Effect of nerve repair after unilateral partial facial paralysis on craniofacial growth and development.

Abstract

The effect of partial transection, coaptation, and freezing of the left facial nerve on craniofacial growth and development was investigated. Twelve-day-old New Zealand White rabbits were randomly assigned to four groups: control group (n = 15), nerve ablation group (n = 15) with a surgically induced partial facial paralysis, nerve coaptation group (n = 15) with a surgically induced partial facial paralysis treated by immediate microsurgical nerve coaptation, and nerve freezing group (n = 13) with a freezing-induced partial facial paralysis. All animals were operated on at the age of 12 days; follow-up evaluations were performed at the ages of 2 months (end-point prepubertal growth) and 6 months (full grown). Computerized dorsoventral roentgencephalometric analysis and computer tomographic three-dimensional volumetric measurements were performed at both ages. Roentgencephalometric analysis revealed that the growth disturbances of the nerve ablation group and the nerve coaptation group were analogous. In contrast, in the nerve freezing group, hardly any growth disturbances as compared with the control group were seen. The CT volume measurements revealed a significant left-right difference in maxillary volume at the ages of 2 and 6 months in the nerve coaptation group as compared with the control group. Muscle histomorphometric analysis revealed a shift in muscle fiber composition in the nerve coaptation group and the nerve freezing group, with an increase of type I fibers at the cost of type IIA fibers. This shift was significantly less pronounced in the latter than in the former. Nerve histomorphometric analysis revealed a significant increase in the number of nerve fibers in the nerve coaptation group as compared with the control group. In the nerve freezing group, the increase in the number of nerve fibers was not significantly different as compared with the control group and the nerve coaptation group. Both the equivalent diameter and the myelin area were equally reduced in the nerve coaptation and nerve freezing groups. Thus, the nerve coaptation group and the nerve freezing group did not differ significantly in the extent of nerve recovery, although they differed in the extent of muscle recovery. The extent of muscle recovery, in turn, was related to the extent of abnormal craniofacial growth and development. Indeed, the growth and development were hardly abnormal in the nerve freezing group and as abnormal as after untreated paralysis in the nerve coaptation group. Therefore, factors related to nerve regeneration, other than those assessed by nerve histomorphology, were considered to be responsible for these differences between both groups. The duration of the denervation time was regarded to be considerably shorter in the nerve freezing group than in the nerve coaptation group, resulting in the observed improved muscle recovery. The difference in the degree of axonal malalignment between both groups was considered to be negligible, because of the tolerance toward axonal malalignment at neonatal age.