New Frontiers in Surgery of Osteoarthritis

Tom Minas

Andreas H. Gomoll

Introduction

Since Hunter’s famous statement over 250 years ago describing cartilage as a “troublesome thing and once destroyed, it is not repaired,”¹ medicine has directed considerable effort toward improving the limited repair potential of chondral lesions. Partial thickness lesions that do not penetrate the subchondral bone are avascular, therefore do not heal, and may enlarge over time. Full-thickness defects, especially with injury to the underlying vascular bone, have the potential to fill with a fibrocartilaginous scar formed by mesenchymal stem cells invading from the marrow cavity. This fibrocartilage, however, is predominantly composed of type I collagen, resulting in inferior mechanical properties compared to the type II collagen-rich hyaline cartilage.

Long implicated in the subsequent development of osteoarthritis (OA), focal chondral defects result from various etiologies. The exact incidence of chondral defects is still poorly established. Traumatic events and developmental etiologies such as osteochondritis dissecans (OCD) predominate in the younger age groups. Traumatic hemarthroses in young athletes with knee injuries are associated with chondral defects in up to 10% of cases;² the incidence of OCD is estimated at 30 to 60 cases per 100,000 people.³ Several large studies have found high-grade chondral lesions (Outerbridge grade III and IV) in 5% to 11% of younger patients (less than 40 years), and up to 60% in the older age groups.⁴^,⁵^,⁶ The most common locations for these defects are the medial femoral condyle and the patella,⁴^,⁶ and most present as incidental findings during procedures such as meniscectomy or anterior cruciate ligament reconstruction.⁵^,⁷

Since articular cartilage lesions have no spontaneous repair potential if left untreated, different techniques have evolved in an attempt to stimulate filling of these defects, ideally with hyaline articular cartilage. Even today, the treatment of chondral defects remains a challenge, and none of the conventional techniques discussed in this chapter has provided predictable long-term clinical results. These conventional techniques, such as abrasion arthroplasty, drilling, or microfracture, attempt to fill the defect with a fibrocartilaginous scar produced by marrow-derived pluripotent stem cells. This scar cartilage, however, is of lesser biological and mechanical quality than the articular, or hyaline cartilage. More recently developed techniques used in current clinical practice, such as autologous chondrocyte implantation (ACI) or matrix autologous chondrocyte implantation (MACI), achieve a tissue that more closely resembles the original hyaline cartilage. Several challenges remain, such as the integration of regenerated cartilage with the surrounding host tissue, and the development of sufficient long-term stability and wear characteristics that will allow the repair tissue to withstand the stresses of physical activity over years.

This chapter will provide a concise overview of current techniques for cartilage repair, and subsequently present several of the more promising new developments in this evolving area.

Surgical Treatment of Chondral Defects

Underlying Abnormalities and Predisposing Factors for Chondropenia

On careful evaluation, the majority of chondral defects is associated with coexisting abnormalities of the knee, including limb malalignment, patellar maltracking, and insufficiency of the ligamentous and meniscal structures.
Varus or valgus malalignment of the lower extremity shifts the load-bearing axis to one compartment, thus resulting in local overload and accelerated degeneration of the articular surface. Ligamentous insufficiency, most commonly of the anterior cruciate ligament, increases shear forces in the knee joint and thus contributes to chondral wear. Meniscal insufficiency, such as after subtotal meniscectomy, increases contact stresses by up to 300% in the respective compartment, and is predictably associated with the development of OA. More recently, the disappointing early results of cartilage repair have been explained by the failure to diagnose and correct these associated bony and ligamentous abnormalities; for example, in early studies of patellar defects treated with ACI alone, good and excellent results were found in only one third of patients.⁸ Later studies, however, identified patellar maltracking as an important associated abnormality, and performance of a corrective osteotomy concurrently with cartilage repair led to 71% good or excellent results.⁹ These reports emphasize the importance of a thorough patient evaluation to correctly identify and treat all associated abnormalities to ensure the long-term success of chondral repair.

When performed concurrently with cartilage repair, osteotomy around the knee should restore the mechanical axis to neutral alignment in cases where the radiographic joint space is maintained. Coventry’s early work with osteotomies popularized this technique for the treatment of OA. However, the population treated for chondral defects is predominantly athletic and cannot tolerate large overcorrection, as has been successfully used in osteoarthrosis patients. Therefore, even in patients with early joint space narrowing, overcorrection of the mechanical axis should be limited to 2 degrees or less.

Subtotal meniscectomy significantly alters the biomechanical environment and frequently results in secondary OA. In carefully selected patients with meniscal insufficiency, meniscal allograft transplantation can provide pain relief and improved function. The ideal candidate for allograft transplantation has a history of prior total or subtotal meniscectomy with persistent pain localized to the involved compartment. Associated abnormalities such as malalignment, discrete chondral defects, or ligamentous instability can be addressed in either staged or concomitant procedures. Following meniscal allograft transplantation, good to excellent results are achieved in nearly 85% of cases, and patients demonstrate a measurable decrease in pain and increase in activity level.¹⁰

Conventional Cartilage Repair Techniques

Prior to the development of modern bioengineering techniques, orthopedists were restricted to procedures that either aimed to palliate the effects of chondral lesions or attempted to stimulate a healing response of the subchondral bone, resulting in the formation of scar tissue to fill the defect. Simple arthroscopic lavage and débridement of arthritic joints has been used since the 1940s¹¹ in an effort to reduce symptoms resulting from loose bodies and cartilage flaps. While lavage alone has not been found to be effective, in combination with débridement it can result in adequate pain reduction in slightly more than half of patients.¹²^,¹³ The goal of débridement of chondral defects is to remove any loose flaps, and to create a defect shouldered by a stable rim of intact cartilage, thus reducing mechanical stresses in the defect bed. Currently, its use is limited to the treatment of small cartilage lesions that are incidental findings during arthroscopic treatment of meniscal or ligamentous pathology.

Marrow stimulation techniques, such as drilling, abrasion arthroplasty, and microfracture, attempt to induce a reparative response in the avascular cartilage. This is achieved by perforation of the subchondral bone after radical débridement of damaged cartilage and removal of the tide mark zone, thus enhancing the integration of repair and surrounding tissue. Perforation of the subchondral bone results in the extravasation of blood and marrow elements with formation of a blood clot in the defect. Over time, this blood clot, and the primitive mesenchymal cells contained within, differentiate into a fibrocartilaginous repair tissue that fills the defect, but may also form bone resulting in an intralesional osteophyte. Unlike hyaline cartilage, this fibrocartilage predominantly consists of type I collagen, and exhibits inferior wear characteristics. Postoperatively, all marrow-stimulating techniques require extended periods of strict non-weight-bearing for 6 weeks or more, as well as the use of continuous passive motion (CPM) therapy for up to 6 hours per day to enhance maturation of the repair tissue, as do other techniques intended to produce hyaline cartilage. Even though marrow stimulation techniques result in a repair tissue with inferior wear characteristics, treatment of smaller defects (<4 cm²) results in good outcomes in 60% to 70% of patients.¹⁴

New Cartilage Repair Techniques

Cartilage Restoration

Restorative cartilage repair techniques introduce chondrogenic cells into the defect area, resulting in the formation of a repair tissue that more closely resembles articular (hyaline) cartilage. The original technique of ACI was developed over 15 years ago, and has been used in the United States to treat more than 10,000 patients since its approval by the FDA in 1997. Second-generation techniques that involve the use of resorbable carrier matrices are available in Europe with over 5-year follow-up results. These techniques offer the benefit of a less-invasive surgical approach, and have demonstrated excellent early results without periosteum-related problems seen in conventional ACI.

Autologous Chondrocyte Implantation

ACI is a technique aimed at treating medium to large size chondral defects by in vitro expansion of an autologous chondrocyte biopsy, followed by staged reimplantation. Originally reported in 1994⁸ for the treatment of chondral defects in the knee, it has more recently been applied to other joints such as the shoulder¹⁵ and ankle.¹⁶

ACI in its current form is a two-stage procedure in which a cartilage biopsy of approximately 200 mg is harvested during an initial arthroscopic procedure. The biopsy is usually obtained from a non-weight-bearing area of the knee, commonly from the superior medial edge of the trochlea or the area of the intercondylar notch. The approximately 200,000 to 300,000 chondrocytes contained within the tissue are released by enzymatic digestion of the surrounding matrix, and expanded in a monolayer culture for several weeks. Initial concerns over cell dedifferentiation and loss of type II collagen expression were addressed by early studies that demonstrated re-expression of the chondrocyte phenotype when the expanded cells were cultured in agarose gels.¹⁷

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