Mesh implants in hernia repair. Inflammatory cell response in a rat model

In the reinforcement of the abdominal wall with mesh implants, various complications including hernia recurrence, abdominal pain, seroma formation and infection are discussed to depend on the biocompatibility of the alloplastic prosthesis. Particularly macrophages, T-cells and mast cells have been shown to play a major role in the inflammatory response to biomaterials. To approach biocompatibility of surgical meshes we therefore examined the infiltrate of these cells as well as the proliferation rate in response to different clinically applied materials.

Three mesh materials (polypropylene: PP, Prolene; polyethylene terephthalate: PET, Mersilene, and polypropylene/polyglactin: PP + PG, Vypro) were compared after inlay implantation in a standardized rodent animal model. A suture-closed laparotomy served as control. After 7 and 90 days of implantation, histochemical analysis of the inflammatory response to all biomaterials was performed: macrophages (ED3), T-cells (CD3), proliferating cells (PCNA) and mast cells (Giemsa) were investigated.

In all groups a persisting T-cell response was observed. Colonization of the interface with macrophages showed a pronounced reduction in the PP + PG-mesh group. Infiltration of mast cells at the tissue graft interface showed a time-dependent decrease in the PET- and PP + PG-mesh groups, whereas in contrast, index of mast cells increased in the PP-mesh group. At both time points, indices of proliferation were highest in the PP-mesh group.

The present data confirm the development of a biomaterial-dependent chronic inflammatory response to surgical meshes with macrophages as the predominant cell type. Further research on the recruitment of inflammatory cells and in particular on the role of mast cells and their granular products should be encouraged.