Osteochondral Defects — Autologous Chondrocyte Implantation (ACI)

Autologous chondrocyte implantation (ACI) is a two-stage biological cartilage restoration technique in which the patient`s own articular chondrocytes are harvested, laboratory-cultured, and then re-implanted into a full-thickness chondral defect to regenerate hyaline-like cartilage. ACI is the preferred treatment for large symptomatic full-thickness chondral defects (>2–4 cm²) in young active patients where single-stage techniques (OATS/mosaicplasty) are insufficient. It produces cartilage that is superior to the fibrocartilage of microfracture and offers a biologically durable repair without the donor site limitations of OATS.

• Indications: full-thickness chondral defect (ICRS Grade III–IV) of the femoral condyle, trochlea, or patella; defect size 2–10 cm² (ideal 2–6 cm²); failed prior cartilage procedure (microfracture, OATS); young active patient (typically <45–50 years); stable knee (concurrent ligament reconstruction and deformity correction is mandatory); adequate subchondral bone stock (significant bony loss (>6–8 mm) requires combined bone grafting before or with ACI)
• ACI is not appropriate for: osteoarthritis (diffuse cartilage loss involving multiple compartments); patients with significant subchondral bone loss (bone grafting required first or combined); patients with inflammatory arthropathy (high cytokine environment prevents chondrocyte survival); malalignment without concurrent correction (high failure rate); patients unwilling to comply with the prolonged rehabilitation

• Stage 1 — Chondrocyte harvest (arthroscopy): a diagnostic arthroscopy is performed to confirm the defect characteristics (size, location, depth, stability) and assess for concurrent pathology; approximately 200–300 mg of articular cartilage is harvested from a low-load-bearing site (the peripheral medial or lateral femoral condyle or the intercondylar notch); this provides approximately 250,000–500,000 chondrocytes; the cartilage is sent to the laboratory for enzymatic digestion and culture; over 4–6 weeks, the chondrocytes are expanded to approximately 12–48 million cells (for MACI, they are then seeded onto the scaffold at approximately 1 million cells/cm²)
• Stage 2 — Chondrocyte implantation (open or mini-open): performed 4–8 weeks after harvest; the defect is debrided to stable cartilage margins and the subchondral bone plate is preserved (the subchondral plate must not be breached to avoid bleeding which impairs chondrocyte differentiation); the scaffold (MACI) is trimmed to the exact defect dimensions and glued with fibrin glue; sutures are used at the margins if needed; any concurrent procedures (ACL reconstruction, tibial osteotomy, meniscal repair) are performed at the same sitting
• Post-operative rehabilitation: non-weight-bearing (NWB) for 6–8 weeks; early passive range of motion; continuous passive motion (CPM) machine in the immediate post-operative period promotes chondrocyte nutrition and cartilage maturation; progressive weight-bearing from 6–8 weeks; return to sport typically at 12–18 months; ACI requires significantly longer rehabilitation than OATS due to the time required for scaffold degradation and matrix maturation

• ACI outcomes: good to excellent results in 70–85% of appropriately selected patients at 5–10 years; the SUMMIT and ROCK trials demonstrate equivalence between ACI and OATS for 2–4 cm² defects; ACI is superior to microfracture for defects >2 cm² in high-demand patients; patellofemoral defects have historically lower success rates than femoral condyle defects; patellar ACI now achieves better results with MACI and concurrent unloading procedures (TTO with anteriorisation)
• Graft hypertrophy: overgrowth of repair tissue above the surrounding articular surface; more common with first-generation periosteal ACI (up to 25%); less common with MACI (<5%); treated with arthroscopic shaving if symptomatic
• Graft delamination: separation of the repair tissue from the subchondral bone; occurs when the subchondral bone plate is damaged during preparation, when there is inadequate fixation, or when the patient loads the knee too early; managed with re-operation (revision ACI or alternative cartilage procedure)
• Failure: graft failure occurs in approximately 10–20% of cases; risk factors — large defect, patellofemoral location, uncorrected malalignment or instability, subchondral bone loss, prior failed cartilage procedure, BMI >35

• Subchondral bone loss and sandwich grafting: when the osteochondral defect involves significant bone loss (>6–8 mm depth), ACI alone will not provide adequate support for the overlying cartilage repair; the standard approach is `sandwich` or combined technique — first stage involves bone grafting the bony defect (autograft from the iliac crest or femoral condyle, or allograft cancellous bone) to restore the subchondral plate; the ACI implantation is performed 4–6 months later once the bone graft has consolidated; alternatively, a fresh osteochondral allograft (which provides both bone and cartilage) can be used for large osteochondral defects as a single-stage procedure
• Patellofemoral ACI: ACI for patellar and trochlear defects is technically more demanding and has historically had inferior outcomes to femoral condyle ACI; the cause is multifactorial — the patellofemoral joint has complex kinematics, high contact pressures, and any malalignment significantly impairs repair tissue survival; current best practice for patellofemoral ACI includes: concurrent TTO with anteromedialisation (reduces PFJ contact pressure), careful patient selection (no patellofemoral malalignment uncorrected), and MACI technique; outcomes have improved significantly with MACI vs first-generation ACI for the patellofemoral joint
• ACI after failed microfracture: previously, failed microfracture was thought to be a negative prognostic factor for ACI; evidence from contemporary series suggests ACI after failed microfracture achieves acceptable outcomes — not as good as primary ACI but still significantly better than continued non-operative management; the fibrocartilage base left by prior microfracture needs to be debrided to stable healthy cartilage before ACI implantation; this reduces the available defect depth and increases the technical demands of the procedure

• ACI indication: full-thickness chondral defect 2–10 cm² (ideal 2–6 cm²); young active patient; failed OATS or microfracture; must address concurrent malalignment, instability, meniscal deficiency
• Two stages: Stage 1 — arthroscopic harvest (200–300 mg cartilage); Stage 2 — implantation 4–8 weeks later; NWB 6–8 weeks; return to sport 12–18 months
• MACI (third generation): chondrocytes seeded on collagen scaffold; trimmed to defect shape; glued in place; lower hypertrophy rate (<5%) vs periosteal ACI (up to 25%); current standard
• Periosteal ACI (first generation): high hypertrophy rate; largely abandoned; collagen membrane (second generation) = intermediate; MACI = current best practice
• ACI vs OATS vs microfracture: ACI for 2–10 cm² defects; OATS for 1–4 cm²; microfracture for <2 cm²; ACI superior to microfracture for large defects in high-demand patients
• Subchondral bone loss >6–8 mm: sandwich technique — bone graft first, ACI 4–6 months later; or fresh osteochondral allograft (single stage for large osteochondral defects)
• Graft hypertrophy: repair tissue overgrowth; arthroscopic debridement if symptomatic; much less common with MACI than first-generation ACI
• Patellofemoral ACI: technically challenging; must correct malalignment (TTO with AMZ) concurrently; historically poorer results now improved with MACI + concurrent unloading
• CPM (continuous passive motion): post-operative; promotes chondrocyte nutrition and scaffold maturation; standard post-operative protocol after ACI implantation
• Failure risk factors: large defect, patellofemoral location, uncorrected malalignment, subchondral bone loss, prior failed cartilage procedure, BMI >35