Logical changes that occur in the ruptured human anterior cruciate ligament during these phases. Myofibroblast-like cells that contain a-smooth muscle actin are present in the midsubstance of the intact human anterior cruciate ligament. A second objective of this study was to determine whether an increased number of myofibroblast-like cells is found in the midsubstance of the ruptured human anterior cruciate ligament because it was thought that those cells might be responsible in part for the retraction of the ruptured anterior cruciate ligament. In the early phase of this study, it was found that the number of myofibroblast-like cells in the midsubstance of the ruptured anterior cruciate ligament was actually decreased, and this hypothesis was abandoned. During the epiligamentous repair phase, synovial tissue was formed that covered the ends of the ruptured anterior cruciate ligament. Most of the synovial lining cells were myofibroblast-like cells that contained a-smooth muscle actin. The primary objective of this study was to determine the location and the characteristics of the a-smooth muscle actin-containing myofibroblast-like cells that appear in the human anterior cruciate ligament following rupture....

This study evaluated the composition of reparative tissue retrieved during revision surgery from full thickness chondral defects in 18 patients in whom abrasion arthroplasty (n = 12), grafting of perichondrial flaps (n = 4), and periosteal patching augmented by autologous chondrocyte implantation in cell suspension (n = 6) failed to provide lasting relief of symptoms. The defects were graded by gross appearance, and all of the tissue filling the defect was retrieved. Histologic evaluation included histomorphometric analysis of the percentage of selected tissue types in cross sections. Immunohistochemistry was performed using antibodies to Types I, II, and X collagen. The histologic appearance of material retrieved after abrasion arthroplasty was that of fibrous, spongiform tissue comprising Type I collagen in 22% ± 9% (mean ± standard error of the mean) of the cross sectional area, and degenerating hyaline tissue (30% ± 10%) and fibrocartilage (28% ± 7%) with positive Type II collagen staining. Three of four specimens obtained after implantation of perichondrium failed as a result of bone formation that was found in 19% ± 6% of the cross sectional area, including areas staining positive for Type X collagen, as an indicator for hypertrophic chondrocytes. Revision after autologous chondrocyte implantation was associated with partial displacement of the periosteal graft from the defect site because of insufficient ongrowth or early suture failure. When the graft edge displaced, repair tissue was fibrous (55% ± 11%), whereas graft tissue attached to subchondral bone displayed hyaline tissue (to 6%) and fibrocartilage (to 12%) comprising Type II collagen at 3 months after surgery. Evaluation of retrieved repair tissue after selected cartilage repair procedures revealed distinctive histologic features reflecting the mechanisms of failure.

Articular cartilage has a limited capacity for repair. In recent clinical and animal experiments, investigators have attempted to elicit the repair of defects of articular cartilage by injecting cultured autologous chondrocytes under a periosteal flap (a layer of periosteum). The objective