Purpose. 1. To evaluate how radiological parameters change during the first 3 years following anterior endoscopic surgery. 2. To report complications encountered in this period. Methods. Between April 2000 and June 2006,106 patients underwent an anterior endoscopic instrumented fusion. There were 95 females and 11 males. Average age was 16.1 years (range 10-46). 103 (97%) had right-sided idiopathic curves. The majority were Lenke type 1 (79%). Patients were assessed at 3, 6, 12, 24, and 36 months. 83 patients had 1 year follow-up, 69 had 2 years or more. The following were investigated; the structural curve, instrumented curve, non-structural curves, skeletal age at operation and sagittal profile (T5-T12). Results. The mean Cobb angle of the structural curve was 52.3 degrees. 2 months following surgery, it was 21.4 degrees, with a correction rate was 59%. There was a partial loss of correction thereafter (29.3 degrees at 3 years, P=<0.001). The instrumented curve did not change significantly. The mean post-operative Cobb angles of the proximal and distal non-structural curves (when present) at 2months were 19.6 and 19.7 degrees respectively. At 3 years they were 18.8 and 24.4. The change in the distal curve was significant (p=<0.05). The pre-operative sagittal profile was 19 degrees. At 2 months it was 28 degrees and 31 degrees at 3 years. Skeletal maturity at time of surgery was not found to influence the structural curve. There were 12 fractured rods. All were 4.5mm rods and all but 2 were using rib autograft. There were 8 cases of proximal screw pullout. Conclusion. Anterior endoscopic surgery is effective in restoring both sagittal and coronal balance. However, there is small loss of coronal correction in the structural curve. 11% of rods fractured, though none occurred in the 94 patients where a larger rod (5.5mm) and femoral allograft was used

Purpose. Internal fixation of fractures in the presence of osteopenia has been associated with a failure rate as high as 25%. Enhancing bone formation and osseointegration of orthopaedic hardware is a priority when treating patients with impaired bone regenerative capacity. Fibroblast Growth Factor (FGF) 18 regulates skeletal development and could therefore have applications in implant integration. This study was designed to determine if FGF 18 promotes bone formation and osseointegration in the osteopenic FGFR3−/− mouse and to examine its effect on bone marrow derived mesenchymal stem cells (MSCs). Method. In Vivo: Intramedullary implants were fabricated from 0.4 × 10mm nylon rods coated with 300nm of titanium by physical vapour deposition. Skeletally mature, age matched female FGFR3−/− and wild type mice received bilateral intramedullary femoral implants. Left femurs received an intramedullary injection of 0.1μg of FGF 18 (Merck Serono), and right femurs received saline only. Six weeks later, femurs were harvested, radiographed, scanned by micro CT, and processed for undecalcified for histology. In Vitro: MSCs were harvested from femurs and tibiae of skeletally mature age matched FGFR3−/− and wild type mice. Cells were cultured in Alpha Modified Eagles Medium (αMEM) to monitor proliferation or αMEM supplemented with ascorbic acid and sodium beta-glycerophosphate to monitor differentiation. Proliferation was assessed through cell counts and metabolic activity at days 3, 6 and 9. Differentiation was assessed through staining for osteoblasts and mineral deposition at days 6, 9 and 12. Results. Wild type mice exhibited more peri-implant bone formation compared to FGFR3−/− mice. Peri-implant bone formation at the proximal metaphyseal-diaphyseal junction was increased in FGF18 treated femurs compared with contralateral control femurs in wild type (p = NS) and FGFR3−/− (p = 0.04) mice. Histological analysis corroborated micro CT findings, with FGF 18 treated FGFR3−/− femurs forming peri-implant bone instead of the fibrous response seen in controls. In vitro studies showed that FGF18 significantly increased MSC proliferation and metabolism in a dose dependent manner in wild type and FGFR3−/− mice. Osteoblast differentiation was inhibited by FGF18 in wild type MSCs, but was increased at physiological concentrations in cells harvested from FGFR3−/− mice. Conclusion. FGF 18 increases bone formation and osseointegration of intramedullary implants in osteopenic mice and increases MSC proliferation in both the presence and absence of FGFR3. FGF18 also promoted osteoblast differentiation in the absence of FGFR3 signalling, most likely via FGFR1 or 2. Additional work is needed to confirm the identity of the alternate FGFR and to evaluate its capacity to improve osseous healing in unfavourable in-vivo environments