A canine knee model of disuse atrophy produced by nonrigid fixation (s
ling) was characterized in respect to variables of proteoglycan size d
istribution, as well as biomechanical properties versus controls. Usin
g this model, we found, in addition to the accepted dogma attributing
changes to reduced protein synthesis by chondrocytes, that there is el
evation of proteases and depression of tissue inhibitor of metalloprot
eases (TIMP) in atrophic knee cartilage. The findings are suggestive o
f cartilage remodelling reminiscent of bone remodelling in disuse atro
phy reported by others, Whether the abnormal changes of protease-TIMP
balance in knee cartilage can be retarded prophylactically by concurre
nt treatment with pentosan polysulfate and insulin like growth factor
1 remains uncertain.