Chondrogenic cells respond to partial-thickness defects of articular cartilage in adult rats: an in vivo study.

The purpose of this study was to establish a partial-thickness articular cartilage defects model in adult rats and explore the respond of chondrogenic cells to the cartilage injury. Forty-five adult Sprague-Dawley rats were divided into operated group, sham-operated group and control group. Partial-thickness cartilage defects were created on the weight-bearing region of femoral condyles by a converted ophthalmic knife. Rats were exposed to 5-bromo-2'-deoxyuridine (BrdU) for five consecutive days and were sacrificed 1, 2 and 4 weeks after surgery. Evaluations of macroscopic and histological changes were made. Chondrocyte apoptosis was evaluated by TUNEL assay. Immunofluorescence staining of CD105 and BrdU, double staining of CD105/integrin α5β1 and CD105-positive cells counting were performed for evaluations of cells around the defects. Cartilage softening and fibrillation with chondrocyte apoptosis were observed around the injury site after surgery. Results of histological scores indicated no significant difference between one time point and a successive time point for either group. CD105-positive cells and BrdU-label-retaining cells were observed around the linear injury. And cells counting showed the number of CD105-positive cells increased at later time points (P < 0.05). Immunofluorescence double staining demonstrated co-localization of CD105 and integrin α5β1 in activated cells around the defects. We establish a partial-thickness cartilage defects model in adult rats and demonstrate this injury may lead to activation of putative progenitor cells. In addition, the activated cells express integrin α5β1 specially, which may help in early discovery of osteoarthritis.