Cartilage regeneration Barbara D. Boyan, PhD a,b,c, * , David D. Dean, PhD a , Christoph H. Lohmann, MD a,d , Gabriele G. Niederauer, PhD e , Jacquelyn McMillan, MBChB, FRCSEd (Orth) a , Victor L. Sylvia, PhD a , Zvi Schwartz, DMD, PhD a,c,f a Department of Orthopaedics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229 – 3900, USA b Department of Biochemistry, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229 – 3900, USA c Department of Periodontics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229 – 3900, USA d Department of Orthopaedics, University of Hamburg Eppendorf, D-20246 Hamburg, Germany e OsteoBiologics, Incorporated, 12500 Network, Suite 112, San Antonio, TX 78249, USA f Department of Periodontics, Hebrew University Hadassah, Jerusalem, Israel Articular cartilage has been a primary focus of the emerging tissue engineering industry. The mar- ket for cartilage repair technologies is considerable for trauma and sports injuries and even greater for regeneration of cartilage in patients with arthritis. Articular cartilage degeneration is accompanied by morbidity, which leads to absenteeism and devel- opment of conditions associated with chronic pain. In severe cases, the loss of function is of sufficient magnitude that it is necessary to replace damaged joint tissue with a bioprosthesis. Problems associated with tissue engineering of cartilage Despite these economic drivers, successful tissue engineering of articular cartilage has been elusive. Unfortunately, cartilage does not heal in the same manner as seen in other tissues, in part because it has only a rudimentary blood supply. When the cartilage is severed, the chondrocytes seal the exposed edges of the wound and in effect create a new cartilage surface [2,66,72]. The two sides of the defect do not fuse, which creates a focal change in the way that the tissue experiences compressive loads. Similarly, when injuries occur that cause loss of a piece of cartilage, the chondrocytes in the surrounding tissue again seal off the edges of the defect site. There is a limited attempt at repair, but the tissue that forms within the defect tends to be fibrocartilage. There are several reasons why fibrocartilage forms within chondral defects. The source of cells is believed to be synoviocytes [39], which are fibroblastic and as such synthesize type I collagen. Even if chondropro- genitor cells migrate into the defect site, they must produce large amounts of matrix quickly to facilitate migration across large regions of space relative to the cell, and type I collagen is favored under such circum- stances. Should the defect penetrate the subchondral plate, a clot is able to form within the defect site and serves as a scaffold for cell attachment and migration. Many of the cells that colonize such defects are derived from the vasculature and marrow stroma [62], how- ever, and possess the capacity to differentiate into various mesenchymal cell types. In the absence of a sufficient supply of chondrogenic factors, these cells tend to select the default pathway and differentiate along a fibroblastic lineage [38,43,49,53,61]. 1042-3699/02/$ – see front matter D 2002, Elsevier Science (USA). All rights reserved. PII:S1042-3699(02)00017-1 * Corresponding author. E-mail address: BoyanB@uthscsa.edu (B.D. Boyan). Oral Maxillofacial Surg Clin N Am 14 (2002) 105 – 116