Articular cartilage repair with autografting under the influence of insulin-like growth factor-1 in rabbits.

Insulin-like growth factor (IGF)-1 has been successfully demonstrated to stimulate proteoglycan synthesis, slow down its catabolism and promote cartilage formation through well defined in vitro studies. It was therefore, assumed that IGF-1 would eventually serve to augment current cartilage repair techniques in vivo. Study was therefore, designed to determine the influence of IGF-1 in cartilage repair with or without autografting. For this purpose articular cartilage repair model was created in the left knee of 48 New Zealand white rabbits of either sex, 6-7 months old, weighing 1-2 kg. The articular cartilage defect was created in the femoral groove of femoro-patellar joint using hand held trephine under xylazine and ketamine anaesthesia in all the animals. The defect created was 3 mm in diameter and 2 mm in depth. For autografting, osteochondral tissues harvested from the proximal patellar groove of the femur were placed in the distal defect and vice versa. The experimental animals were divided mainly into four groups, i.e. Group A (control), Group B (autografting), Group C (control + IGF-1) and Group D (autografting + IGF-1). Animals of group A and B were provided only with collagen scaffolds at 10 mug/cm(2) whereas animals of treatment group C and D were provided with collagen scaffolds holding 30 ng/30 mul of IGF-1 into the defect. Evaluation of cartilage repair was done on days 15, 30 and 45 after ethically killing the animals. Initially IGF-1 had shown the tendency for either in the maintenance of autografted cartilage or helped in proliferation of chondroblast for the repair process. However, later in the process, cartilage formation apparently declined and appeared to converge to osseous tissue. Collectively, non-responsiveness of osteoarthritic chondrocytes to IGF-1 could be partially attributed to either increased IGF-binding proteins in the joint space, micromovement of the graft, lack of nutrition, dose of IGF-1 or its half life in the current study.