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Osteochondral Defects of the Knee

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Osteochondral Defects of the Knee

Comprehensive guide to osteochondral defects and cartilage restoration of the knee for FRCS exam preparation

complete
Updated: 2025-12-25
High Yield Overview

OSTEOCHONDRAL DEFECTS

Cartilage Lesions | MACI | OAT | Restoration

MFCMost common location
less than 2 cm²Microfracture limit
MACI/ACILarger lesions
OATSmall contained lesions

ICRS Grade

Grade I
PatternSoftening, superficial
TreatmentObservation
Grade II
PatternPartial thickness less than 50%
TreatmentConsider treatment
Grade III
PatternPartial greater than 50% or to subchondral
TreatmentTreat
Grade IV
PatternFull thickness to bone
TreatmentTreat

Critical Must-Knows

  • Medial femoral condyle is most common location
  • ICRS grading classifies cartilage damage
  • Microfracture for small (less than 2cm²) contained lesions
  • MACI/ACI for larger lesions (greater than 2-4cm²)
  • OAT (mosaicplasty) for small-moderate lesions

Examiner's Pearls

  • "
    Address alignment, meniscal, and ligament issues concurrently
  • "
    Microfracture produces fibrocartilage (Type I collagen)
  • "
    ACI/MACI produces hyaline-like cartilage (Type II)
  • "
    OAT transfers hyaline cartilage with bone from non-weight-bearing area

Clinical Imaging

Imaging Gallery

In vivo animal study procedure. Microfracture done at the femoral condyle cartilage of a rabbit, and the lesion was covered with scaffolds. a Microfracture done at the femoral condylar cartilage lesio
Click to expand
In vivo animal study procedure. Microfracture done at the femoral condyle cartilage of a rabbit, and the lesion was covered with scaffolds. a MicrofraCredit: Kim J et al. via J Orthop Surg Res via Open-i (NIH) (Open Access (CC BY))
Saggital PD-weighted TSE MRI of the same patient depicted in Figure 5. A dislocated fragment lying in the intercondylar notch (short white arrow) corresponds to the full thickness cartilage defect at
Click to expand
Saggital PD-weighted TSE MRI of the same patient depicted in Figure 5. A dislocated fragment lying in the intercondylar notch (short white arrow) corrCredit: von Engelhardt LV et al. via BMC Musculoskelet Disord via Open-i (NIH) (Open Access (CC BY))
Axial PD-weighted TSE MRI of a 15-year-old male with a recurrent LPD. At the medial facet of the patella, a full-thickness defect of the cartilage (grade 4) with ulceration of the bone is demonstrated
Click to expand
Axial PD-weighted TSE MRI of a 15-year-old male with a recurrent LPD. At the medial facet of the patella, a full-thickness defect of the cartilage (grCredit: von Engelhardt LV et al. via BMC Musculoskelet Disord via Open-i (NIH) (Open Access (CC BY))

Clinical Imaging

Imaging Gallery

Critical OCD Knee Exam Points

Microfracture

Small lesions (less than 2cm²). Marrow stimulation. Creates fibrocartilage (Type I collagen). Good short-term but deteriorates at 5+ years. Contained lesion ideal.

MACI/ACI

Larger lesions (greater than 2-4cm²). Two-stage: harvest chondrocytes, culture, implant. MACI uses membrane. Produces hyaline-like cartilage. Better long-term than microfracture for large lesions.

OAT

Osteochondral autograft transfer (mosaicplasty). Small-moderate lesions. Plugs from non-weight-bearing area (trochlea, notch). True hyaline cartilage. Limited by donor site.

OCA

Osteochondral allograft. Large lesions (greater than 4cm²). Fresh allograft. Good for young patients with large defects. Disease transmission risk, availability issues.

At a Glance

Osteochondral defects involve damage to articular cartilage and underlying subchondral bone, with the medial femoral condyle (MFC) being the most common weight-bearing location. Treatment selection is size-dependent: microfracture for small lesions (less than 2cm²) produces fibrocartilage (Type I collagen), while MACI/ACI for larger lesions (greater than 2-4cm²) produces hyaline-like cartilage (Type II). OAT (mosaicplasty) transfers true hyaline cartilage with bone from non-weight-bearing areas. Critical principle: always address concomitant alignment, meniscal, and ligamentous pathology for successful outcomes.

Mnemonic

SIZETreatment Selection by Size

S
Small (less than 2cm²)
Microfracture, OAT
I
Intermediate (2-4cm²)
OAT, MACI
Z
Zone matters
Weight-bearing = treat
E
Enormous (greater than 4cm²)
MACI, OCA

Memory Hook:SIZE determines treatment: Small = microfracture/OAT, Large = MACI/OCA!

Overview and Classification

Osteochondral defects of the knee involve damage to the articular cartilage and potentially underlying subchondral bone. Goals of treatment are pain relief, improved function, and prevention of osteoarthritis.

ICRS Classification

Grade I: Superficial softening, fibrillation Grade II: Partial thickness lesion (less than 50% depth) Grade III: Deep lesion (greater than 50% depth) or down to subchondral bone Grade IV: Full thickness with exposed subchondral bone

Grade III and IV are generally treated.

Location

Medial femoral condyle (MFC): Most common weight-bearing location for symptomatic lesions.

Treatment Options

📊 Management Algorithm
Management algorithm for Osteochondral Defects Knee
Click to expand
Management algorithm for Osteochondral Defects KneeCredit: OrthoVellum

Mechanism: Create holes in subchondral bone. Marrow elements (MSCs, blood) fill defect. Forms fibrocartilage.

Indications: Small lesions (less than 2cm², ideally less than 1.5cm²). Contained with healthy shoulder. First-line for small lesions.

Technique: Debride edges to stable margins. Create microfracture holes 3-4mm apart, 3-4mm deep.

Outcomes: Good short-term (2-5 years). Deteriorates over time. Fibrocartilage (Type I collagen) less durable than hyaline (Type II).

MACI: Matrix-induced autologous chondrocyte implantation.

ACI: Autologous chondrocyte implantation.

Two-Stage:

  1. Harvest chondrocytes arthroscopically
  2. Culture and expand cells (3-4 weeks)
  3. Implant: Inject under periosteal patch (ACI) or on collagen membrane (MACI)

Indications: Larger lesions (greater than 2-4cm²). Failed microfracture. Younger patients.

Outcomes: Hyaline-like cartilage (Type II collagen). Good 10+ year results. Better than microfracture for larger lesions.

OAT (Mosaicplasty):

  • Harvest osteochondral plugs from non-weight-bearing area (trochlea edge, intercondylar notch)
  • Transplant to defect
  • Single-stage
  • Small-moderate lesions (1-4cm²)
  • Limited by donor site morbidity

OCA (Osteochondral Allograft):

  • Fresh allograft
  • Large lesions (greater than 4cm²)
  • No donor site morbidity
  • Disease transmission, availability, cost

Both provide true hyaline cartilage with bone.

Key Considerations

Address Concurrent Pathology

Alignment: Varus/valgus malalignment must be corrected (HTO, DFO). Uncorrected alignment leads to failure.

Meniscus: Meniscal deficiency increases contact stress. Consider MAT if previous meniscectomy.

Ligaments: ACL deficiency causes abnormal kinematics. Reconstruct if unstable.

Patient Selection

  • Young (typically under 40-50)
  • Active, motivated
  • Single compartment disease
  • Focal lesion (not diffuse OA)
  • Normal or correctable alignment
  • Stable knee

Evidence Base

I (RCT)
📚 Saris et al (SUMMIT)
Key Findings:
  • MACI vs microfracture for knee cartilage defects
  • MACI superior at 5 years
  • Better cartilage repair tissue with MACI
  • MACI recommended for larger lesions
Clinical Implication: MACI superior to microfracture for larger lesions.
Source: Am J Sports Med 2014

III
📚 Mithoefer et al
Key Findings:
  • Microfracture systematic review
  • Good short-term results
  • Deterioration at 5+ years
  • Lesion size matters
Clinical Implication: Microfracture for small lesions, deteriorates long-term.
Source: Am J Sports Med 2009

Exam Viva Scenarios

Practice these scenarios to excel in your viva examination

VIVA SCENARIOStandard

Scenario 1: Cartilage Defect Treatment

EXAMINER

"A 28-year-old has a 3cm² full-thickness cartilage defect on the medial femoral condyle. Knee is stable with normal alignment. What are your treatment options?"

EXCEPTIONAL ANSWER
This young patient has a moderate-sized (3cm²) focal cartilage defect on the MFC which is the most common location for symptomatic lesions. With a stable knee and normal alignment, he is a good candidate for cartilage restoration. The goals are pain relief, improved function, and prevention of OA. For a lesion of this size, my options include microfracture, OAT (mosaicplasty), or MACI. Microfracture is simple but best for lesions less than 2cm², and 3cm² is borderline. It produces fibrocartilage which deteriorates at 5+ years. OAT (osteochondral autograft transfer) is an option - I would harvest plugs from non-weight-bearing areas (lateral trochlea, notch) and transplant. It's single-stage and provides hyaline cartilage with bone. Limitation is donor site morbidity. For a 3cm² lesion, multiple plugs needed. My preferred option would be MACI (matrix-induced autologous chondrocyte implantation). This is a two-stage procedure: first arthroscopy to harvest chondrocytes, culture for 3-4 weeks, then implant on a collagen membrane. Evidence shows MACI is superior to microfracture for lesions greater than 2cm², producing hyaline-like cartilage with better long-term durability. Post-operatively he would need protected weight-bearing for 6-8 weeks, progressive ROM, and a lengthy rehabilitation. Return to sport at 9-12 months.
KEY POINTS TO SCORE
3cm² = microfracture borderline, consider MACI or OAT
MACI superior for larger lesions (greater than 2cm²)
Produces hyaline-like cartilage
Address alignment, meniscus, ligaments
COMMON TRAPS
✗Using microfracture for large lesions
✗Not considering concurrent pathology
✗Not knowing MACI is two-stage
LIKELY FOLLOW-UPS
"What type of cartilage does microfracture produce?"
"What is the SUMMIT trial?"
VIVA SCENARIOChallenging

Scenario 2: Failed Microfracture - Revision Decision-Making

EXAMINER

"You are seeing a 32-year-old recreational footballer in your clinic 3 years after he underwent arthroscopic microfracture for a 1.8cm² ICRS grade IV cartilage defect on the medial femoral condyle. At the time, microfracture was appropriate given the lesion size (under 2cm²) and he was a suitable candidate - young, active, stable knee with normal alignment. He did well initially, returning to football at 9 months post-operatively with significant improvement in his knee pain. However, over the past 6-8 months, his medial knee pain has gradually returned and is now limiting his ability to play football. He has tried physiotherapy, activity modification, and NSAIDs with minimal benefit. On examination, he has medial joint line tenderness, a small effusion, and pain with deep knee flexion. Range of motion is full (0-135°). His knee is stable to ligamentous examination and there is no malalignment on standing alignment. You order an MRI which shows deterioration of the previously treated cartilage lesion - the microfractured area now has poor fill with irregular surface and underlying bone marrow edema. The lesion measures approximately 2.2cm² (slightly larger than original). There is no evidence of other cartilage damage, meniscal pathology, or ligamentous injury. The patient is frustrated and asks what can be done - he wants to continue playing football. How do you counsel him and what is your management plan?"

EXCEPTIONAL ANSWER
This patient represents a classic case of failed microfracture with deterioration of the repair tissue at 3 years, which is consistent with the known natural history of microfracture. I would counsel him that his initial treatment was appropriate - microfracture is the standard first-line treatment for small (less than 2cm²) focal cartilage defects, and his lesion at 1.8cm² was ideal for this approach. The issue is that microfracture produces fibrocartilage (Type I collagen) rather than hyaline cartilage (Type II), and while fibrocartilage provides good short-term pain relief (2-5 years), it is biomechanically inferior and deteriorates over time, particularly in active patients with high demands on the knee. Studies (Mithoefer et al 2009) show that microfracture results deteriorate at 5+ years, and he is unfortunately experiencing this at 3 years, likely due to his high activity level with football. The lesion has now enlarged slightly to 2.2cm² due to breakdown of the fibrocartilage and potentially propagation of the defect. For revision treatment, I have several options to discuss: (1) Conservative management - accept that the microfracture has failed and manage symptomatically with activity modification (reduce/stop football), physiotherapy for strength and unloading strategies, weight management if needed, analgesia, and consider viscosupplementation or corticosteroid injections for symptom control; however, at 32 years old wanting to continue sport, this is unlikely to meet his goals; (2) Revision microfracture - technically possible but has poor success rates in this scenario (30-40% vs 70-80% for primary microfracture) because the first microfracture has depleted the marrow elements and created a sclerotic base that doesn't respond well to repeat marrow stimulation; generally not recommended; (3) MACI (matrix-induced autologous chondrocyte implantation) - this is my preferred option for this patient. MACI is specifically indicated for failed microfracture and for lesions now measuring 2.2cm² (in the 2-4cm² range where MACI excels). Evidence from the SUMMIT trial (Saris et al 2014) shows MACI is superior to microfracture for lesions greater than 2cm², producing hyaline-like cartilage (Type II collagen) with better long-term durability. The procedure is two-stage: first arthroscopy to harvest chondrocytes from a non-weight-bearing area (trochlea), send for culture and expansion (3-4 weeks), then second surgery (mini-arthrotomy or arthroscopic) to debride the failed microfracture tissue back to healthy bone, prepare the lesion with stable shoulders, and implant the cultured chondrocytes on a collagen membrane secured with fibrin glue or sutures. Post-operatively, he would need protected weight-bearing (non-weight-bearing or touch-toe weight-bearing) for 6-8 weeks to allow graft incorporation, progressive ROM starting early but avoiding deep flexion initially, then gradual strengthening. Return to sport would be at minimum 9-12 months, possibly 12-18 months given this is revision surgery. Expected outcomes: 70-80% good-excellent results at 10 years with MACI for failed microfracture, superior to revision microfracture. Important point - I would verify on repeat imaging that alignment is truly neutral (full-length standing alignment films) because even subtle varus/valgus can overload the compartment and cause cartilage failure. If any malalignment detected, would need to combine MACI with corrective osteotomy (HTO/DFO). Similarly, I would confirm meniscal integrity - if he has had partial medial meniscectomy previously (not mentioned but possible), the increased contact stress could contribute to failure and I might consider staged MAT + MACI. ACL status is stable so no concern there. I would counsel realistic expectations - MACI is not a guarantee and there is still 20-30% failure rate even in ideal circumstances, and this being revision surgery may have slightly worse outcomes than primary MACI. Alternative option (4) is osteochondral allograft (OCA) for the lesion, which would provide true hyaline cartilage with bone support, but this is typically reserved for larger lesions (greater than 4cm²) or failed MACI, so I would not use as first-line revision option for 2.2cm² lesion. My recommendation would be to proceed with MACI for failed microfracture, with counseling that return to football at previous level is possible but not guaranteed, and he needs to accept a lengthy rehabilitation (12+ months). If he is not willing to undergo two-stage surgery and prolonged rehab, then conservative management is the alternative.
KEY POINTS TO SCORE
Microfracture deterioration at 3 years - expected natural history of fibrocartilage repair: Microfracture produces fibrocartilage (Type I collagen, inferior mechanical properties to hyaline cartilage Type II); Good short-term results (70-80% at 2-5 years) but deteriorates over time, particularly in young active patients (Mithoefer 2009 systematic review); Fibrocartilage breakdown typically occurs 5+ years but can be earlier in high-demand patients (football involves pivoting, cutting, high shear forces); Lesion enlargement from 1.8cm² to 2.2cm² represents progression as fibrocartilage fails and defect propagates; This is biological failure of repair tissue, not technical failure of original surgery
MACI is treatment of choice for failed microfracture - evidence-based revision strategy: MACI specifically indicated for failed marrow stimulation techniques and for lesions 2-4cm² (this patient now 2.2cm²); Two-stage procedure: (1) arthroscopic chondrocyte harvest from non-weight-bearing trochlea, culture 3-4 weeks, (2) mini-arthrotomy or arthroscopic implantation on collagen membrane; Debride failed microfracture tissue back to stable base (remove all fibrocartilage and sclerotic bone), ensure healthy shoulders for graft; SUMMIT trial (Saris 2014 Level I RCT): MACI superior to microfracture for lesions greater than 2cm² at 5 years - better cartilage repair tissue, improved clinical outcomes; Produces hyaline-like cartilage (Type II collagen) with better durability than fibrocartilage; Expected outcomes: 70-80% good-excellent results at 10 years, superior to revision microfracture (30-40% success)
Revision microfracture has poor success - not recommended for failed primary microfracture: Repeat marrow stimulation in previously microfractured area has 30-40% success vs 70-80% for primary; Mechanism of failure: (1) depleted marrow stem cell reservoir (already used in first microfracture), (2) sclerotic subchondral bone (poor bleeding response to repeat awls/drilling), (3) poor biological milieu (scar tissue, fibrosis); Only consider revision microfracture if patient refuses MACI (cost, time commitment, two-stage), accepts poor prognosis, or has medical contraindications to MACI; Generally should counsel patient that revision microfracture unlikely to provide durable benefit and MACI is better evidence-based option
Verify alignment and meniscal status - concurrent pathology causes cartilage procedure failure: Even subtle varus malalignment (2-3° mechanical varus) overloads medial compartment and causes cartilage repair failure; Must obtain full-length standing alignment films to confirm mechanical axis passes through knee center - if varus detected, MUST combine MACI with high tibial osteotomy to correct alignment and unload compartment; Similarly, previous partial meniscectomy increases contact stress 20-30% and can contribute to cartilage failure - if significant meniscal deficiency identified, consider staged meniscal allograft transplant (MAT) before or concurrent with MACI; ACL deficiency causes abnormal kinematics and shear forces - confirm ACL stable (this patient is stable); Fundamental principle: cartilage procedures fail if concurrent pathology not addressed
Post-operative protocol and return to sport - lengthy rehabilitation for MACI: Initial 6-8 weeks: non-weight-bearing or touch-toe weight-bearing to allow chondrocyte incorporation and early matrix formation; ROM started early but gentle - continuous passive motion (CPM) if available, active-assisted ROM, avoid deep flexion (greater than 90°) first 6 weeks; 6-12 weeks: progressive weight-bearing, advance ROM to full, begin strengthening (quad sets, straight leg raises, cycling); 3-6 months: advanced strengthening, proprioception training, sport-specific rehab (agility, cutting drills); 9-12 months minimum before return to pivoting sport like football, possibly 12-18 months given revision surgery; Serial MRI at 6 and 12 months to assess graft incorporation; Patient must understand this is significantly longer recovery than microfracture (6-9 months), requires patience and compliance with protocol
COMMON TRAPS
✗Recommending revision microfracture for failed primary microfracture - poor evidence and outcomes: Revision microfracture has only 30-40% success rate because marrow elements depleted and bone sclerotic; Doing same procedure that already failed and expecting different result is not sound clinical reasoning; MACI is evidence-based choice for failed microfracture (SUMMIT trial, multiple case series); Not offering MACI denies patient best chance at successful revision; Only scenario where revision microfracture acceptable is if patient absolutely refuses MACI and understands poor prognosis
✗Not counseling realistic expectations for return to sport - setting patient up for disappointment: While MACI has good outcomes (70-80% at 10 years), return to pre-injury sport level is not guaranteed, particularly pivoting sport like football; Studies show 60-70% return to sport after MACI, lower than ACL reconstruction (80-85%); This being revision surgery (failed microfracture) may have slightly inferior outcomes to primary MACI; Should counsel that goal is pain relief and improved function, return to football is possible but not certain; If he cannot accept uncertainty or prolonged rehab (12+ months), conservative management may be better choice than gambling on MACI
✗Not verifying alignment before revision cartilage procedure - guaranteed failure if malaligned: Even 2-3° varus malalignment overloads medial compartment and causes MACI failure; Cannot assume alignment is normal because 'standing alignment looked okay' - need full-length weight-bearing films with mechanical axis measurement; If varus present and not corrected with HTO, MACI will fail just like microfracture did; Doing MACI without addressing malalignment is surgical malpractice; Must measure mechanical axis from femoral head to ankle center - should pass through knee center (50% tibial width); If passes medial (varus) or lateral (valgus), need osteotomy to correct
✗Choosing osteochondral allograft (OCA) as first-line revision for 2.2cm² lesion - not appropriate: OCA is typically reserved for large lesions (greater than 4cm²) or failed MACI, not first-line revision for failed microfracture; For 2.2cm² lesion, MACI is more appropriate size match and has excellent evidence; OCA involves fresh allograft with logistical challenges (sourcing, timing, disease transmission risk small but real), higher cost, and technically more demanding than MACI; Save OCA for larger lesions or if MACI fails - don't skip over MACI to OCA; Treatment ladder should be: microfracture (small lesions) → MACI (medium lesions, failed microfracture) → OCA (large lesions, failed MACI)
✗Not addressing meniscal status if previous meniscectomy - increased contact stress contributes to failure: If patient had partial medial meniscectomy (common after traumatic cartilage injury), the 20-30% increase in contact stress in medial compartment contributes to both microfracture failure and will contribute to MACI failure if not addressed; Should review any previous operative notes - if significant meniscectomy (greater than 50% meniscus removed), consider staged meniscal allograft transplant (MAT) 6-12 months before MACI, or possibly concurrent MAT + MACI; Doing MACI without addressing meniscal deficiency reduces success rate; Patient may need to accept multi-stage reconstruction (MAT then MACI) to optimize biology
LIKELY FOLLOW-UPS
"What type of cartilage does microfracture produce and why does it deteriorate?"
"What is the SUMMIT trial and what did it show?"
"What are the technical steps of the MACI procedure?"
"If this patient had 4° of varus malalignment, would you still do MACI alone?"
"What would you do if MACI also fails in 3-4 years?"
VIVA SCENARIOCritical

Scenario 3: Large Cartilage Defect with Multiple Concurrent Pathologies - Complex Staged Reconstruction

EXAMINER

"You are seeing a 35-year-old woman in your knee reconstruction clinic who was referred by a colleague. She has severe medial knee pain following a skiing injury 4 years ago where she sustained an ACL rupture which was reconstructed at the time. However, her pain has progressively worsened despite a stable ACL reconstruction. She has tried conservative management including physiotherapy, weight loss (BMI now 28, down from 32), activity modification, and multiple courses of injections with minimal sustained benefit. She is now unable to walk more than 500 meters without severe pain and has had to stop her active lifestyle completely. On examination, she has marked medial joint line tenderness, moderate effusion, full range of motion (0-130°), stable ACL reconstruction (negative Lachman and pivot shift), but varus thrust during gait. Standing alignment films show 6° of mechanical varus with the mechanical axis passing well medial to the knee center, loading the medial compartment. MRI shows a large ICRS grade IV cartilage defect on the medial femoral condyle measuring 5cm² with significant bone marrow edema. Additionally, the MRI shows that she had a previous total medial meniscectomy (you review the notes - at the time of her ACL reconstruction 4 years ago, the medial meniscus was found to be complex and degenerative with extensive tearing, and the surgeon performed a total meniscectomy). There is no evidence of significant arthritis in other compartments - the lateral compartment is pristine. The patient is desperate for help and wants to avoid knee replacement as long as possible. A previous surgeon told her nothing could be done and she would need a knee replacement within 5 years. How do you counsel her and what is your surgical plan if you proceed?"

EXCEPTIONAL ANSWER
This is a complex case requiring careful planning, realistic counseling, and potentially multi-stage reconstruction. The patient has three major concurrent pathologies contributing to her medial compartment overload and pain: (1) large 5cm² cartilage defect on MFC, (2) 6° varus malalignment, and (3) total medial meniscectomy (meniscal deficiency). The fundamental principle in cartilage restoration is that you cannot successfully treat the cartilage defect without addressing the concurrent pathology - the alignment and meniscal issues must be corrected or the cartilage procedure will fail. I would explain to her that while this is a challenging situation, she is NOT a candidate for knee replacement at age 35 - TKR in young patients (under 50) has poor long-term outcomes with high revision rates, and we should exhaust all joint preservation options first. Her case is complex but potentially salvageable with staged reconstruction. The problems: (1) The 5cm² cartilage defect is large and requires MACI (matrix-induced autologous chondrocyte implantation) or OCA (osteochondral allograft) - too large for microfracture or OAT. MACI is preferred first-line (two-stage, produces hyaline-like cartilage, good evidence for lesions 2-10cm²). (2) The 6° varus malalignment is severe and MUST be corrected with high tibial osteotomy (HTO) - cannot do cartilage procedure in malaligned knee as it will fail due to mechanical overload. Target is 3-5° valgus overcorrection (mechanical axis at 60-65% tibial width from medial, Fujisawa point) to unload the medial compartment and protect the cartilage repair. (3) The total medial meniscectomy has increased medial compartment contact stress by 50-100% (complete loss of load distribution), contributing to both cartilage defect progression and ongoing pain. She will need meniscal allograft transplantation (MAT) to restore meniscal function and protect the cartilage repair. My recommended surgical plan is a staged approach: Stage 1 - High Tibial Osteotomy (HTO): Perform opening or closing wedge HTO to correct the varus and achieve 3-5° valgus. This is the foundation - must correct alignment first before addressing cartilage and meniscus. Opening wedge HTO using medial approach, biplanar cut, achieve correction, fix with locking plate, bone graft to defect. Post-op: NWB 6 weeks, progressive weight-bearing, expect 3-4 months for bone healing. At 6 months post-HTO, confirm alignment correction with repeat full-length standing films and assess pain improvement. Stage 2 - Concurrent MAT + MACI (6-12 months after HTO): Once HTO healed and alignment confirmed corrected, proceed with combined meniscal allograft transplantation and cartilage restoration. MAT: Use fresh-frozen medial meniscal allograft, size-matched (within 5% using Pollard method or contralateral MRI), bone bridge technique for root fixation, suture periphery to capsule. MACI: For 5cm² lesion, this is ideal size. First arthroscopy to harvest chondrocytes (concurrent with MAT if single-stage, or separate if two-stage MACI). Then 3-4 weeks later (or concurrent if using stored chondrocytes), debride cartilage defect back to stable base, implant chondrocytes on collagen membrane, secure with fibrin glue/sutures. Mini-arthrotomy for both MAT and MACI implantation. Post-op for combined MAT + MACI: NWB or partial weight-bearing 6-8 weeks, ROM limited initially (0-90°) for 6 weeks to protect MAT and MACI, then progressive rehabilitation. Return to full activities 12-18 months. Alternative staging: Some surgeons prefer three-stage (HTO → MAT → MACI) to optimize biology, but I would favor two-stage (HTO, then MAT + MACI) to reduce total number of surgeries. Rationale for staging HTO first: (1) HTO creates biological milieu (bone marrow elements, growth factors from osteotomy healing) that may improve subsequent MAT and MACI incorporation, (2) Allows confirmation of alignment correction before committing to MAT + MACI, (3) Some patients (20-30%) get significant pain relief from HTO alone by unloading compartment - can reassess at 6 months if MAT + MACI still needed, (4) Doing all three procedures simultaneously is technically feasible but has high stiffness risk (15-20% vs 5-8% for single procedures) and very complex rehabilitation. Expected outcomes and counseling: This is joint preservation, not cure. With successful staged reconstruction (HTO + MAT + MACI), she has 60-70% chance of good-excellent pain relief and improved function. Goal is to delay knee replacement by 10-15 years (to age 45-50 when TKR is more appropriate). She will require 2-3 surgeries over 12-18 months, prolonged rehabilitation, significant time commitment, and multiple risks (infection, stiffness, graft failure for MAT or MACI, nonunion of HTO, neurovascular injury). Each procedure has 20-30% failure rate, compounded risk with multiple procedures. Alternative is to accept knee replacement now at age 35, which has poor long-term outcomes in young patients (50% revision rate by age 55-60) but is single surgery with predictable short-term relief. I would strongly recommend attempting joint preservation given her age, but she must understand the complexity, commitment, and uncertain outcomes. This is a marathon, not a sprint. If she proceeds, meticulous surgical technique, addressing all three pathologies, and compliant rehabilitation give her best chance. If she is not willing or able to commit to this process, conservative management and eventual TKR is the alternative.
KEY POINTS TO SCORE
Three concurrent pathologies requiring staged reconstruction - cannot address cartilage alone: (1) Large 5cm² cartilage defect requiring MACI or OCA, (2) Severe varus malalignment 6° requiring HTO to correct, (3) Total medial meniscectomy (meniscal deficiency) requiring MAT to restore load distribution; Fundamental principle: cartilage procedures FAIL if concurrent pathology not addressed - varus overloads compartment, meniscal deficiency increases contact stress 50-100%; Must address all three pathologies for successful outcome - treating cartilage alone will fail within 2-3 years due to mechanical overload; This is complex joint preservation surgery requiring multi-stage approach, NOT simple cartilage repair
Staged surgical plan - HTO first, then MAT + MACI: Stage 1 (HTO): Correct varus alignment first, achieve 3-5° valgus overcorrection (mechanical axis 60-65% tibial width from medial, Fujisawa point), opening or closing wedge technique, 3-4 months healing; Rationale: Creates biological environment for subsequent procedures, allows confirmation of correction, some patients improve with HTO alone; Stage 2 (MAT + MACI): At 6-12 months post-HTO, perform combined meniscal transplant and cartilage restoration; MAT: Fresh-frozen allograft, bone bridge technique, peripheral sutures; MACI: Two-stage (harvest chondrocytes, culture 3-4 weeks, implant on membrane) for 5cm² defect; Why combined MAT + MACI same stage: Both require similar post-op (NWB 6-8 weeks, ROM limited), biological synergy (MAT protects MACI by reducing contact stress, MACI benefits from growth factors); Total timeline: 12-18 months for complete staged reconstruction
Varus malalignment MUST be corrected before cartilage procedure - HTO is foundation: 6° mechanical varus is severe (normal is 0-2° varus, greater than 3° is abnormal), mechanical axis passes well medial to knee center; Varus overloads medial compartment by 20-40%, accelerates cartilage degeneration, causes MACI/MAT failure if not corrected; Target HTO correction: 3-5° valgus overcorrection to shift load to pristine lateral compartment (Fujisawa point = mechanical axis at 60-65% tibial width from medial); Opening wedge HTO (medial approach, easier to control correction, bone graft to gap, locking plate fixation) or closing wedge (lateral approach, more stable, no graft needed); Post-HTO healing: 3-4 months, confirm correction on repeat full-length standing films before proceeding to Stage 2; Some patients (20-30%) improve significantly from HTO alone (unloading effect) - can reassess at 6 months if MAT + MACI still needed
Total medial meniscectomy creates massive contact stress - MAT essential for cartilage protection: Complete loss of medial meniscus increases contact stress 50-100% (loss of load distribution across compartment); Explains why cartilage defect has progressed to 5cm² and why pain is severe despite stable ACL; MAT restores meniscal function, reduces contact stress back toward normal, protects MACI graft from overload; Fresh-frozen allograft standard, sizing critical (within 5% using Pollard method on AP/lateral X-rays or MRI contralateral knee); Bone bridge technique for root fixation (bone-to-bone healing superior to soft tissue), peripheral sutures to capsule; Expected MAT outcomes: 70-80% pain relief, 70-80% graft survival 10 years in ideal candidates (she has concurrent pathologies so may be lower); Cannot do MACI without MAT - increased contact stress from meniscal deficiency will cause MACI failure
MACI for 5cm² lesion - size-appropriate cartilage restoration: 5cm² defect too large for microfracture (less than 2cm²) or OAT (optimal less than 4cm²), ideal for MACI (2-10cm² range); MACI two-stage: (1) Arthroscopy harvest chondrocytes from non-weight-bearing trochlea, send for culture/expansion 3-4 weeks, (2) Mini-arthrotomy debride defect to stable base, implant cultured chondrocytes on collagen membrane (secured with fibrin glue or sutures); Produces hyaline-like cartilage (Type II collagen) with good long-term durability (70-80% at 10 years); Alternative is OCA (osteochondral allograft) which provides true hyaline cartilage with bone, but logistical challenges (fresh allograft sourcing, disease transmission risk), higher cost, technically demanding; MACI preferred first-line for 5cm², save OCA for failed MACI; Post-MACI protocol: NWB 6-8 weeks, ROM limited initially, return to activity 12-18 months (combined with MAT)
COMMON TRAPS
✗Attempting to treat cartilage defect without addressing varus alignment and meniscal deficiency - guaranteed failure: Single biggest error in cartilage restoration is ignoring concurrent pathology; Doing MACI alone in 6° varus knee with meniscal deficiency = mechanical overload will cause MACI failure within 2-3 years; Must correct all three pathologies (HTO for alignment, MAT for meniscal deficiency, MACI for cartilage) for any chance of success; Literature clearly shows cartilage procedures fail in malaligned knees - HTO is MANDATORY, not optional; Similarly, meniscal deficiency from total meniscectomy increases contact stress and must be addressed with MAT; Treating only cartilage is surgical negligence - patient will fail and blame surgeon
✗Telling patient 'nothing can be done' or recommending TKR at age 35 - inappropriate nihilism: Previous surgeon told patient nothing could be done and TKR in 5 years - this is wrong and denies patient chance at joint preservation; TKR in patients less than 50 has poor long-term outcomes: 30-40% revision rate by age 50-55, 50% revision rate by age 55-60; At 35, patient would almost certainly need multiple TKR revisions in lifetime (primary at 35, revision at 45-50, re-revision at 55-60); Joint preservation with staged HTO + MAT + MACI is challenging but offers 60-70% chance of delaying TKR by 10-15 years to age 45-50 (more appropriate age); While complex, she is NOT a TKR candidate now - must exhaust preservation options first; Counseling TKR now is giving up prematurely
✗Attempting single-stage HTO + MAT + MACI without considering stiffness risk - patient safety concern: Technically feasible to do all three procedures in single surgery, but significantly higher complication risk; Stiffness risk with single-stage combined procedure: 15-20% vs 5-8% for individual procedures; Also higher infection risk (longer operative time, larger incisions), DVT/PE risk (prolonged anesthesia), patient stamina required; Post-op rehabilitation extremely complex - protecting HTO healing, MAT, and MACI simultaneously with conflicting requirements; Only attempt single-stage if patient extremely fit, motivated, and surgeon very experienced with all three procedures; For most patients, staged approach (HTO first, then MAT + MACI) safer and allows optimization between stages
✗Not counseling realistic expectations about outcomes and commitment - recipe for patient dissatisfaction: This is complex multi-stage reconstruction over 12-18 months requiring 2-3 surgeries, prolonged rehabilitation, significant patient commitment; Outcomes are uncertain - each procedure has 20-30% failure rate, compounded with multiple procedures; Best case: 60-70% good-excellent pain relief, improved function, delay TKR 10-15 years; Worst case: one or more procedures fail, patient still needs TKR at 37-40, having undergone multiple surgeries and prolonged rehab for nothing; Must counsel both scenarios - under-promising and over-delivering better than overselling complex reconstruction; Patient must understand this is joint preservation attempt, not cure, and may still need TKR eventually; If not willing to commit to process or cannot accept uncertainty, conservative management and eventual TKR is valid alternative
✗Doing MACI before HTO - wrong surgical sequence causes MACI failure: If you do MACI first while knee is still in 6° varus, the varus overload will damage the MACI graft before it can mature and integrate; Cartilage repair requires favorable mechanical environment to heal - doing MACI in malaligned knee ensures failure; Must correct alignment FIRST with HTO to create unloaded compartment, THEN do MACI once alignment corrected; Staging sequence is critical: HTO → MAT + MACI (not MACI → HTO); Some surgeons argue for MAT first (restore meniscus to protect compartment) but this is controversial - most agree HTO must be first stage; Getting sequence wrong causes graft failure and wastes patient's time and surgical effort
LIKELY FOLLOW-UPS
"Why do you stage HTO first rather than doing all three procedures simultaneously?"
"What is the target alignment correction with HTO and why?"
"How does total meniscectomy affect contact stress in the medial compartment?"
"What would you do if the MACI fails 3 years after this staged reconstruction?"
"What are the risks of TKR in a 35-year-old patient?"

MCQ Practice Points

Exam Pearl

Q: What lesion size thresholds guide treatment selection for osteochondral defects?

A: Less than 2 cm²: Microfracture or drilling preferred. 2-4 cm²: OATS (osteochondral autograft) or ACI (autologous chondrocyte implantation). Greater than 4 cm²: ACI or osteochondral allograft (fresh). Microfracture produces fibrocartilage (Type I collagen), while ACI/OATS produce hyaline-like cartilage (Type II collagen).

Exam Pearl

Q: What is the ICRS classification for cartilage lesions?

A: Grade 0: Normal. Grade 1: Superficial lesions (soft, fissures). Grade 2: Less than 50% depth. Grade 3: Greater than 50% depth, not reaching subchondral bone. Grade 4: Full thickness with exposed subchondral bone. Guides treatment: Grade 3-4 lesions with symptoms are candidates for cartilage restoration procedures.

Exam Pearl

Q: What are the advantages and disadvantages of OATS versus ACI?

A: OATS advantages: Single-stage, immediate hyaline cartilage, structural bone support. OATS disadvantages: Donor site morbidity, limited graft availability, plug mismatch. ACI advantages: Larger lesions, no donor morbidity. ACI disadvantages: Two-stage, requires periosteal flap or collagen membrane, expensive.

Exam Pearl

Q: What MRI findings indicate an unstable osteochondritis dissecans lesion?

A: Unstable OCD signs: High T2 signal rim surrounding fragment (fluid interface), cystic changes in subchondral bone, breach of articular cartilage, loose body formation. Unstable lesions require surgical fixation or fragment removal. Stable lesions may be treated nonoperatively in skeletally immature patients.

Exam Pearl

Q: What is the preferred harvest site for OATS in the knee?

A: Lateral femoral trochlea (superolateral, above sulcus terminalis) and intercondylar notch. These areas are non-weight-bearing. Harvest plugs perpendicular to surface. Maximum 2-3 plugs to avoid significant donor morbidity. Plug diameter typically 6-10mm. Match recipient site curvature.

Australian Context

Australian Epidemiology and Practice

Osteochondral Lesion Epidemiology in Australia:

  • Osteochondral defects of the knee represent a significant cause of knee pain and dysfunction in the Australian population
  • High sporting participation rates contribute to increased incidence of traumatic osteochondral injuries
  • AFL, rugby, and football-related knee injuries frequently involve chondral or osteochondral damage
  • Increasing awareness has led to earlier diagnosis and referral for cartilage restoration procedures

RACS Orthopaedic Training Relevance:

  • Osteochondral defects are a core topic in the FRACS Orthopaedic examination syllabus
  • Viva scenarios commonly test understanding of classification systems (ICRS, Outerbridge), diagnostic approach, and treatment algorithms
  • Key examination focus: indications for microfracture vs OAT vs ACI/MACI, size thresholds for treatment selection
  • Candidates should understand the principles of malalignment correction and meniscal pathology that affect treatment outcomes

Australian Cartilage Restoration Practice:

  • Microfracture remains widely used for smaller lesions (less than 2cm²) in primary treatment settings
  • Osteochondral autograft transfer (OAT/mosaicplasty) performed for contained lesions 1-4cm² with good outcomes
  • Matrix-induced autologous chondrocyte implantation (MACI) available through specialised centres for larger defects
  • TGA-approved MACI products are accessible in Australia for appropriate candidates
  • Subspecialty knee surgeons in major metropolitan centres typically manage complex cartilage restoration cases

AOANJRR Considerations:

  • The Australian Orthopaedic Association National Joint Replacement Registry tracks long-term outcomes of knee procedures
  • Patients with prior cartilage procedures who progress to arthroplasty are captured in registry data
  • Registry data informs understanding of cartilage restoration failure rates and subsequent management

Rehabilitation and Recovery:

  • Australian physiotherapy protocols align with international standards for post-cartilage restoration rehabilitation
  • Protected weight-bearing and graduated return to activity are essential components
  • Sports medicine physicians and physiotherapists play key roles in the multidisciplinary team

OSTEOCHONDRAL DEFECTS

High-Yield Exam Summary

Treatment by Size

  • •Small (less than 2cm²): Microfracture, OAT
  • •Medium (2-4cm²): OAT, MACI
  • •Large (greater than 4cm²): MACI, OCA

Cartilage Quality

  • •Microfracture: Fibrocartilage (Type I)
  • •MACI/ACI: Hyaline-like (Type II)
  • •OAT/OCA: True hyaline with bone

Address Concurrent

  • •Malalignment (HTO/DFO)
  • •Meniscal deficiency (MAT)
  • •ACL instability (ACLR)

MACI

  • •Two-stage procedure
  • •Larger lesions (greater than 2cm²)
  • •Better than microfracture long-term
  • •Hyaline-like cartilage
Quick Stats
Reading Time97 min
Related Topics

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