BACKGROUND: The healing potential of articular cartilage in response to injury is poor, because articular cartilage lacks blood vessels or perichondrium. Costal cartilage is covered with a vascularized perichondrium, which is known to have chondrogenic potential. The purpose of this study was to determine whether costal cartilage can heal in response to mechanical injury. METHODS: Sixty-five ICR mice were used. Under anesthesia, the left tenth costal cartilage was dissected using microscissors. At 1 day and at 1, 2, 3, and 12 weeks after injury, the mice were killed and paraffin sections were prepared. Safranin O staining, in situ hybridization of type II collagen, and immunostaining for CD44 were performed. Localization of cell proliferation was performed using immunohistochemistry with bromodeoxyuridine monoclonal antibody. In situ detection of apoptosis (deoxynucleotidyl transferase-mediated dUTP nick end labeling) was performed using an Apop Tag Kit. RESULTS: From 1 to 2 weeks after costal cartilage injury, bromodeoxyuridine-positive cells were observed in the perichondrium. Two weeks after injury, the dissected cartilage fragments had combined with newly formed safranin O-positive tissue. Type II collagen mRNA was strongly expressed in the cells of the newly formed tissue. Apoptosis was detected in newly formed cartilaginous tissue at 1 and 2 weeks after injury. The cartilage fragments failed to unite at 12 weeks after injury. CD44 immunoreactivity was detected on the surface of the cavity between the cartilage fragments. CONCLUSION: Although the dissected fragments of costal cartilage can combine with newly formed cartilaginous tissue temporarily, they fail to unite ultimately.
BACKGROUND: The healing potential of articular cartilage in response to injury is poor, because articular cartilage lacks blood vessels or perichondrium. Costal cartilage is covered with a vascularized perichondrium, which is known to have chondrogenic potential. The purpose of this study was to determine whether costal cartilage can heal in response to mechanical injury. METHODS: Sixty-five ICR mice were used. Under anesthesia, the left tenth costal cartilage was dissected using microscissors. At 1 day and at 1, 2, 3, and 12 weeks after injury, the mice were killed and paraffin sections were prepared. Safranin O staining, in situ hybridization of type II collagen, and immunostaining for CD44 were performed. Localization of cell proliferation was performed using immunohistochemistry with bromodeoxyuridine monoclonal antibody. In situ detection of apoptosis (deoxynucleotidyl transferase-mediated dUTP nick end labeling) was performed using an Apop Tag Kit. RESULTS: From 1 to 2 weeks after costal cartilage injury, bromodeoxyuridine-positive cells were observed in the perichondrium. Two weeks after injury, the dissected cartilage fragments had combined with newly formed safranin O-positive tissue. Type II collagen mRNA was strongly expressed in the cells of the newly formed tissue. Apoptosis was detected in newly formed cartilaginous tissue at 1 and 2 weeks after injury. The cartilage fragments failed to unite at 12 weeks after injury. CD44 immunoreactivity was detected on the surface of the cavity between the cartilage fragments. CONCLUSION: Although the dissected fragments of costal cartilage can combine with newly formed cartilaginous tissue temporarily, they fail to unite ultimately.