The pathogenesis of collagen pathway on the metabolism disorder of bone and cartilage induced by chronic aluminum (Al) exposure was studied. One hundred Wistar rats were divided randomly into two groups. Experimental rats were given drinking water containing Al chloride (400 mg/L, Al3+), while control rats were given distilled water for up to 150 days. Ten rats were sacrificed in each group every 30 days. The weights of rats, the Al levels of serum, bone and cartilage and the serum levels of carboxyterminal propeptide of type I procollagen (PICP), C-telopeptide of type I collagen (CTX-I), typeII collagen and C-telopeptide of type II collagen (CTX-II) were detected. The Al-poisoning model was established successfully in rats. Al-treated rats showed lower body weight and higher Al accumulation compared with control rats. The serum levels of PICP and type II collagen decreased gradually, and were significantly lower than those in the control group (P<;0.05, P<;0.01). The serum levels of CTX-I and CTX-II were higher in the Al-treated group than in the control group from day 90 and 60, respectively (P<;0.01). The results indicate that chronic Al exposure can induce the dysequilibrium of bone formation and bone absorption. As a result, bone and cartilage metabolism disorder were induced.