MODEL ESTABLISHING OF PARTIAL-THICKNESS ARTICULAR CARTILAGE INJURY AND RELATIONSHIPS BETWEEN ACTIVATION OF CELLS AND EXPRESSION OF INTEGRIN β₁IN A RAT MODEL

OBJECTIVE: To investigate the relationships between the expression of integrin β₁and activated cells in a partial-thickness articular cartilage injury model of adult rats.

METHODS: Forty-five male Sprague Dawley rats (aged 10 weeks and weighing 300-400 g) were randomly divided into operated group (n = 15), sham-operated group (n = 15), and control group (n = 15). Partial-thickness articular cartilage injury model was made by scarification in operated group, direct suture after opening of the knee joint was performed in sham-operated group, and no operation was done in control group. Five rats were sacrificed at 1, 7, and 14 days after operation respectively for macroscopic evaluation, HE staining, Safranin O staining, CD105, BrdU, CD105/integrin β₁immunofluorescence and double labeling staining. The histological score of HE staining, gray value of Safranin O staining and CD105-positive cells count were compared among groups at each time point.

RESULTS: Macroscopic evaluation showed chondromalacia and cartilage fibrosis around the linear injury with aggravating tendency with time in operated group, but no chondromalacia and cartilage fibrosis in sham-operated and control groups. HE staining demonstrated a number of activated cells accumulating around the linear injury with nonuniform distribution in operated group, and uniform size and distribution in sham-operated and control groups. The histological scores at each time point in operated group were significantly higher than those in sham-operated group and control group (P < 0.05), but no significant difference was found between different time points in 3 groups (P > 0.05). Safranin O staining was nonuniform with hypochromasia around linear injury in operated group, but the staining was uniform in sham-operated group and control group. Gray value of Safranin O staining had no significant difference among groups and among different time points in the same group (P > 0.05). BrdU-positive and CD105-positive cells distributed unevenly around the linear injury in operated group, uniform distribution was observed in sham-operated group and control group. CD105-positive cells count in operated group was significantly higher than those in sham-operated group and control group at each time point (P < 0.05); CD105-positive cells increased significantly with time in operated group (P < 0.05). CD105/integrin β₁-positive cells were observed around the linear injury in operated group, but was not observed in sham-operated group and control group.

CONCLUSION: The partial-thickness articular cartilage injury model is successfully established in rats, and cartilage injury could not be repaired completely in the model. The activated cells aggregation around the linear injury can be observed, but there is no obvious relationships between activated cells and cartilage matrix. These activated cells are in proliferation and could express both CD105 and integrin β₁.