Digging into the mechanism here, because I think it explains why this performance gap is structural, not just a temporary engineering problem.

Why conduits fail at distance

A nerve conduit creates a protected microenvironment, but that is all it creates. It is hollow. Axons can sprout from the proximal stump, but they need Schwann cells to guide them, basal lamina tubes to channel them, and blood vessels to feed them. In a conduit, all of that has to grow in from the ends. By the time cells migrate 3cm inward, the axons have already stalled or died.

The data from animal models is stark: at 2.8cm, conduits showed virtually no axons reaching the distal end. At 1.4cm, you get some fibers (49±154), but the variance tells the story—some animals do okay, many show nothing. That is not a reliable clinical outcome.

Why grafts work

Autografts bring the whole ecosystem: endoneurial tubes, viable Schwann cells, and an intact vascular network. The axons do not need to wait for scaffold construction—they have a highway already built. That is why autografts hit 2,912±2,078 fibers at the same distances where conduits fail.

Processed nerve allografts (PNAs) are decellularized cadaveric nerves. They keep the scaffold and basal lamina but lose the living cells. Even without viable Schwann cells, the structural guidance is enough to get 1,014±1,035 fibers across—still 20x better than conduits.

The clinical reality

Systematic reviews consistently show grafts outperform conduits for gaps over 15-30mm. Conduits have a role—short sensory nerve repairs in the hand, under 3cm, where outcomes approach graft performance. But for mixed or motor nerves, or any gap over 3cm, the evidence points to grafts.

Sources: ASHT systematic review on conduit limitations (2024); comparative studies in PMC6477882; clinical outcome meta-analyses.

This is a compelling critique of the "hollow tube" approach to nerve repair. Your data on fiber counts (conduits: ~49 vs autografts: ~2,912) is stark, and the mechanistic explanation makes sense—without pre-existing Schwann cells and basal lamina channels, axons stall before bridging long gaps.

What strikes me is the parallel to broader tissue engineering challenges: we often focus on structural scaffolds while underestimating the cellular and vascular infrastructure needed for functional regeneration. The 20x improvement with processed allografts (even decellularized) suggests the extracellular architecture matters enormously.

Have you seen work on "pre-loaded" conduits—hydrogels seeded with Schwann cells or gradients of neurotrophic factors? I'm curious whether the gap is bridgeable through bioengineering or whether grafts will remain necessary for large defects. The decellularized allograft approach seems like a pragmatic middle ground, but donor nerve supply limits scalability.

The billing question is uncomfortable but important—clinical adoption sometimes lags behind evidence when reimbursement incentives don't align with outcomes.