Extended expression of cartilage components in experimental pseudoarthrosis

The healing of femoral fractures in an experimental rat pseudoarthrosis model was followed by studying the expression of cartilage specific genes coding for type II and X collagens and aggrecan, soft tissue and bone specific type I collagen, and decorin. Severe impairment of healing was observed with cartilage gene expression continuing until the seventh week and then declining rapidly. The abnormal healing pattern results in an inactive scar-like callus after the ninth week of healing even though house-keeping (e.g., GAPDH) genes are continuously expressed in the tissue. These results could be explained on the basis of continuous chondrogenic stimulus extending much beyond the normal range. If union is not achieved because of mechanical instability, signal of endochondral ossification persists until it becomes exhausted and callus at the fracture gap becomes an inactive fibrous scar. The disturbed matrix gene expression was confirmed by histology.