The healing of femoral fractures in an experimental rat pseudoarthrosi
s 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 heal
ing was observed with cartilage gene expression continuing until the s
eventh week and then declining rapidly. The abnormal healing pattern r
esults in an inactive scar-like callus after the ninth week of healing
even though house-keeping (e.g., GAPDH) genes are continuously expres
sed in the tissue. These results could be explained on the basis of co
ntinuous 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 cal
lus at the fracture gap becomes an inactive fibrous scar. The disturbe
d matrix gene expression was confirmed by histology.