Foreign Body Response to Subcutaneous Implants in Diabetic Rats

Abstract

Implantation of synthetic matrices and biomedical devices in diabetic individuals has become a common procedure to repair and/or replace biological tissues. However, an adverse foreign body reaction that invariably occurs adjacent to implant devices impairing their function is poorly characterized in the diabetic environment. We investigated the influence of this condition on the abnormal tissue healing response in implants placed subcutaneously in normoglycemic and streptozotocin-induced diabetes in rats. In polyether-polyurethane sponge discs removed 10 days after implantation, the components of the fibrovascular tissue (angiogenesis, inflammation, fibrogenesis, and apoptosis) were assessed. Intra-implant levels of hemoglobin and vascular endothelial growth factor were not different after diabetes when compared with normoglycemic counterparts. However, there were a lower number of vessels in the fibrovascular tissue from diabetic rats when compared with vessel numbers in implants from non-diabetic animals. Overall, the inflammatory parameters (neutrophil accumulation - myeloperoxidase activity, tumor necrosis factor alpha, and monocyte chemotactic protein-1 levels and mast cell counting) increased in subcutaneous implants after diabetes induction. However, macrophage activation (N-acetyl-β-D-glucosaminidase activity) was lower in implants from diabetic rats when compared with those from normoglycemic animals. All fibrogenic markers (transforming growth factor beta 1 levels, collagen deposition, fibrous capsule thickness, and foreign body giant cells) decreased after diabetes, whereas apoptosis (TUNEL) increased. Our results showing that hyperglycemia down regulates the main features of the foreign body reaction induced by subcutaneous implants in rats may be relevant in understanding biomaterial integration and performance in diabetes.

Efficient cutaneous wound healing using bixin-loaded PCL nanofibers in diabetic mice

“…Cutaneous wound healing in streptozotocin‐induced diabetic mice is a model established in the literature . Hyperglycemic condition in streptozotocin‐induced diabetic mice alters inflammation, angiogenesis and fibrogenesis, which result a delayed wound closure and increased scar area . We observed that Bix‐PCL1 nanofiber and Bix‐PCL2 nanofiber‐treated mice exhibited a significant increase in the percentage of wound closure.…”

“…[65][66][67] Hyperglycemic condition in streptozotocin-induced diabetic mice alters inflammation, angiogenesis and fibrogenesis, which result a delayed wound closure and increased scar area. 66,68 We observed that Bix-PCL1 nanofiber and Bix-PCL2 nanofibertreated mice exhibited a significant increase in the percentage of wound closure. This result suggests that, although the Bixin release from the PCL nanofibers is acting since initial days of wound healing and is more effective than PCL alone, increasing Bixin concentration on PCL higher hydrophobic nanofibers produced an unfavorable healing environment.…”

Venous Stenosis and Occlusion in the Presence of Endocardial Leads

“…In consequence, diabetes affects the cellular response to tissue injury and delays wound healing. In a study conducted on rats it was observed that fibrous formation and presence of foreign body giant cells, the typical features of the foreign body reaction, were attenuated in the hyperglycemic environment [19]. We assume that these effects may contribute to a decreased risk of venous stenosis in patients with indwelling endocardial leads.…”

Activated macrophages as key mediators of capsule formation on adipose constructs in tissue engineering chamber models

“…(Socarras et al, 2014;Lee et al, 2015;Lytle et al, 2015). (Socarras et al, 2014;Lee et al, 2015;Lytle et al, 2015).…”

“…It has been shown that capsular fibrosis appeared after chamber implantation due to an unavoidable foreign body reaction resulting from acute and chronic inflammation. (Socarras et al, 2014;Lee et al, 2015;Lytle et al, 2015). Generally, it is only a few days that acute inflammation could last, depending on the shape, size, and physicochemical properties of the implants .…”