The role of neurofibromin and melatonin in pathogenesis of pseudarthrosis after spinal fusion for neurofibromatous scoliosis.

摘要

We might hypothesize that the high rate of pseudarthrosis after spinal fusion for neurofibromatous scoliosis is related to two factors: the absence of neurofibromin and melatonin deficiency. Loss of the up-regulation of neurofibromin during the healing process might abolish the bone-forming effects mediated through platelet-derived growth factor (PDGF) and transforming growth factor (TGF) beta1. The absence of neurofibromin might cause an increase in the Ras activity that increases the mitogen-activated protein kinase (MAPK) with resultant disturbance of the regulatory mechanism of core binding transcription factor (Cbfa 1) and increase of osteocalcin. These effects might inhibit bone formation. Melatonin deficiency might cause defective bone formation and favour excess fibrous tissue formation.