Four methods of nerve terminolateral neurorrhaphy (TLN) were studied in rat experimental model. In Group A, the distal end of a severed peroneal nerve was sutured end-to-side with an intact tibial nerve trunk, without removal of the tibial epineurium at the suture site. In Group B, the distal end of a severed peroneal nerve was sutured end-to-side with the intact tibial nerve trunk, with removal of the tibial epineurium at the suture site. In Group C, a nerve segment was bridged between the distal part of the severed peroneal nerve and the intact tibial nerve with two end-to-side sutures. In Group D, the proximal end of a severed tibial nerve was sutured end-to-side with the peroneal nerve trunk. Through electrophysiologic, histologic, and ultrastructural examinations, the following conclusions were drawn: 1. Nerve regeneration is possible after TLN. 2. The regenerating fibers after TLN have the ability to penetrate the endoneurium, perineurium, and epineurium. 3. After different methods of TLN, the regenerating fibers grow in both a flowing-out and a filling-in fashion.

The osteogenic growth peptide (OGP) is a naturally occurring tetradecapeptide that has attracted considerable clinical interest as a bone anabolic agent and hematopoietic stimulator. In vitro studies have demonstrated that OGP directly regulates the bone marrow mesenchymal stem cells' (BMSCs) differentiation into osteoblasts. However, the exact mechanism of this process remains unknown. In the present study, we investigated the role of RhoA/ROCK signaling in differentiation along this lineage using human BMSCs. OGP treatment increased the mRNA level of bone morphogenetic protein-2 and alkaline phosphatase activity after osteogenic induction. Analysis of BMSCs induced in the presence of OGP revealed an increase in RhoA activity, and phosphorylation of FAK and cofilin. The ROCK-specific inhibitors, Y27632, blocked the OGP-induced regulation of BMSC differentiation. Taken together, these data suggest that OGP not only acts on BMSCs to stimulate osteogenic differentiation, but also in a dose-dependent manner, and this effect is mediated via the activation of RhoA/ROCK pathway.

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