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IMMUNOHISTOCHEMICAL TRENDS OF THE CONSEQUENCES OF MESH AND AUTODERM IMPLANTATION INTO THE ANTERIOR ABDOMINAL WALL IN RATS

Archiv Euromedica 2023 Score: 30 ? 0–100 AI score estimating relevance to the microplastics field. Papers below 30 are filtered from public browse.
Dmitry Parshin, A.M. Topchiev, Andrey Protasov, Mikhail Topchiev, А В Федосеев, Lev Brusnev, Lev Brusnev, Vladislav Murzov, Misrikhan Misrikhanov, Misrikhan Misrikhanov

Summary

This study compared the immune response triggered by polypropylene mesh implants versus biological tissue implants in the abdominal walls of rats. As polypropylene is a common surgical plastic, understanding its long-term tissue interactions helps assess risks from medical plastic implants that can shed microparticles over time.

Polymers
Models

This research involves a comparative study of the immunohistochemical features of the inflammatory response of the anterior abdominal wall tissues after implantation of the autoderm and polypropylene mesh in rats. The object of the study were 36 Wistar rats, which were divided into two groups of 18 specimens each. In the first group, a polypropylene mesh was implanted; in the second group, de-epithelialized skin (autoderm) was implanted. On days 3, 7, 14, 30, and 90, we studied: CD68 as a pan-macrophage marker, CD3 as a pan-lymphocyte marker, and Bcl-2 the apoptosis regulator. Statistical analysis was performed using the Spearman-Rho-Test. The peak of an acute inflammatory response in the tissues after the implantation of polypropylene mesh and autoderm occurs 72 hours after the surgery. Arresting of acute inflammatory response after autodermal implantation is achieved 30 days after surgery. A specific reaction of the anterior abdominal wall tissues to polypropylene, in contrast to the autoderm, is the formation of a persistent chronic inflammatory response 90 days after the operation, which is due to the starting biodegradation of the synthetic implant. The Spearman-Rho-Test showed a highly significant correlation between CD68 and CD3 (r = 0.341, p = 0.001). A high correlation was found between CD68 and Bcl-2 (r = 0.195, p = 0.033) and CD3 and Bcl-2 (r = 0.220, p = 0.021). CD3, CD68 and Bcl-2 markers give evidence of the severity of the inflammatory response.

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