A comparative assessment of lengthening followed by end-to-end repair and isograft repair of chronically injured peripheral nerves.

In order to repair chronic nerve injuries (injuries repaired after a long delay), the damaged nerve segments are resected and stumps are bridged by grafts. Autografts remain the gold-standard, but outcomes are typically poor, even after long periods of recovery. In a recent study, we described the use of a nerve lengthening device to gradually elongate the proximal stump of a transected nerve towards the distal stump, enabling a tension-free end-to-end repair.

Nerve lengthening and subsequent end-to-end repair yield more favourable outcomes compared with autograft repair of rat sciatic nerve defects.

Outcomes of end-to-end nerve repairs are more successful compared with outcomes of repairs bridged by nerve grafts. However, end-to-end repairs are not always possible for large nerve gaps, as excessive tension may cause catastrophic failure. In this study, we built on previous nerve-lengthening studies to test the hypotheses that gradual lengthening of the proximal stump across a large nerve gap enables an end-to-end repair and such a repair results in more favourable regenerative outcomes than autografts, which represent the gold standard in bridging nerve gaps.

Redistribution of nerve strain enables end-to-end repair under tension without inhibiting nerve regeneration.

End-to-end repair under no or low tension leads to improved outcomes for transected nerves with short gaps, compared to repairs with a graft. However, grafts are typically used to enable a tension-free repair for moderate to large gaps, as excessive tension can cause repairs to fail and catastrophically impede recovery. In this study, we tested the hypothesis that unloading the repair interface by redistributing tension away from the site of repair is a safe and feasible strategy for end-to-end repair of larger nerve gaps.

Pannexin 1 Modulates Axonal Growth in Mouse Peripheral Nerves.

The pannexin family of channels consists of three members-pannexin-1 (Panx1), pannexin-2 (Panx2), and pannexin-3 (Panx3) that enable the exchange of metabolites and signaling molecules between intracellular and extracellular compartments. Pannexin-mediated release of intracellular ATP into the extracellular space has been tied to a number of cellular activities, primarily through the activity of type P2 purinergic receptors. Previous work indicates that the opening of Panx1 channels and activation of purinergic receptors by extracellular ATP may cause inflammation and apoptosis.