Peri-implantitis is currently a topic of major interest in implantology. Considered one of the main reasons of late implant failure, there is an emerged concern whether implant characteristics could trigger inflammatory lesion and loss of supporting bone. The purpose of this narrative review is to provide an evidence based overview on the influence of implant-based factors in the occurrence of peri-implantitis. A literature review was conducted addressing the following topics: implant surface topography; implant location; occlusal overload; time in function; prosthesis-associated factors (rehabilitation extension, excess of cement and implant-abutment connection); and metal particle release. Although existing data suggests that some implant-based factors may increase the risk of peri-implantitis, the evidence is still limited to consider them a true risk factor for peri-implantitis. In conclusion, further evidences are required to a better understanding of the influence of implant-based factors in the occurrence of peri-implantitis. Large population-based studies including concomitant analyses of implant- and patient-based factors are required to provide strong evidence of a possible association with peri-implantitis in a higher probability. The identification of these factors is essential for the establishment of strategies to prevent peri-implantitis.

It is believed that penetration of dentinal fluid into natural enamel caries (NEC) is negligible because of the barrier created by underlying sclerotic dentine, but there are conflicting evidences on whether dentine subjacent to NEC is sclerotic or demineralized. This study aimed at investigating the relationship between NEC, subjacent dentine reactions, modification of dentinal fluid, and composition of cariogenic biofilm formed on the NEC surface. Proximal NEC (PNEC) lesions of human permanent posterior teeth were included in five experiments. Histologically, microradiographic analysis with contrast solution (MRC) in dentine revealed a decreased proportion of sclerotic dentine and an increased proportion of deep dentine demineralization compared to the classical stereomicroscopic histological analysis based on dentin color and translucency. Real-time MRC and 3D optical profilometry, and 3D microtomographic analysis evidenced a facilitated transport of modified dentinal fluid towards PNEC lesions. Cariogenic biofilm formed in vitro on the PNEC surface presented lower amounts of insoluble and soluble matrix polysaccharides when 2% chlorexidine was inserted in the pulp chamber. In conclusion, this study evidenced that dentine subjacent to PNEC is mostly demineralized, providing facilitated pathway for dentinal fluid to penetrate into PNEC and alter the composition of the biofilm formed on the PNEC surface.