Chondrogenesis in cartilage repair is induced by members of the transforming growth factor-beta superfamily.

The authors recently reported on the principle of an intrinsic repair strategy for partial-thickness articular cartilage defects, which is based on the introduction of a biocompatible and biodegradable matrix loaded with a free chemotactic and mitogenic agent (transforming growth factor-beta 1, at low concentration) and a liposome-encapsulated chondrogenic factor (transforming growth factor-beta 1 at high concentration). In the current study, the potential of other members of the transforming growth factor-beta superfamily (transforming growth factor-beta 2, transforming growth factor-beta 3, bone morphogenetic protein-2 and bone morphogenetic protein-13), and of insulinlike growth factor-1, epidermal growth factor, transforming growth factor-alpha, and Tenascin-C, to induce chondrogenesis within the authors' adult miniature pig articular cartilage defect model, was evaluated. The degree of chondrogenic tissue differentiation was assessed 6 weeks after surgery, on a semiquantitative basis, histologic assessment of cell morphologic features, and intercellular matrix staining being used as the relevant criteria. All selected members of the transforming growth factor-beta superfamily were efficacious in inducing chondrogenic tissue transformation, whereas the other signaling substances tested were not. When encapsulated at high activity levels, bone morphogenetic proteins were less prone than transforming growth factor-beta 1, transforming growth factor-beta 2, and transforming growth factor-beta 3 to evoke undesired side effects as a result of incidental leakage into the joint cavities and subsynovial connective tissue spaces, and therefore they are potentially more suitable candidates for use in human patients.