Current concepts in the treatment of articular cartilage defects.
Over time, articular cartilage loses the capacity to regenerate itself, making repair of articular surfaces difficult. Lavage and debridement may offer temporary relief of pain for up to 4.5 years, but offer no prospect of long-term cure. Likewise, marrow-stimulation techniques such as drilling, microfracture, or abrasion arthroplasty fail to yield long-term solutions because they typically promote the development of fibrocartilage. Fibrocartilage lacks the durability and many of the mechanical properties of the hyaline cartilage that normally covers articular surfaces. Repair tissue resembling hyaline cartilage can be induced to fill in articular defects by using perichondrial and periosteal grafts. However, these techniques are limited by the amount of tissue available for grafting and the tendency toward ossification of the repair tissue. Autogenous osteochondral arthroscopically implanted grafts (mosaicplasty), or open implantation of lateral patellar facet (Outerbridge technique), requires violation of subchondral bone. Osteochondral allografts risk viral transmission of disease and low chondrocyte viability, in addition to removal of host bone for implantation. Autologous chondrocyte implantation offers the opportunity to achieve biologic repair, enabling the surgeon to repair the joint surface with autologous articular cartilage. With this technique, care must be taken to ensure the safety, viability, and microbial integrity of the autologous cells while they are expanded in culture over a 4- to 5-week period prior to implantation. Surgical implantation requires equal attention to meticulous technique. In the future, physiologic repair also may become possible using mesenchymal stem cells or chondrocytes delivered surgically in an ex vivo-derived matrix. This would allow in vitro manipulation of cells with growth factors, mechanical stimuli, and matrix sizing to allow implantation of mature biosynthetic grafts which would allow treatment of larger defects with decreased rehabilitation and morbidity.
Minas
T
T
Department of Orthopedics, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass, USA.
Nehrer
S
S
D002358:Cartilage, Articular / Q000166:cytology / Q000293:injuries / Q000473:pathology / Q000601:surgery*; D017690:Cell Transplantation; D006801:Humans; D007592:Joint Diseases / Q000601:surgery*; D010521:Periosteum / Q000637:transplantation; D014182:Transplantation, Autologous; D014184:Transplantation, Homologous; D014945:Wound Healing / Q000502:physiology