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Page 2 of 4 Chi et al. Plast Aesthet Res 2023;10:70 https://dx.doi.org/10.20517/2347-9264.2023.89

In a study by Peters et al., a special cohort of patients offered the rare clinical opportunity where the failed
allograft was close enough to the nerve end-target to justify a simultaneous acellular nerve allograft excision
[3]
and autograft reconstruction . Histologic analyses in these patients demonstrated the presence of
[3]
myelinated axons proximal to the allograft and a paucity of regenerating axons through the allograft .
Figure 1 includes a gross image with corresponding histologic sections demonstrating the presence of
myelinated axons proximal to, within, and distal to the ANA. For proximal nerve injuries, the time and
distance to end target are usually too long and are thereby prohibitive of autograft reconstruction. The failed
ANA is then frequently left in place as the senescent axons traveling through the allograft have dwindled
and are thus useful for pain control while distal nerve transfers are performed .
[4,5]

Nerve autografts have been considered the gold standard, with the cellular and extracellular components
serving as a biologic scaffold to guide axonal regeneration. However, there are limits to autograft efficacy as
dictated by nerve gap length and diameter. For example, 6 cm appears to be a useful approximate ceiling for
what outcomes may be expected in reconstructing motor nerve gaps, as demonstrated in a study assessing
outcomes from common peroneal nerve decompression and reconstruction . However, in another study,
[6-8]
gaps greater than 5 cm were associated with 10% meaningful motor recovery and 52.9% meaningful sensory
recovery . Additionally, large diameter nerve gaps represent a greater challenge to revascularization
[9]
demand for autografts and acellular nerve allografts. Increasing nerve diameter increases central necrosis
during the period of nerve recovery. In a study by Leckenby et al., ANA nerve diameters greater than 3 mm
[9]
were inhibitory to axonal growth . Autografts revascularize via longitudinal inosculation, while acellular
nerve allografts require the reconstitution of entirely vascular networks de novo [10,11] . Hence, even with
matched diameters, allografts have been demonstrated to take several times longer than autografts to
[12]
revascularize .

Fortunately, for shorter or smaller-diameter nerve gaps, acellular nerve allografts and nerve conduits may
return function to some degree since only 25%-30% of nerve fibers are necessary, given the compensatory
expansion of motor and sensory units [13,14] . However, when critical functions are being restored, it would be
reasonable to utilize “gold standard” autografts to maximize functional recovery. In one of the few studies
not funded by industry, meaningful motor recovery after ANA declined notably with diameters exceeding 2
[9]
mm and lengths of 2 cm . Utilizing an off-the-shelf allograft is less time-consuming than harvesting an
autograft, but in keeping with the principles of reconstructive surgery, the solution must match the
demands and functional importance of the defect. For example, cortical bone allografts certainly have their
place in skeletal reconstruction; however, when bone gap distance and weight-bearing criteria are
considered, vascularized bone flaps may be the suitable treatment [15,16] . Therefore, in modern nerve surgery,
it remains the practice of the senior author to treat critical motor and sensory nerves with nerve autograft.
By contrast, acellular nerve allografts are utilized for noncritical or small-diameter sensory nerves and to
prevent neuroma formation by utilizing the dwindling regeneration that occurs over a long distance .
[17]