The Utilisation of Osteochondral Autografts
in the Treatment of Articular Cartilage Lesions (Part 1 of 3)

Vladimir Bobic, M.D.
Consultant Orthopaedic Knee Surgeon
The Royal Liverpool University Hospitals, Broadgreen Hospital Knee Service, Liverpool, The Grosvenor Nuffield Hospital Knee Clinic, Chester, UNITED KINGDOM

Introduction

It is well known that the capacity of articular cartilage for repair is limited. Partial-thickness defects in the articular cartilage do not heal spontaneously. Injuries of the articular cartilage that do not penetrate the subchondral bone do not heal and usually progress to the degeneration of the articular surface. A short-lived tissue response fails to provide sufficient cells and matrix to repair even small defects. Injuries that penetrate the subchondral bone undergo repair through the formation of fibrocartilage, instead of the normal hyaline cartilage. From the biomechanical standpoint, the problem is that the fibrocartilage is made to resist tension forces, while the hyaline cartilage is made to resist compression forces, to enable smooth articulation, and to withstand long-term variable cyclic load and shearing forces.

In selecting methods of restoring damaged articular surface, it is important to distinguish articular cartilage repair from articular cartilage regeneration. Repair refers to the healing of injured cartilage or replacement of lost cartilage by cell proliferation and synthesis of new extracellular matrix. Unfortunately, the repaired articular cartilage generally fails to replicate the structure, composition, and function of normal hyaline articular cartilage. Regeneration refers to the formation of an entirely new articulating surface that essentially duplicates the original hyaline articular cartilage, which is still beyond all current surgical techniques.

With this in mind it seems that the articular cartilage defect should be diagnosed and treated early, before it becomes large and deep osteochondral defect. The concept that small lesions are insignificant is not supported in the study of 23 isolated chondral defects in 15 high-caliber soccer players: 33% of the lesions were less than 10 mm in diameter, but all players had knee pain. Pain probably occurs because of the stimulation of nerve endings of the subchondral bone. This is caused by the compromised load-transmitting and energy-absorbing capabilities.⁹

Indications for Osteochondral Autograft Transplantation (OAT)

The "ideal" chondral lesion is a relatively small, 10 to 20 mm in diameter, full-thickness chondral defect. Quite frequently this type of the lesion will be present in the weight-bearing area of the medial femoral condyle, in an ACL deficient knee (picture opposite). Although it may be easier to microfracture or drill this lesion, this will produce fibrocartilage or hyaline-like cartilage cover. Osteochondral autograft transplantation can repair the defect with the autologous hyaline cartilage, which will survive and restore the height and the shape of the defect. The main reason for the long-term survival of transplanted hyaline cartilage seems to be the preservation of an intact tidemark and cancellous bone carrier.

Deep and large osteochondral defects (picture opposite) are not suitable for osteochondral autograft transplantation, mainly because of the limited availability of autologous osteochondral grafts. Also, it is difficult to reconstruct subchondral bone and restore the contour of the large defect area, and to cover the entire defect area with hyaline articular cartilage.

OAT Clinical Experience

Wilson et al. in 1952, Müller¹¹ in 1978, and Yamashita et al.¹⁶ in 1985, published results of the transplantation of an autogenic osteochondral grafts, with the successful outcome and survivorship of the hyaline cartilage, from six months to over 10 years. A similar clinical study, on treating osteochondritis dissecans lesions with osteochondral autografts, was reported at the annual AOSSM conference, by Fabbriciani et al.⁵ in 1991.

In 1993, Matsusue et al.¹⁰ published the first case report and the technique of the arthroscopic osteochondral autograft transplantation in an ACL deficient knee.

In 1995 Outerbridge et al.¹³ treated osteochondral defects of the femoral condyle with patellar osteochondral grafts in ten patients and found that the function of the knee improved and symptoms were alleviated in all patients at an average of six and one-half years after transplantation. Hyaline cartilage survived up to nine years.

In 1996 Bobic published the series of 12 patients with chronic ACL deficiency and osteochondral autograft transplantation for the full-thickness femoral condyle chondral defects larger than 10 mm in diameter². Seventy seven percent of 309 patients in this series had some form of chondral damage, ranging from deep chondral fissures, to large crater-like osteochondral defects. In most cases intra-articular fluid contained numerous chondral slivers and particles of delaminated articular cartilage. Small chondral defects were "microfractured" with an arthroscopic awl. Twelve patients underwent ACL reconstruction with patellar tendon graft, and osteochondral autograft transplantation with modified tubular instruments and multiple osteochondral cylinders, harvested mainly from the notch and roofplasty area. On second look arthroscopy at two years grafts appeared satisfactory in ten patients, visually and on probing. A specimen obtained from the transplanted area after two years, in two patients, was composed of histologically normal hyaline cartilage.

In 1996 and 1997 Hangody et al. published several animal and clinical studies^6,7 on the multiple osteochondral autograft transplantation (Mosaicplasty technique). The animal trials and extensive clinical experience (over 370 procedures), demonstrate long-term survivorship of the hyaline articular cartilage. The longest follow-up is 6 years. The histological analysis of transplanted cartilage demonstrates that the specimens were composed of 70% to 80% hyaline cartilage. The biopsy at 4.5 years (picture below) demonstrated normal appearing chondrocytes, high GAG content, normal orientation of chondrocytes and matrix elements, and matrix integration between the hyaline and the fibrocartilage.⁷

Next Section: OATS Surgical Technique: Step-by-Step Guide