Evaluation of Different Polymerisation Methods of Ocular Prosthesis Acrylic Resins on Subcutaneous Tissue Inflammatory Response in Rats.

Objectives: This study aimed to evaluate the influence of different polymerisation methods of acrylic resin for ocular prostheses on the subcutaneous tissue inflammatory response of rats. Methods: The study was conducted at the Basic Sciences Department, Araçatuba Dental School, São Paulo State University (UNESP), Brazil, from 2016 to 2018. The samples were prepared by water bath (WB), microwave energy (MW) or autopolymerisation (AP) (n = 20 samples per group). The inflammatory response (cell count and immunohistochemical analysis of interleukin [IL]-1ß, IL-6, tumour necrosis factor [TNF]-α, IL-17 and macrophage inflammatory protein-3α) was analysed by the implantation of a sample from each group in the subcutaneous tissue of 20 Wistar rats and evaluated after seven, 15, 30 and 60 days. The quantitative and qualitative data were analysed using analysis of variance and Tukey tests (P <0.05) and visual comparison, respectively. Results: There was a moderate inflammatory infiltrate for the MW and AP groups and a light infiltrate for the WB group after seven days. The inflammatory infiltrate and the immunolabeling of tested targets decreased gradually during the 60-day period. The AP group had the highest immunolabeling of TNF-α (seven days), IL-1ß and IL-17 (at 15 and 30 days) and IL-6 (at 30 and 60 days). The WB and MW groups showed greater immunolabeling at 15 and 30 days, while the MW group also had high results at 60 days. Conclusion: Polymerisation by microwave energy and by chemical activation resulted in a higher inflammatory response.

Neutrophil migration in inflammation: nitric oxide inhibits rolling, adhesion and induces apoptosis.

There is controversy in the literature over whether nitric oxide (NO) released during the inflammatory process has a pro- or inhibitory effect on neutrophil migration. The aim of the present investigation was to clarify this situation. Treatment of rats with non-selective, NG-nitro-L-arginine (nitro), or selective inducible NO synthase (iNOS), aminoguanidine (amino) inhibitors enhanced neutrophil migration 6h after the administration of low, but not high, doses of carrageenan (Cg) or Escherichia coli endotoxin (LPS). The neutrophil migration induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) was also enhanced by nitro or amino treatments. The enhancement of Cg-induced neutrophil migration by NOS inhibitor treatments was reversed by co-treatment with L-arginine, suggesting an involvement of the L-arginine/NOS pathway in the process. The administration of Cg in iNOS deficient (iNOS(-/-)) mice also enhanced the neutrophil migration compared with wild type mice. This enhancement was markedly potentiated by treatment of iNOS(-/-) mice with nitro. Investigating the mechanisms by which NOS inhibitors enhanced the neutrophil migration, it was observed that they promoted an increase in Cg-induced rolling and adhesion of leukocytes to endothelium and blocked the apoptosis of emigrated neutrophils. Similar results were observed in iNOS(-/-) mice, in which these mechanisms were potentiated and reverted by nitro and L-arginine treatments, respectively. In conclusion, these results suggest that during inflammation, NO released by either constitutive NOS (cNOS) or iNOS down-modulates the neutrophil migration. This NO effect seems to be a consequence of decreased rolling and adhesion of the neutrophils on endothelium and also the induction of apoptosis in migrated neutrophils.