Dural cell culture. A new approach to study duraplasty.

Fistulas of the cerebrospinal fluid are often repaired by insertion of grafts of various kinds. However, current knowledge of wound healing after graft insertion is limited, and only a few animal studies are available. The objective of this study is to test whether an in vitro model is suited to analyze cellular healing aspects after duraplasty and to assess dura substitutes in such conditions in regard to their surface attractiveness for cellular migration from the dura margins. Harvested dura pieces from minipigs were perforated to mimic central dura lesions, placed on various coated surfaces (collagen, laminin, poly-L-lysine) or grafts, and investigated in a cell culture for cellular closure of the perforation. Cellular migration from the dura into the central perforation was noted on collagen-coated surfaces and when defects were filled with collagen gels, but there was no cell growth on surfaces with poly-L-lysine or laminin coating. Immunocytochemistry identified the migrating cells mainly as fibroblasts with some intermingled epithelial cells. Scanning electron microscopy proved cellular closure of defects after dura placement on allogenic non-crosslinked collagen transplants. Less cellular migration was observed on poly-P-dioxanon sheets, while no cells migrated into the central dura perforation after placement on a cartilage substitute. Cell counting indicated enhanced cellular closure of the dura opening after introduction of insulin or fibroblast growth factor (sign test for both: 0.031). Our study succeeded in establishing a cell culture model for duraplasty and indicated cellular migration from the dura borders at the site of the defect during the wound healing process. The cell culture model presented in this report shows that collagen grafts are best suited for duraplasty. In accordance with the immunocytological finding of fibroblast migration from the dura borders additional application of fibroblast-stimulating growth factors accelerated cellular defect closure.