Impact of polymer pore size on the interface scar formation in a rat model.
BACKGROUND
The surgical therapy of hernias is increasingly based on reinforcement with alloplastic material, in particular surgical meshes. The biological response to these foreign bodies largely depends on the selected material and its structure. In comparison to the physiological scar process following a simple abdominal wall incision, the chronic inflammation at the interface to the polymers lead to specific morphological alterations.


METHODS
In the present study two meshes with different pore sizes were implanted into rats: a heavy-weight and small-pore-sized mesh (hw-mesh) made of nonabsorbable polypropylene monofilaments and a low-weight large-pore-sized mesh consisting of polypropylene and of absorbable polyglactin multifilaments (lw-mesh). A suture repair of a laparotomy served as control. After 7, 14, 21, and 90 days the mesh area was analyzed with regard to tissue and cellular response.


RESULTS
Over the whole observation period morphometric analysis indicated an improved integration of the lw-mesh with reduction of both inflammation and fibrosis, whereas the hw-mesh induced an intense chronic inflammation concomitant with an intensified bridging scar reaction. On the cellular level these findings correspond to an elevated cell turnover, characterized by increased rates of apoptotic and proliferating cells. In contrast, the tissue reaction to the lw-mesh achieved levels almost similar to those of the physiological scaring process in the control group.


CONCLUSIONS
In conclusion, the present data confirm the development of a chronic inflammatory foreign body reaction at the interface to both hw-meshes and lw-meshes; however, the use of lw-meshes showed superior tissue integration. With regard to the quite similar polymer surface the pore size appears to be of major importance in tissue reaction and for the biocompatibility of mesh structures.
Klinge
U
U
Department of Surgery, Institute of Pathology, The Technical University of Aachen, Pauwelsstrasse 30, Aachen, D-52057, Germany.
Klosterhalfen
B
B
Birkenhauer
V
V
Junge
K
K
Conze
J
J
Schumpelick
V
V
D000818:Animals; D017209:Apoptosis; D001672:Biocompatible Materials; D002455:Cell Division; D055598:Chemical Phenomena; D002627:Chemistry, Physical; D002921:Cicatrix / Q000209:etiology* / Q000473:pathology; D004195:Disease Models, Animal; D005355:Fibrosis; D006098:Granulocytes / Q000473:pathology; D018840:HSP70 Heat-Shock Proteins / Q000032:analysis; D007249:Inflammation / Q000209:etiology / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D011108:Polymers / Q000737:chemistry*; D019736:Prostheses and Implants; D051381:Rats; D017207:Rats, Sprague-Dawley; D013526:Surgical Mesh / Q000009:adverse effects*; D013537:Sutures
D001672:Biocompatible Materials; D018840:HSP70 Heat-Shock Proteins; D011108:Polymers