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abstract

108 - VAGINAL EXPOSURES CONNECTED TO REGIONAL MICROBIOMES: UNDERSTANDING FOREIGN BODY REACTIONS TO MESH IMPLANTATION

108

VAGINAL EXPOSURES CONNECTED TOREGIONAL MICROBIOMES: UNDERSTANDING FOREIGN BODY REACTIONS TO MESHIMPLANTATION

C. ELWOOD 1, E. PARK 2,N. A. KOENIG 3, G. W. CUNDIFF 3, J. HILL 4,R. GEOFFRION 3, D. MONEY 1, D. LANGE2;
1OBSTETRICS AND GYNECOLOGY, Univ. of British Columbia,Vancouver, Canada, 2Urology, Univ. of British Columbia,Vancouver, Canada, 3Univ. of British Columbia, Vancouver,Canada, 4Veterinary Microbiology, Univ. of Saskatchewan,Saskatoon, Canada.

Introduction: Vaginal meshexposure is a serious complication of surgery for pelvic organprolapse and stress urinary incontinence occurring in 10-30% ofwomen, causing chronic complications including pain and discharge andoften requiring re-operation 1,2. The underlying etiology of erosionis unknown, but may be associated with a foreign body response (FBR)driven by chronic inflammation. Little is known of this reaction inclinically utilized mesh in the vaginal environment as previousstudies evaluated vaginal mesh engraftment in the abdominalwall.
Objective: To determine the FBR to mesh engraftmentin a novel long-term vaginal mesh in vivo model of vaginal surgery tobetter understand the macrophage-specific response to implantedmesh.
Methods: 24 Sprague Dawley rats were used, 12 animalsunderwent mesh implantation in the anterior vaginal compartment,while 12 underwent sham surgery which included dissection of theanterior compartment and closure with suture but no meshimplantation. Following recovery animals were monitored visually forsigns of exposure. Three animals were sacrificed at 48h, 7d, 30d and90d post-operatively and tissue containing the mesh removed forhistological analysis. The expression of markers characteristic ofFBRs, iNOS and Arginase 1, was analyzed via qPCR.
Results:Mesh was implanted successfully. Histologic analysis demonstratedsignificantly more low level inflammation and giant cell formation inthe rats with mesh, a requirement for successful engraftment of meshlong term. qPCR demonstrated no significant difference in iNOS andarginase 1 expression, indicating equal distribution of M1 and M2type macrophages which drive mesh engraftment.
Conclusions:The normal FBR to implanted vaginal mesh material appears to bedriven by a balance between M1 and M2-type macrophages, suggesting amechanism that involves well-balanced inflammatory and wound-healingresponses. Our model allows for future studies identifying factorsthat disrupt this balance leading to mesh exposure potentiallyleading to the identification of modifiable risk factors prior tosurgical engraftment. Current efforts focus on translating thesefindings to clinical samples and evaluating a role for members of thevaginal microbiome in mediating mesh exposure.
References:1.Committee on Gynecologic Practice. (2011, December). CommitteeOpinion no. 513: vaginal placement of synthetic mesh for pelvic organprolapse. Obstetrics & Gynecology2. Abed H, Rahn DD,Lowenstein L, Balk EM, Clemons JL, Rogers RG. Incidence andmanagement of graft erosion, wound granulation, and dyspareuniafollowing vaginal prolapse repair with graft materials: a systematicreview. Int Urogynecol. J. 2011 Jul;22(7):789-98.