Deficiency of tenascin-C delays articular cartilage repair in mice

Objective In human articular cartilage, tenascin-C (TN-C) expression decreases during maturation of chondrocytes. and almost disappears in adults, however, it reappears in damaged cartilage To examine the effects of TN-C on cartilage degeneration and repair, we compared articular cartilage degeneration between wild-type (WT) and tenascin-C knockout mouse (TNKO) mice using a spontaneous osteoarthritis (OA) in aged joints and surgical OA model In addition, we made full-thickness cartilage defects and compared the cartilage repair process between the two groups Methods The surgical procedure to create degenerative OA model was performed by transecting the anterior eructate ligament and medial collateral ligament Full-thickness defects were created in the center of the femoral trochlea to evaluate cartilage repair Sections of cartilage were stained with hematoxylin and eosin or safranin-O. and immunostaining for TN-C The degrees of degeneration and repair were graded Results In the WT surgical OA model, the articular cartilage was almost nor mal at 2 weeks, but safranin-O-decreased staining at 4 weeks In TNKO mice, saftanin-O decreased staining at 2 weeks, and cartilage was injured intensely at 4 weeks In the cartilage repair model, TN-C was expressed after 1 week, was strongly expressed in the upper layer of regenerated tissue after 3 weeks, and disappeared after 6 weeks The defects were restored until 6 weeks in WT mice; however, defects in TNKO mice were filled with fibrous tissue with no cartilage-like tissue. Conclusions This study revealed that cartilage repair in TNKO mice was significantly slower than that in WT mice and that the deficiency of TN-C progressed during cartilage degeneration (C) 2010 Osteoarthritis Research Society International Published by Elsevier Ltd. All rights reserved