Cellular proliferation and macrophage populations associated with implanted expanded polytetrafluoroethylene and polyethyleneterephthalate

Abstract

The chronic inflammatory response associated with the abluminal surface of polymeric vascular grafts has been suggested to affect adversely graft neovascularization, the cellular response at the luminal surface of vascular grafts, and overall graft patency. To better understand the source for this chronic inflammation, this study examined two types of macrophages and the amount of cellular proliferation around two widely used graft materials, expanded polytetrafluoroethylene (ePTFE) and polyethyleneterephthalate (PET or Dacron) implanted in the rat for 3 and 5 weeks. Serial sections of explants were analyzed for recruited macrophages (ED1), resident macrophages (ED2), and proliferating cells (PCNA). Results show that Dacron is more inflammatory than ePTFE and that there is a segregated macrophage response; the first 54 micrometer of perigraft tissue were composed predominantly of recruited macrophages (ED1+) while the more distal tissue consisted of resident macrophages (ED2+). Proliferating cells were located predominantly in this same 54 micrometer perigraft region. In subcutaneous tissue they accounted for 23% of all cells present around Dacron after 3 weeks of implantation and 8% after 5 weeks. Conversely, cellular proliferation around ePTFE increased from 4% at 3 weeks to 21% at 5 weeks. In adipose tissue, proliferation levels around the implanted polymers were lower and more similar after 3 and 5 weeks. Serial sections revealed the coordinate expression of PCNA and ED1 antigens by the same individual cells, suggesting that proliferation is a mechanism used to perpetuate the chronic inflammatory response. These results suggest a new target for designing treatments to alter inflammation and improve the healing associated with these biomaterials.

High 18F-FDG Uptake in Synthetic Aortic Vascular Grafts on PET/CT in Symptomatic and Asymptomatic Patients

“…The chronic aseptic inflammation in synthetic graft material, mediated primarily by macrophages, fibroblasts, and foreign-body giant cells, constitutes a potential base for 18 F-FDG uptake, even a long time after the operation (13)(14)(15).…”

“…However, synthetic grafts provoke a chronic low-grade inflammation (13)(14)(15). This chronic inflammation constitutes a potential site for 18 F-FDG uptake and, therefore, a risk for false-positive results.…”

18F-FDG Uptake in Noninfected Prosthetic Vascular Grafts: Incidence, Patterns, and Changes over Time

“…Diffuse 18 F-FDG uptake in noninfected grafts is the result of a local sterile inflammatory process around the prosthesis due to a foreign bodyrelated reaction. During this process, a relatively small number of inflammatory cells-such as macrophages, fibroblasts, and foreign body giant cells, known to take up small amounts of 18 F-FDGlocalized in the region of the graft (21,22,25). Notably, none of the noninfected grafts showed focal 18 F-FDG uptake.…”

“…18 F-FDG is also taken up by scar tissue and native vessels. Synthetic grafts often induce a foreign-body chronic low-grade inflammatory reaction, which can also exhibit increased 18 F-FDG activity, thus representing potential causes for false-positive results and erroneous interpretation of 18 F-FDG PET/CT studies (21)(22)(23). At present, there is only limited information regarding the incidence and patterns of 18 F-FDG uptake in noninfected vascular grafts, mainly in relationship to type and location of the implants.…”

Biocompatibility and Systemic Safety of a Novel Implantable Annuloplasty Ring for the Treatment of Mitral Regurgitation in a Minipig Model

“…The grade of granulomatous reaction was intermediate at the 64-day time point, but tended to subside (i.e., minimally present), in the 109-day terminal sacrifice time point. The presence of time-related reduction in the intensity of the foreign body granulomatous reaction toward the fabric is reported by Hagerty et al (2000). The granulomatous response was limited to the immediate interface between the ring and the endocardium and did not spill over in the adjacent neoendocardium, annulus, or myocardium.…”