Chronic nerve compression (CNC), as in carpal tunnel syndrome, is a common cause of peripheral nerve dysfunction in humans. Previous studies using animal models have demonstrated progressive demyelination and a slowing of nerve conduction velocity. To characterize the Schwann cell response to CNC, we evaluated total Schwann cell number, apoptosis, and proliferation in an animal model of CNC. Design-based stereologic techniques revealed a striking transient increase in Schwann cell number following CNC. Schwann cell number increased sixfold relative to the normal nerve at the site of compression at 1 month and then slowly declined toward control levels. Nevertheless, assays of apoptosis (TUNEL and an antipoly-ADP-ribose polymerase labeling assays) revealed extensive Schwann cell apoptosis at 2 weeks postcompression, which is during the time when Schwann cell number was increasing. Electron microscopic analysis confirmed that these dramatic changes in Schwann cells occurred in the absence of axon degeneration and axonal swelling and before there were any detectable alterations in nerve conduction velocity. Counts of bromodeoxyuridine-labeled Schwann cells revealed that proliferation occurred concurrently with ongoing apoptosis. To define further the possible mitogenic properties of mechanical stimuli on Schwann cells, we used an in-vitro model to deliver shear stress in the form of laminar fluid flow to pure populations of Schwann cells and confirmed that mechanical stimuli induce Schwann cell proliferation. Our findings indicate that chronic nerve compression induces Schwann cell turnover with minimal axonal injury and support the idea that mechanical stimuli have a direct mitogenic effect on Schwann cells.

Background: Detachment of a tendon from its osseous insertion, as can be the case with severe rotator cuff injuries,

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