title: Calcitonin enhanced lumbar spinal fusion in a New Zealand rabbit model: a study with morphologic and molecular analysis.
abstract: METHODS
  In this study, the effect of calcitonin on lumbar spinal fusion was studied in a New Zealand rabbit model.
  
  
  OBJECTIVE
  To investigate whether calcitonin can enhance lumbar spinal fusion in a New Zealand rabbit model and whether calcitonin can enhance expression genes involved in osteogenesis and angiogenesis.
  
  
  BACKGROUND
  Calcitonin is used to treat osteoporosis and diseases involving accelerated bone turnover. Studies have shown that calcitonin might also promote bone cell proliferation and bone formation, suggesting its possible role in promoting spinal fusion, but few data are available.
  
  
  METHODS
  The effect of calcitonin on lumbar spinal fusion was analyzed in 32 New Zealand rabbits. Each rabbit received 2 autologous iliac bone grafts (one between L4-L5 without fixation, one between L6-L7 with fixation). Sixteen rabbits received calcitonin (calcitonin group, 1 U/kg daily from day 1 to the day of sacrifice), whereas the other 16 did not (control). At weeks 1, 2, 4, and 8, after examination for spinal fusion with radiography, 4 rabbits from each group were sacrificed. Each graft was histologically scored under light microscopy. In addition, we analyzed the messenger RNA (mRNA) levels of collagen I (Col I), bone morphometric protein 2 (BMP-2), insulinlike growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF), genes known to be involved in osteogenesis and angiogenesis, in each graft.
  
  
  RESULTS
  With both fixation and without fixation, the bone grafts in rabbits receiving calcitonin showed a higher spinal fusion rate and higher histologic scores from week 2 to week 8, and had higher mRNA levels of Col I, BMP-2, IGF-1, and VEGF at all time points except BMP-2 and IGF-1 at week 1, than grafts in rabbits without receiving calcitonin.
  
  
  CONCLUSIONS
  Calcitonin can enhance lumbar spinal fusion. One mechanism might be through upregulating genes involved in osteogenesis and angiogenesis.
authors: Department of Orthopedic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
authors: Yong
authors: Y
authors: Liu
authors: Yu
authors: Y
authors: Fan
authors: Dengfeng
authors: D
authors: Cao
authors: Jianguo
authors: J
authors: Zhang
authors: Zhihong
authors: Z
authors: Wu
authors: Guixing
authors: G
authors: Qiu
mesh_terms: D000818:Animals; D050071:Bone Density Conservation Agents / Q000494:pharmacology; D055396:Bone Morphogenetic Protein 2 / Q000235:genetics; D002116:Calcitonin / Q000502:physiology*; D024042:Collagen Type I / Q000235:genetics; D005786:Gene Expression Regulation / Q000502:physiology*; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D008159:Lumbar Vertebrae / Q000502:physiology* / Q000601:surgery; D008297:Male; D023421:Models, Animal; D018919:Neovascularization, Physiologic / Q000502:physiology*; D010012:Osteogenesis / Q000235:genetics; D011817:Rabbits; D013123:Spinal Fusion / Q000379:methods*; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
chemical_list: D050071:Bone Density Conservation Agents; D055396:Bone Morphogenetic Protein 2; D024042:Collagen Type I; D042461:Vascular Endothelial Growth Factor A; D007334:Insulin-Like Growth Factor I; D002116:Calcitonin