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The limited physical and mechanical properties of polymethyl methacrylate (PMMA), the current gold standard, necessitates exploring improved denture base materials. While three-dimensional (3D) printing offers accuracy, efficiency, and patient comfort advantages, achieving superior mechanics in 3D-printed denture resins remains challenging despite good biocompatibility and esthetics. This review investigates the potential of innovative materials to address the limitations of 3D-printed denture base materials. Thus, this article is organized to provide a comprehensive overview of recent efforts to enhance 3D-printed denture base materials, highlighting advancements. It critically examines the impact of incorporating various nanoparticles (zirconia, titania, etc.) on these materials' physical and mechanical properties. Additionally, it delves into recent strategies for nanofiller surface treatment and biocompatibility evaluation and explores potential future directions for polymeric composites in denture applications. The review finds that adding nanoparticles significantly improves performance compared to unmodified resins, and properties can be extensively enhanced through specific modifications, particularly silanized nanoparticles. Optimizing 3D-printed denture acrylics requires a multifaceted approach, with future research prioritizing novel nanomaterials and surface modification techniques for a novel generation of superior performance, esthetically pleasing, and long-lasting dentures.

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BACKGROUND: Evolutionary arms race plays a major role in shaping biological diversity. In microbial systems, competition often involves chemical warfare and the production of bacteriocins, narrow-spectrum toxins aimed at killing closely related strains by forming pores in their target's membrane or by degrading the target's RNA or DNA. Although many empirical and theoretical studies describe competitive exclusion of bacteriocin-sensitive strains by producers of bacteriocins, the dynamics among producers are largely unknown. METHODOLOGY/PRINCIPAL FINDINGS: We used a reporter-gene assay to show that the bacterial response to bacteriocins' treatment mirrors the inflicted damage Potent bacteriocins are lethal to competing strains, but at sublethal doses can serve as strong inducing agents, enhancing their antagonists' bacteriocin production. In contrast, weaker bacteriocins are less toxic to their competitors and trigger mild bacteriocin expression. We used empirical and numerical models to explore the role of cross-induction in the arms race between bacteriocin-producing strains. We found that in well-mixed, unstructured environments where interactions are global, producers of weak bacteriocins are selectively advantageous and outcompete producers of potent bacteriocins. However, in spatially structured environments, where interactions are local, each producer occupies its own territory, and competition takes place only in "no man's lands" between territories, resulting in much slower dynamics. CONCLUSION/SIGNIFICANCE: The models we present imply that producers of potent bacteriocins that trigger a strong response in neighboring bacteriocinogenic strains are doomed, while producers of weak bacteriocins that trigger a mild response in bacteriocinogenic strains flourish. This counter-intuitive outcome might explain the preponderance of weak bacteriocin producers in nature. However, the described scenario is prolonged in spatially structured environments thus promoting coexistence, allowing migration and evolution, and maintaining bacterial diversity.

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Explaining the coexistence of competing species is a major challenge in community ecology. In bacterial systems, competition is often driven by the production of bacteriocins, which are narrow-spectrum proteinaceous toxins that serve to kill closely related species, providing the producer better access to limited resources. Bacteriocin producers have been shown to competitively exclude sensitive, nonproducing strains. However, the dynamics between bacteriocin producers, each lethal to its competitor, are largely unknown. In this study, we used in vitro, in vivo and in silico models to study competitive interactions between bacteriocin producers. Two Escherichia coli strains were generated, each carrying a DNA-degrading bacteriocin (colicins E2 and E7). Using reporter-gene assays, we showed that each DNase bacteriocin is not only lethal to its opponent but, at lower doses, can also induce the expression of its opponent's toxin. In a well-mixed habitat, the E2 producer outcompeted its adversary; however, in structured environments (on plates or in mice colons), the two producers coexisted in a spatially 'frozen' pattern. Coexistence occurred when the producers were initiated with a clumped spatial distribution. This suggests that a 'clump' of each producer can block invasion of the other producer. Agent-based simulation of bacteriocin-mediated competition further showed that mutual exclusion in a structured environment is a relatively robust result. These models imply that colicin-mediated colicin induction enables producers to successfully compete and defend their niche against invaders. This suggests that localized interactions between producers of DNA-degrading toxins can lead to stable coexistence of heterogeneously distributed strains within the bacterial community and to the maintenance of diversity.

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