bone. Chondrocyte viability requires fresh tissue.

Patient factors. The ideal candidate:

• Age under 45 years
• Single, contained defect
• Normal alignment
• Stable knee (intact ligaments)
• Intact menisci
• High demand, motivated for rehabilitation
• Normal BMI

Relative contraindications, for whom alternative options should be considered:

• Age over 55 (consider HTO or UKA instead)
• Multiple or kissing (bipolar) lesions, or diffuse osteoarthritis
• Uncorrected malalignment (address alignment first)
• Ligament insufficiency
• Meniscal deficiency
• Low-demand patient
• BMI over 35
• Inflammatory arthritis

Concomitant pathology. Each is paired with the cartilage procedure:

• Malalignment - HTO or DFO, staged or concurrent, to unload the diseased compartment: a varus knee with a medial defect needs a medial opening-wedge HTO, and a valgus knee with a lateral defect needs a DFO
• ACL deficiency - ACL reconstruction
• Meniscal deficiency - meniscal allograft
• Patellofemoral lesion - tibial tubercle osteotomy; anteromedialisation (Fulkerson) unloads a distal or lateral patellar facet lesion

Microfracture and ACI/MACI share the protocol below: CPM, and NWB or TTWB for 6-8 weeks. After microfracture, impact is avoided for 4-6 months.

Microfracture. 70-80% good or excellent at 5 years. Durability is limited, the fibrocartilage degrades over time, and it is best regarded as a bridge procedure.

OATS. 80-90% good outcomes, limited by the number of plugs that can be taken.

ACI/MACI. 80-90% satisfaction at 10 or more years, and the best long-term hyaline restoration, at the cost of an expensive two-stage procedure.

Osteochondral allograft. 75-85% survival at 10 years; the best option for large defects with bone loss.

Prognosis. Young age, a single defect, femoral condyle location, normal alignment, intact menisci and a first-time procedure predict a good result. Age over 40, bipolar lesions, patellofemoral location, malalignment and revision surgery predict a poor one.

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The knee dominates cartilage teaching, but the talar dome is the second most common site and behaves differently enough to be a favourite viva extension. The same biological ladder applies, but the thresholds, morphology and classification are talus-specific.

Morphology by location. Posteromedial lesions are the commonest: typically deeper and cup-shaped, and often atraumatic or degenerative. Anterolateral lesions are usually shallower and wafer-shaped, and more clearly traumatic, following an inversion injury. This shapes both diagnosis and the choice of resurfacing.

Imaging and access. MRI assesses cartilage, bone oedema and subchondral cysts; CT best defines the bony geometry and cyst size for planning. Posteromedial lesions are hard to reach and may need a medial malleolar osteotomy for open grafting.

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