Abstract Bioabsorbable materials enable temporary implantation without the need for subsequent implant removal. The aim of the present experimental study was to evaluate the suitability of a fibrous bioabsorbable implant made of poly-L/D-lactide (PLDLA) 96/4 fibres as an episcleral implant. The general tissue reactions were evaluated in subcutaneous tissues in rats in follow-up periods ranging from 3 days to 48 weeks. The episcleral tissue reactions were studied in rabbits with follow-up periods of one, three, five and 48 weeks. A silicone sponge implant was used as a control material and operations were performed using similar technique with both implants. Tissue reactions were located just around the implant area and consisted of an acute inflammatory reaction in the early follow-up periods, continuing as a foreign body inflammatory reaction. With episcleral implants there were no inflammatory cells seen within the sclera or in the retinal layers, and the structure of the retina and the cornea was also normal. The biocompatibility was good in the 48 week follow-up despite the relatively high surface area of the fibrous implant. The material had not degraded by 48 weeks. The indentation effect by the PLDLA implant (diameter of 3–3.5mm) was lower than that achieved with the silicone sponge implant (diameter 4mm). The depth of indentation decreased over time in both groups with comparable rates over the follow-up period of 5 months. The duration of the indentation effect was sufficient to be used for scleral buckling in retinal detachment surgery. In conclusion, the biocompatibility of a fibrous implant made of PLDLA 96/4 placed subcutaneously and episclerally was good in the follow-up lasting 48 weeks despite the relatively high surface area of the implant. The fibrous implant made of PLDLA 96/4 seemed to be well-tolerated by ocular tissues and the indentation effect was sufficiently long.

Metal ions released from implantable biomaterials have been associated with adverse biological reactions that can limit implant longevity. Previous studies have shown that, in macrophages, Co2+, Cr3+, and Ni2+ can activate the NLR family pyrin domain-containing protein 3 (NLPR3) inflammasome, which is responsible for interleukin(IL)-1β production through caspase-1. Furthermore, these ions are known to induce oxidative stress, and inflammasome priming is known to involve nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling. However, the mechanisms of inflammasome activation by metal ions remain largely unknown. The objectives of this thesis were to determine if, in macrophages: 1. IL-1β release induced by metal ions is caspase-1-dependent; 2. caspase-1 activation and IL-1β release induced by metal ions are oxidative stress-dependent; and 3. IL-1β release induced by metal ions is NF-κB signaling pathway-dependent. Lipopolysaccharide (LPS)-primed murine bone-marrow-derived macrophages were exposed to Co2+, Cr3+, or Ni2+, with or without an inhibitor of caspase-1, oxidative stress, or NF-κB. Culture supernatants were analyzed for active caspase-1 (immunoblotting) and/or IL-1β (ELISA). Overall, results showed that while both Cr3+ and Ni2+ may be inducing inflammasome activation, Cr3+ is likely a more potent activator, acting through oxidative stress and the NF-κB signaling pathway. Further elucidation of the activation mechanisms may facilitate the development of therapeutic approaches to modulate the inflammatory response to metal ions, and thereby increase implant longevity.