Abstract

Articular cartilage defects have been addressed using microfracture, abrasion chondroplasty, or osteochondral grafting, but these strategies do not generate tissue that adequately recapitulates native cartilage. During the past 25 years, promising new strategies using assorted scaffolds and cell sources to induce chondrocyte expansion have emerged. We reviewed the evolution of autologous chondrocyte implantation and compared it to other cartilage repair techniques. Methods. We searched PubMed from 1949 to 2014 for the keywords “autologous chondrocyte implantation” (ACI) and “cartilage repair” in clinical trials, meta-analyses, and review articles. We analyzed these articles, their bibliographies, our experience, and cartilage regeneration textbooks. Results. Microfracture, abrasion chondroplasty, osteochondral grafting, ACI, and autologous matrix-induced chondrogenesis are distinguishable by cell source (including chondrocytes and stem cells) and associated scaffolds (natural or synthetic, hydrogels or membranes). ACI seems to be as good as, if not better than, microfracture for repairing large chondral defects in a young patient's knee as evaluated by multiple clinical indices and the quality of regenerated tissue. Conclusion. Although there is not enough evidence to determine the best repair technique, ACI is the most established cell-based treatment for full-thickness chondral defects in young patients.

Highlights

  • Articular cartilage (AC) lines the surface of diarthrodial joints, provides a low-friction interface for motion, and distributes forces to underlying subchondral bone

  • Advances in magnetic resonance imaging (MRI), combined with a longitudinal human trial [3], have shown that cartilage defects often progress to large, higher grade lesions over time, resulting in osteoarthritis

  • Within AC, metabolic and morphologic profiles of deep-zone chondrocytes are distinct from those populating the superficial tangential zone

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Summary

Introduction

Articular cartilage (AC) lines the surface of diarthrodial joints, provides a low-friction interface for motion, and distributes forces to underlying subchondral bone. AC lesions do not heal spontaneously and are often intractable clinical problems. Curl et al [1] retrospectively reviewed 31516 arthroscopies, noting a 63% incidence of knee cartilage lesions and Outerbridge grade IV [2] chondral lesions in patients less than 40 years old accounting for 4% of all lesions noted at arthroscopy [1]. Advances in magnetic resonance imaging (MRI), combined with a longitudinal human trial [3], have shown that cartilage defects often progress to large, higher grade lesions over time, resulting in osteoarthritis. There is a need for effective methods of repairing cartilage early, which can potentially delay osteoarthritis development

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