Purpose: Untreated symptomatic osteonecrosis of the femoral head (ONFH) often leads to femoral head collapse and advanced secondary osteoarthritis (OA). The primary goal in the treatment of ONFH is to treat it in early enough stage to preserve the femoral head and avoid total hip arthroplasty. The use of growth factors have been proposed. The purpose of this paper is to evaluate the effects of basic fibroblast growth factor (bFGF) on the repair of ONFH in rabbits. Methods: To evaluate the in vivo effect of implanted bFGF, we created drill hole (1mm in diameter and 5mm in depth) in the femoral head of rabbit ONFH model. Animal model were induced by the treatment combining the administration of high dose corticosteroids (40mg/kg of methylprednisolone) and capsule resection, accompanied by coagulating of the softtissue attachments from femoral surgical neck and acetabulum. 8 weeks after induction of ONFH, we implanted gelatin hydrogel microspheres containing 100mg bFGF or PBS into the femoral head and articular surface. Thirty-five male Japanese white rabbits underwent ONFH were divided three groups as follows: (1) Control group, in which the rabbits received no further treatment after ONFH; (2) PBS group, in which 8 weeks after ONFH, PBS contained in gelatin hydrogel microspheres were directly injected; (3) bFGF group, in which 8 weeks after ONFH, 100mg bFGF contained in gelatin hydrogel microspheres were directly injected. The right hip was experimented on in all treated rabbits. Animals in control group were killed at 0, 4, 8, 12, 24 weeks after ONFH (n= 5 each). Animals in the treatment groups were killed at 24 weeks after ONFH (n= 5). Gross morphologic and histologic examinations, and radiographic assessment by micro CT scans were performed. Results: Injections of bFGF contained in gelatin hydrogel microspheres suppressed the progression of OA in the ONFH rabbit model. Macroscopically, the area of articular surface of the right femoral head involved OA change was significantly less in the bFGF group (14.1±9.0%) compared with the PBS group (42.1±5.4%, P <0.01) or control group (62.5±11.4%, P <0.01). The roundness index of the right femoral head was significantly less in the bFGF group (52.4±4.9%) than that in the PBS group (62.2±4.3%, P < 0.05) Radiographic assessment by micro CT scans showed significantly better preservation of the femoral head structure and better osteogenesis in the bFGF group compared with the PBS group or control group. The irregularity of subchondral bone of the femoral head in the bFGF group (17.5±6.6%) was less than that in the PBS group (59.1±13.6%, P <0.01) or control group (54.2±10.7%, P <0.01). Bone formation rate of/around implant area was significantly higher in the bFGF group (71.2±3.3%, 37.9±11.5%) compared with the PBS group (47.8±8.6%, 11.5±4.2%, P <0.01). According to the modified Mankin’s histological score, the severity of OA in the bFGF group (3.4±1.6) was significantly less than that in the PBS group (8.8±2.6, P < 0.01) or control group (7.8±0.4, P <0.05). Conclusions: To our knowledge, this is the first study to show that bFGF induces osteogenesis and suppresses the progression of secondary OA in the ONFH animal model. Our findings demonstrated that bFGF into the femoral head and articular surface had therapeutic effects on secondary OA development in the ONFH. Our results suggest the potential feasibility of a new conservative treatment for ONFH. 77 ASSOCIATION OF OSTEOCHONDRAL ANGIOGENESIS, CARTILAGE LESION AND BEHAVIOURAL PAIN IN A RAT MODEL OF OSTEOARTHRITIS