Enhancing tissue integration in cartilage repair procedures

• Published in: Journal of anatomy 2006-10, Vol.209 (4), p.481-493
• Main Authors: Archer, Charles W., Redman, Samantha, Khan, Ilyas, Bishop, Joanna, Richardson, Kirsty
• Format: Article
• Language: English
• Subjects: cartilage; Cartilage, Articular - injuries; Cartilage, Articular - pathology; Cell Proliferation; chondrocyte; Chondrocytes - pathology; Chondrocytes - transplantation; Humans; osteoarthritis; Osteoarthritis - pathology; Osteoarthritis - therapy; repair; Review; tissue; tissue integration; Transplantation, Autologous; Wound Healing - physiology; Wounds, Nonpenetrating - pathology; Wounds, Nonpenetrating - therapy
• ISSN: 0021-8782; 1469-7580
• DOI: 10.1111/j.1469-7580.2006.00624.x

Arguably, the gold standard of biological repair of articular cartilage lesions is autologous chondrocyte transplantation. Although the clinical outcomes appear to range between good and excellent in most cases, there are, nevertheless, both clinical and biological challenges that remain to improve rehabilitation and clinical outcome. One of the major biological problems relates to tissue integration of the reparative tissue into the host tissue at a predictable level. Often within a single lesion, varying degrees of integration can be observed from total integration through to non‐integration as one passes through the defect. Here we briefly review some of the literature relating to this problem and include some of our own data drawn from questions we have posed about the biological nature of cartilage/cartilage integration. The nature and status of the tissue that comprises the wound lesion edge is central to tissue integration, and controlling aspects of trauma and free‐radical‐induced cell death together with matrix synthesis are identified as two components that require further investigation. Interestingly, there appears to be a limited ability of chondrocytes to be able to infiltrate existing cartilage matrices and even to occupy empty chondrocyte lacunae. Proliferation as a result of blunt and sharp trauma shows differential responses. As expected, blunt trauma induces a greater proliferative burst than sharp trauma and is more widespread from the lesion edge. However, in the case of sharp trauma, the basal cells enter proliferation before surface zone chondrocytes, which is not the case in blunt wounds. Regulation of these and associated processes will be necessary in order to devise strategies that can predict successful integration in biological repair procedures.