Several hundred thousand peripheral nerve injuries occur each year in Europe and the United States alone, mainly as a result of trauma to the upper extremity. Even after optimal surgical repair, functional outcome--especially sensory recovery--is disappointingly poor. This poor outcome is largely due to death of primary sensory neurons, but also lack of fiber regeneration over the nerve trauma zone and target-organ denervation. The type of nerve repair performed is dependent on the size of the nerve gap between the proximal and distal stumps. Short gaps can be repaired directly by end-to-end coaptation and epineural suturing, whereas long nerve gaps require additional material to bridge the defect, which further reduces the functional outcome. The current repair method to bridge nerve defects is the use of autologous nerve grafts (autografts), which provide the regenerating axons with a natural guidance channel populated with functioning Schwann cells (SC) surrounded by their basal lamina. The first use of nerve grafts in humans was reported in 1878, but the wide use of this technique was developed during World War II when nerve grafting became the standard method for nerve-gap repair. Harvesting of nerve grafts results in co-morbidity that includes scarring, loss of sensation, and possible formation of painful neuroma. The donor nerves often are of small calibre and limited number. As functional recovery in peripheral nerve reconstruction is poor, clearly, alternative method for bridging nerve gaps is needed.