OPTIONS

Before the development of modern bioengineering techniques, orthopedists were restricted to procedures that aimed to palliate the effects of chondral lesions or attempted to stimulate a healing response initiated from the subchondral bone resulting in the formation of fibrocartilage to fill the defect. Simple arthroscopic lavage and debridement of lesions has been used since the 1940s in an effort to reduce symptoms resulting from loose bodies and cartilage flaps, and it is a common first-line treatment, especially for coincidental defects. Marrow stimulation techniques (MST), such as abrasion arthroplasty, drilling, and microfracture, attempt to induce a reparative response by perforation of the subchondral bone after radical debridement of damaged cartilage and removal of the tide mark “calcified” zone to enhance the integration of repair tissue. The resultant blood clot, and the primitive mesenchymal cells contained within, may differentiate into a fibrocartilaginous repair tissue that fills the defect. Unlike hyaline cartilage, this fibrocartilage largely consists of type I collagen and is mechanically less stable and less durable.⁵ The pluripotential marrow-derived cells may also form bone, another mode of MST-related failure that is increasingly becoming recognized.⁶ Although closely related, MSTs vary by the degree of trauma to the subchondral bone, which has been recognized as a factor in the failure of these techniques. Abrasion arthroplasty (or also abrasion chondroplasty) decorticated the superficial subchondral bone with a bur to expose the more porous bone below but also destabilized the subchondral bone with the risk for fracture. Drilling utilizes small drill bits or K-wires to perforate the subchondral bone, which can result in heat necrosis; microfracture avoids this issue by using special awls (microfracture or Steadman awls). Currently, most surgeons have abandoned the older methods in favor of microfracture, which is usually performed in an all-arthroscopic fashion.

Restorative cartilage repair techniques such as autologous chondrocyte implantation (ACI) introduce chondrogenic cells into the defect area, resulting in the formation of a repair tissue that more closely resembles the collagen type-II rich hyaline cartilage. The original technique of ACI was developed in the 1980s⁷ and has been used in the United States to treat more than 10,000 patients since its approval by the U.S. Food and Drug Administration (FDA) in 1997. ACI is indicated for the treatment of medium to large chondral defects with no or shallow associated osseous deficits. It originally received FDA approval for application in the femoral condyle (medial, lateral, and trochlea) but has also been used successfully to treat patellar defects. ACI in its current form is a two-stage procedure with an initial arthroscopic cartilage biopsy, followed by a staged reimplantation through an arthrotomy. The next generation ACI-c (collagen-covered) technique was developed to reduce the reoperation rate because of hypertrophy of the periosteal patch used to cover the defect. This was achieved by substitution of periosteum with a collagen membrane, frequently consisting of a porcine type-I/III collagen bilayer membrane. The latest generation of ACI, termed MACI (membrane associated), cultures the chondrocytes directly on the aforementioned collagen membrane, which is then implanted arthroscopically or through a mini-open approach with fibrin glue or limited suturing.

Cartilage replacement techniques include osteochondral autograft and allograft transfers, such as the osteochondral autograft transfer system (OATS; Arthrex, Naples, FL), mosaicplasty (Smith & Nephew, Andover, MA), and mega-OATS techniques. Osteochondral autograft transplantation is used to address small to medium defects (1–4 cm²), often with associated bone loss. Osteochondral cylinders are harvested from lesser marginal weight-bearing areas of the knee joint and press-fitted into the prepared defect. Commonly, multiple cylinders have to be transplanted to fill larger defects. Osteochondral autografting is limited by the amount of cartilage that can be harvested without violating the weight-bearing articular surface.⁸ The main advantage lies in its autogenicity, avoidance of disease transmission, immediate graft availability through harvesting of the patient’s own tissue, and decreased cost of this single-stage procedure.

The treatment of chondral defects with fresh osteochondral allografts has garnered significant attention because of its potential to restore and resurface even extensive areas of damaged cartilage and bone. Osteochondral allograft transplantation is used predominantly in the treatment of large and deep osteochondral lesions resulting from OCD, osteonecrosis, and traumatic osteochondral fractures, but it can also be used to treat peripherally uncontained cartilage and bone defects. Furthermore, osteochondral allografting presents a viable salvage option after failure of other cartilage resurfacing procedures. The main advantages over autograft transplantation are the ability to closely match the curvature of the articular surface by harvesting the graft from a corresponding location in the donor condyle, the ability to transplant large grafts, and the avoidance of donor-site morbidity. The main concerns with allograft transplantation are failure to incorporate with subchondral collapse and the risk for disease transmission (estimated at 1 in 1.6 million for the transmission of HIV⁹).

EVIDENCE

Table 96-1 provides an overview of cartilage repair studies. Table 96-2 provides a summary of treatment recommendations and respective levels of evidence for chondral defects in the knee.

TABLE 96-2 Treatment Recommendations and Respective Level of Evidence

ACI, autologous chondrocyte implantation; ACI-c collagen-covered autologous chondrocyte implantation; BMI, body mass index; MACI, membrane-associated autologous chondrocyte implantation.